Ipamorelin Peptide

Ipamorelin is a synthetic peptide that is composed of five amino acids, otherwise known as a pentadecapeptide (Aib-His-D-2-Nal-D-Phe-Lys-NH2), formally classified as a Growth Hormone Secretagogue (GHS). Its name is derived from the intention of its development. Ipamorelin peptide was designed to act via ghrelin receptor binding. The ghrelin receptors on the pituitary gland (the gland naturally involved with growth hormone, or hGH synthesis) are also known as Growth Hormone Secretagogue receptors (GHS-R). Through its implied action, Ipamorelin may host the potential to trigger the GHS-Rs on the pituitary gland and potentially stimulate the release of growth hormone.(1)

Overview

Ipamorelin is the first synthetic GHS that appears highly selective and may have the potential to augment the production of hGH without affecting other pituitary hormones such as prolactin or adrenocorticotropic hormone (ACTH). The potential increase in hGH might promote lipolysis and insulin-like growth factor-1 (IGF-1) production synthesis. Consequently, IGF-1 may become a mediator of hGH’s anabolic actions, and thereby the peptide may act to increase cellular proliferation and bone and muscle anabolism.(1)

Chemical Makeup

Molecular Formula: C38H49N9O5
\nMolecular Weight: 711.86 g/mol
\nOther Known Titles: NNC 26-0161

Research and Clinical Studies
\nIpamorelin Peptide and Selective Agonism

Based on one 1998 murine model-based research study, researchers suggested that Ipamorelin may release growth hormones from the pituitary cells. When Ipamorelin was presented to swine and pentobarbitone anesthetized rats, it reportedly exhibited release in growth hormones. Upon further observation, the researchers hypothesized that similar to other growth hormone (GH) stimulating peptides, Ipamorelin may be a growth receptor agonist stimulating GH release through potential affinity in growth hormone receptors. Moreover, the researchers commented that Ipamorelin appears to be the first GHS-R “agonist with a selectivity for GH release similar to that displayed by GHRH. The specificity of Ipamorelin makes this compound a very interesting candidate for future clinical development.”(1) Scientific research studies have also suggested that Ipamorelin may lead to increased hGH secretion, possibly without significantly affecting other pituitary hormones such as the levels of prolactin or ACTH.(2)

Ipamorelin Peptide and Growth Hormone Synthesis

Studies conducted in vitro suggest that the interaction of Ipamorelin with GHS receptors may potentially affect somatotroph cells in the anterior pituitary gland by triggering a series of cellular signaling events.(3) This theorized pathway involves the activation of phospholipase C (PLC), which some researchers believe may lead to the increased release of inositol triphosphate (IP3) and diacylglycerol (DAG). This release of secondary messenger molecules such as IP3 might potentially stimulate the discharge of calcium ions (Ca2+) from the cell’s internal stores, while DAG might activate protein kinase C (PKC). The subsequent rise in intracellular calcium levels and the possible activation of PKC are thought to result in the exocytosis of vesicles filled with growth hormones from these pituitary cells.(3)

In late 1999, a clinical trial was carried out on eight test subjects where Ipamorelin was presented every 15 minutes for a set period. Two hours post-study, it was suggested by the researchers that the levels of growth hormone had apparently increased. More specifically, Ipamorelin appeared to have tended to boost growth hormone levels, potentially soaring to as much as 80mIU/l (roughly equivalent to a concentration of about 26.6ng/ml). When this increase is measured as a percentage compared to a placebo (with a baseline of 1.31mIU/l or 0.4ng/ml), the enhancement appeared to have exceeded a 60-fold uplift.(4)

Ipamorelin Peptide and Bone Tissue

It is conceivable that Ipamorelin may positively influence bone mineral density. The theory posits that Ipamorelin might stimulate osteoblasts (cells responsible for bone formation) via hGH-mediated mechanisms, potentially leading to their enhanced proliferation, growth, and specialization. In a particular study, murine models were exposed to either Ipamorelin or a placebo.(5) The impact of Ipamorelin on bone mineral density in these mice was monitored closely through real-time dual X-ray absorptiometry (DEXA) assessments at critical sites, including the femur and L6 vertebra. Post-experiment, the femur bones were further examined using mid-diaphyseal peripheral quantitative computed tomography (pQCT) scans. Preliminary findings implied that the peptide may have contributed to increased body mass and a probable elevation in the overall tibial and vertebral BMC (bone mineral content) as detected by DEXA compared to the placebo group. Further, the pQCT data appeared to suggest that the observed augmentation in cortical BMC may have stemmed from an enlargement in the cross-sectional area of the bone. In contrast, the cortical volumetric bone mineral density (BMD, which denotes the ratio of BMC to area) appeared to remain steady. Thus, there may have been an enlargement in the volumes of the femur and the L6 vertebrae since BMC appeared to increase while the volumetric BMDs appeared unchanged.(5)

Ipamorelin Peptide and Digestion

Researchers have delved into the potential of Ipamorelin in the functionality of the stomach, with a keen interest in its ability to possibly expedite the process of gastric emptying. For example, one study employed a technique to ascertain gastric emptying rates, which entailed monitoring the proportion of a marked substance that lingered in the stomach 15 minutes after its introduction through intragastric gavage.(6) The scientists conducted surgeries to purposefully decelerate the gastric emptying process in murine models. This deceleration was particularly noticeable in the control group. In contrast, Ipamorelin appeared to have markedly accelerated the emptying process compared to the control. This observation led the team to hypothesize that Ipamorelin might be able to increase the velocity of gastric emptying. Additional research was initiated to delve deeper into the action of the compound on the contractile potential of the stomach’s smooth muscles, which were activated by acetylcholine and electrical field stimulation. Indeed, the decelerated peristalsis appeared to be mitigated when Ipamorelin and ghrelin were studied together, suggesting the idea that Ipamorelin may enhance the contractility of gastric smooth muscles.(6)

Ipamorelin Peptide and Appetite

The potential actions of Ipamorelin on ghrelin receptors may lead to an enhancement in hunger signals and, perhaps, an ensuing augmentation in body mass. Research suggests that research models exposed to Ipamorelin were observed to sustain an estimated 15% surge in body weight.(7) Researchers speculate that this substance might have led to a proportional increase in the weight of fat pads in comparison to the total body weight. Consequently, DEXA scans might indicate a comparative rise in body fat percentage. Moreover, there is speculation among researchers that Ipamorelin might elevate serum leptin levels, a hormone considered to play a crucial role in energy balance and hunger regulation. This observation has prompted scientists to consider increased food consumption as a potential contributor to the weight gain noted in research models exposed to Ipamorelin. They have posited that “GHSs increase body fat by GH-independent mechanisms that may include increased feeding.”(7)

Ipamorelin Peptide and Nitrogen Balance

Researchers have suggested that Ipamorelin may potentially mediate anabolic action, which may be due to its potential in hGH and IGF-1 synthesis and may be assessed through its impact on nitrogen balance. In a distinct investigation, researchers aimed to explore the action of Ipamorelin on specific liver markers associated with alpha-amino-nitrogen conversion during induced catabolic states.(8) The study focused on the liver’s capacity to synthesize urea-N (CUNS), which may serve as an indicator of the organ’s ability to process nitrogen. The levels of messenger RNA (mRNA) related to liver urea cycle enzymes were scrutinized, alongside an assessment of the overall nitrogen balance and a hypothesis regarding nitrogen distribution across various organs. The findings suggested that Ipamorelin might have contributed to a possible 20% reduction in CUNS compared to the artificially induced catabolic condition. Furthermore, it might have diminished the expression of urea cycle enzymes, possibly restored nitrogen balance, and, in theory, altered or improved nitrogen concentrations in different organs.(8)

Ipamorelin peptide is available for research and laboratory purposes only. Please review and adhere to our before ordering.

References:
\nK. Raun et al., Ipamorelin, the first selective growth hormone secretagogue, Endocrinology, November 1998.
\nSinha DK, Balasubramanian A, Tatem AJ, Rivera-Mirabal J, Yu J, Kovac J, Pastuszak AW, Lipshultz LI. Beyond the androgen receptor: the role of growth hormone secretagogues in the modern management of body composition in hypogonadal males. Transl Androl Urol. 2020 Mar;9(Suppl 2):S149-S159. doi: 10.21037/tau.2019.11.30. PMID: 32257855; PMCID: PMC7108996
\nJiménez-Reina, L., Cañete, R., de la Torre, M. J., & Bernal, G. (2002). Influence of chronic treatment with the growth hormone secretagogue Ipamorelin, in young female rats: somatotroph response in vitro. Histology and histopathology, 17(3), 707–714.
\nGobburu, J.V.S., Agersø, H., Jusko, W.J. et al. Pharmacokinetic-Pharmacodynamic Modeling of Ipamorelin, a Growth Hormone Releasing Peptide, in Human Volunteers. Pharm Res 16, 1412–1416 (1999).
\nSvensson, J., Lall, S., Dickson, S. L., Bengtsson, B. A., Rømer, J., Ahnfelt-Rønne, I., Ohlsson, C., & Jansson, J. O. (2000). The GH secretagogues ipamorelin and GH-releasing peptide-6 increase bone mineral content in adult female rats. The Journal of endocrinology, 165(3), 569–577.
\nGreenwood-Van Meerveld, B., Tyler, K., Mohammadi, E., & Pietra, C. (2012). Efficacy of ipamorelin, a ghrelin mimetic, on gastric dysmotility in a rodent model of postoperative ileus. Journal of experimental pharmacology, 4, 149–155.
\nLall, S., Tung, L. Y., Ohlsson, C., Jansson, J. O., & Dickson, S. L. (2001). Growth hormone (GH)-independent stimulation of adiposity by GH secretagogues. Biochemical and biophysical research communications, 280(1), 132–138.
\nAagaard, N. K., Grøfte, T., Greisen, J., Malmlöf, K., Johansen, P. B., Grønbaek, H., Ørskov, H., Tygstrup, N., & Vilstrup, H. (2009). Growth hormone and growth hormone secretagogue effects on nitrogen balance and urea synthesis in steroid treated rats. Growth hormone & IGF research: official journal of the Growth Hormone Research Society and the International IGF Research Society, 19(5), 426–431.

Dr. Marinov (MD, Ph.D.) is a researcher and chief assistant professor in Preventative Medicine & Public Health. Prior to his professorship, Dr. Marinov practiced preventative, evidence-based medicine with an emphasis on Nutrition and Dietetics. He is widely published in international peer-reviewed scientific journals and specializes in peptide therapy research.

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AOD 9604 Peptide

AOD 9604 peptide is a synthetic analog of growth hormone designed with the intention of mitigating obesity and aiding weight loss. The peptide is a modified fragment of the growth hormone where the last 16 amino acids (176-191) have been reproduced as a specific peptide, called GH Fragment 176-191 or simply AOD 9604. It also has a tyrosine residue to replace the first amino acid at the N-terminus, which researchers consider to help increase the stability of the peptide.(1)

More specifically, AOD 9604 is considered the lipolytic fragment of GH as different parts of the GH molecule appease to have different potentials. For instance, studies suggest that out of its 191 amino acid structure “the N-terminal region exhibits an insulin-potentiating action, while amino acids 108 – 129 of hGH were found to evoke high mitogenic responses.”(2)

Overview

AOD 9604 peptide was developed in the 1990s in an effort to develop proteins which might exhibit anti-obesity properties similar to Growth Hormone (hGH). Rigorous scientific studies and experiments have since been conducted to determine the potential action of AOD 9604 in lipolysis.(1) Lipolysis is a term to describe the process through which stored fats or triglycerides in fat cells are broken down into glycerol and free fatty acids, which may be used as an energy source by other cells. Enzymes such as lipase appear to play a critical role in this process, helping in the breakdown of these fats. It’s possible that AOD9604 may influence the fat cells and lipolytic receptors, particularly given its observed association with changes in weight and fat in murine models. Research study findings indicate that the fragment seems to have the capacity to amplify lipolytic sensitivity following its introduction. Furthermore, the study hypothesizes a potential interaction of AOD9604 with the beta-adrenergic pathway, especially concerning the beta(3)-adrenergic receptors (beta(3)-AR), which are considered to be key lipolytic receptors found in fat cells. While it is not entirely clear, the expression level of beta(3)-AR RNA, the primary lipolytic receptor in fat cells, was observed to increase in the presence of AOD 9604. This could possibly suggest that the peptide might be playing a role in enhancing the sensitivity of these lipolytic receptors, potentially making them more responsive to lipolytic stimuli. However, it is essential to note that while the peptide appears to elevate the expression of beta(3)-AR, it may not act directly through the beta(3)-AR to induce its potential lipolytic action.

Scientists and researchers have suggested that the modified portion of the hGH in the AOD 9604 peptide may be responsible for significantly inducing the fat burning process, possibly without stimulating the production of Insulin-like Growth Factor IGF 1, as opposed to the natural growth hormone.

Chemical Makeup

Molecular Formula: C78H123N23O23S2
\nMolecular Weight: 1815.12 g/mol
\nOther Known Titles: Tyr-hGH Fragment 177-191

Research and Clinical Studies
\nAOD 9604 Peptide and Lipolytic Activity

Early studies were carried out on obese mice where the AOD 9604 peptide was periodically introduced for 14 days. Following the experiment, the results reported a reduction in weight and excess fat. These results appeared directly correlated with the increased levels of major lipolytic receptors, beta(3)-AR, found in the fat cells. AOD 9604 peptide appeared to exhibit action similar to hGH wherein both may be capable of increasing repressed levels of lipolytic receptors in obese mice as compared to the lean mice. To confirm whether the lipolytic action of AOD 9604 might merely be associated with the increased lipolytic receptor levels, additional studies were carried out where AOD 9604 was given to mice with knocked out lipolytic receptors. Further analysis suggested that the AOD 9604 peptide enacted the lipolytic action via increased energy expenditure and fat oxidation.(1) Both these findings on chronic and acute action of AOD 9604 suggested that while enhanced beta(3)-AR expression may have played a role in the chronic action of the compound, beta(3)-AR might not be the sole arbiter in this reaction. Oxidation and enhanced energy expenditure appeared to be vital in the proposed action of the peptide.

In 2000, a research study was carried out in obese Zucker rats where the AOD 9604 peptide was given daily for 19 consecutive days. Following the study, it was reported that weight appeared to be reduced in all rats by over 50%, in comparison to the rats given a placebo. Further analysis suggested that the adipose tissues of the AOD 9604 peptide animals had increased lipolytic activity and no marked insulin sensitivity interruption in the animals.(3)

AOD 9604 Peptide and Obesity

In 2004, clinical trials observed the actions of the peptide in 300 obese subjects who were given the peptide for 12 weeks. The rate of weight loss remained consistent throughout the study period. The trial results noted minor improvement exhibited in the subjects’ cholesterol profiles and glucose tolerance levels.(4)

AOD 9604 Peptide and Cell Regeneration

Additional research was conducted to study the regenerative potential of the peptide. In 2015, 32 white rabbits were divided into four groups of eight, and each group was given a placebo, AOD 9604, hyaluronic acid, or a combination of AOD 9604 and hyaluronic acid for 4 to 7 weeks. After the study, these rabbits were assessed morphologically and histopathologically to determine the degree of cartilage degeneration. It was concluded that rabbits given the combination of AOD 9604 with hyaluronic acid apparently exhibited the least degeneration. Thus, it was suggested by the researchers that AOD 9604 might exhibit potential to enhance cartilage regeneration and cartilage repair in some capacity.(5)

This may be due to the potential role of AOD 9604 in cellular differentiation processes and, potentially, in the synthesis of proteins important for tissue repair. According to an in vitro study, AOD 9604 may possibly enhance the differentiation of adipose mesenchymal stem cells into bone(5). These stem cells, which are typically found within fat tissue, may have the potential to evolve into various cell types. It has been hypothesized that under the influence of AOD 9604, these stem cells may show a predisposition to differentiate into bone cells. Moreover, when the research was conducted on isolated bovine chondrocytes, it appeared that there might be an increased production of proteoglycan and collagen. Chondrocytes are cells believed to be found within cartilage tissue, and they possibly play a role in producing and maintaining the extracellular matrix, which consists of components like collagen and proteoglycans. It is posited that the presence of AOD 9604 could stimulate these chondrocytes to produce more of these vital components. The study also hints at the idea that AOD 9604 might promote the differentiation of myoblasts into C2C12 cells. Myoblasts are thought to be precursor muscle cells, and C2C12 cells are a type of murine model muscle cell line. From what the study suggests, AOD 9604 may assist in the transition of these precursor cells into a more mature form. The research seems to underline the potential role AOD 9604 might have in processes connected to the repair of bone, cartilage, and muscle tissues.

AOD 9604 and Research in Cancer Cells

The peptide may be able to bind (target) tumor-related proteins to enhance tumor drug accumulation and local cytotoxicity.(6) The hGH fragment AOD 9604 may potentially play a pivotal role in cancer cell research, as it has been observed to enhance the anticancer efficacy of doxorubicin, a commonly recognized chemotherapeutic agent. One study utilized chitosan nanoparticles, a biocompatible and biodegradable polymer, as a carrier for doxorubicin and AOD 9604.(6) The research team hypothesized that AOD 9604 possibly enhanced the doxorubicin binding to multiple breast cancer cell protein targets, thereby exhibiting greater anti-proliferative activity against the MCF-7 breast cancer cell line compared to chitosan loaded with doxorubicin alone. This suggests that AOD 9604 may potentially augment the anti-cancer potency of doxorubicin while possibly minimizing unintended actions associated with non-target tissue exposure. In conclusion, multiple clinical studies have suggested that the peptide may significantly induce lipolysis and possibly prevent lipogenesis by mimicking natural hGH.

AOD 9604 is available for research and laboratory purposes only. Please review and adhere to our before ordering.

References:
\nMark Heffernan, Roger J. Summers, Anne Thorburn, Esra Ogru, Robert Gianello, Woei-Jia Jiang, Frank M. Ng, The Effects of Human GH and Its Lipolytic Fragment (AOD 9604) on Lipid Metabolism Following Chronic Treatment in Obese Mice and β 3-AR Knock-Out Mice, Endocrinology, Volume 142, Issue 12, 1 December 2001, Pages 5182–5189.
\nMoré, M. I., & Kenley, D. (2014). Safety and metabolism of AOD9604, a novel nutraceutical ingredient for improved metabolic health. Journal of Endocrinology and Metabolism, 4(3), 64-77.
\nFrank M. Ng, J Sun et.al, Metabolic Studies of a Synthetic Lipolytic Domain (AOD 9604) of Human Growth Hormone, Hormone Research, February 2000.
\nNews, Medical and Life Sciences, Obesity drug codenamed AOD 9604 highly successful in trials, 16 December 2004.
\nDong Rak Kwon and GI Young Park, Effect of Intra-articular Injection of AOD9604 with or without Hyaluronic Acid in Rabbit Osteoarthritis Model, Annals of Clinical and Laboratory Science, Volume 45, July-August 2015.
\nHabibullah, M. M., Mohan, S., Syed, N. K., Makeen, H. A., Jamal, Q. M. S., Alothaid, H., Bantun, F., Alhazmi, A., Hakamy, A., Kaabi, Y. A., Samlan, G., Lohani, M., Thangavel, N., & Al-Kasim, M. A. (2022). Human Growth Hormone Fragment 176-191 Peptide Enhances the Toxicity of Doxorubicin-Loaded Chitosan Nanoparticles Against MCF-7 Breast Cancer Cells. Drug design, development and therapy, 16, 1963–1974.

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Acetate",43,93,"https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/913c43a6-c5c6-4233-bfbb-90f4dbd6e423.png",[509],[505,506],{"_124":508,"_153":154,"_155":500,"_141":142,"_134":-5},{"_124":507,"_153":174,"_155":501,"_141":142,"_134":-5},"5297d68a-d5f8-437e-9442-ccf93dc32dd3","52fe5961-6d2e-4401-983a-eb9416dfb866","https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/gallery/beda881c-6efd-4877-a362-5d40e0374633.png","78511bca-0507-437b-9fdb-9f141611d844","HCG",90,"https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/0fd6059e-1311-448a-b391-45e61bbdfbf2.png",[522],[516,517],{"_124":520,"_153":521,"_155":512,"_141":142,"_134":-5},{"_124":518,"_153":519,"_155":198,"_141":142,"_134":-5},"dfab7390-a192-4664-a3ef-c4d3a36d5d9e","10000iu*10vials","ca04b692-c869-4efb-b9c1-28dc72c1ed04","5000iu*10vials","https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/gallery/05af356f-d7c7-4ce0-af83-3e9633c6e02f.png","7df7cda8-427c-4203-bc6c-808789c9c34c","FOXO4-DRI",384,"https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/2c111339-05c3-43ec-a1c0-3066f7d09f62.png",[531],[529],{"_124":530,"_153":172,"_155":525,"_141":142,"_134":-5},"9866257a-4aae-40fa-9655-18522979bf65","https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/gallery/490657e4-c27b-4556-a378-f6a8964bd34a.png","28aee0b9-56fc-4e1a-bb96-b0252f756688","FOX04",360,"https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/df3d277f-bbc8-4aa7-99c7-d5e01e2932d4.png",[542],[538,539],{"_124":541,"_153":154,"_155":285,"_141":142,"_134":-5},{"_124":540,"_153":172,"_155":534,"_141":142,"_134":-5},"e7ad7857-ad4b-43e2-8ddc-72c163b92140","9d3b1b28-595f-4291-86c1-d4f28b9d5e13","https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/gallery/8444a795-3b00-40f9-94fa-c912b2308d2b.png","4c27fe61-795a-46c5-b187-8a0d79a092a2","Cagrilintide",120,160,"https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/9f5bc50b-a347-46a3-a828-6b18d2b78fae.png",[554],[550,551],{"_124":553,"_153":174,"_155":545,"_141":142,"_134":-5},{"_124":552,"_153":172,"_155":546,"_141":142,"_134":-5},"2ba3d377-706f-4ecd-a293-6cbd1c399390","548ae786-f120-47c4-a502-eafcfa466b85","https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/gallery/b51ee0c4-26a1-4d89-a9a8-ce7c41aef914.png","677f268e-6962-45f6-97b8-8dd7aefe6aca","Aicar","AR50",103,"https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/8c5ce78f-6621-4fb1-a79b-592d21fbd5fa.png",[566],[562,563],{"_124":565,"_153":336,"_155":223,"_141":142,"_134":-5},{"_124":564,"_153":397,"_155":558,"_141":142,"_134":-5},"c685cd4c-4da0-4bab-bc6e-6583bf56e2dc","e58d993d-46ce-42e9-a930-f852d61f791a","https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/gallery/63a99a18-63c8-4a03-a8ef-5ff64d5b4fc4.png","f4809ce0-f6d4-4029-8123-a0f624d11eb2","Adipotide_FTTP",122,"https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/1d2b16bc-9c9f-4347-846e-6fcdab8f34c0.png",[575],[573],{"_124":574,"_153":174,"_155":569,"_141":142,"_134":-5},"46829503-65ea-4e72-a317-0759c93a628e","https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/gallery/b4305d00-902b-4f95-86f7-45b779d0aaef.png","e2deea85-7fdc-42e6-bba5-74f0808f3b33","Retatrutide","retatrutide",92,582,"https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/32d6de74-ea4a-4bef-b2b4-58d5a0613ad2.png",[611],[584,585,586,587,588,589,590,591,592],{"_124":610,"_153":174,"_155":579,"_141":142,"_134":-5},{"_124":608,"_153":172,"_155":609,"_141":142,"_134":-5},{"_124":605,"_153":606,"_155":607,"_141":142,"_134":-5},{"_124":603,"_153":383,"_155":604,"_141":142,"_134":-5},{"_124":600,"_153":601,"_155":602,"_141":142,"_134":-5},{"_124":598,"_153":205,"_155":599,"_141":142,"_134":-5},{"_124":597,"_153":336,"_155":374,"_141":142,"_134":-5},{"_124":594,"_153":595,"_155":596,"_141":142,"_134":-5},{"_124":593,"_153":397,"_155":580,"_141":142,"_134":-5},"e22bf75d-ae7f-4c1f-b888-9970f1de6ed1","6cf8815b-7cd5-4b74-82e0-4ee1e4344eda","60mg*10vials",434,"cb423c14-86ae-49a9-9fa4-7ad177889e04","0fecfe4a-e4c8-421b-82df-7adfb24ac893",310,"a09b9f6a-cba2-4e85-a7be-17e4f5b7e833","30mg*10vials",285,"5155cd24-03e8-48bc-809b-67fabfcba666",183,"f876d38d-32a4-44f9-9aad-57fda8706c46","15mg*10vials",140,"eec117ed-e04c-4dbb-b50f-4acd38e64445",130,"f2cf776b-c0ce-459b-ac83-00acb72bd1e6","https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/gallery/5435a52e-4c83-4137-abca-99de51b7cb3f.png","cf04bd0f-f7d1-4d41-9313-3ecaaa429349","Tirzepatide","tirzepatide","

Tirzepatide is a synthetic analogue of gastric inhibitory polypeptide (GlP) that wasdeveloped for its ability to stimulate insulin release and thus address both type 2 diabetesand non-alcoholic fatty liver disease. Made up of 39 amino acids, the relatively largeTirzepatide stimulates the release of insulin from the pancreas by binding to both GIP andGLP-1 (glucagon-like peptide-1)receptors. Taken over longer periods of time, Tirzepatideincreases adiponectin levels by as much as 26% as well[1].

Amino Acid Sequence: YE-Aib-GTFTSDYSI-Aib-LDKIAQ (C20 fattyacid)AFVQWLIAGGPSSGAPPPS

Note: Aib is a non-coded (non-proteinogenic) amino acid – HzH-C(CH3)2-COOH

Molecular Formula: C225H348N48O68

Molecular Weight: 4813.527 g/mol

PubChem ClD: 156588324

CAS Number: 2023788-19-2

Synonyms: P1206,LY3298176

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NAD+ Peptide

NAD+ is an acronym for Nicotinamide Adenine Dinucleotide, an endogenous nucleotide that is considered to regulate primary functions such as metabolism, energy production, and DNA repair. It is also considered to act as a secondary messenger via calcium-dependent signaling mechanisms, possibly serving as an immunoregulatory component.(1)(2) NAD+ is considered by researchers to be naturally synthesized via the de novo mechanism of converting the amino acid tryptophan through several enzymatic steps. Researchers posit that there are five components to NAD+ synthesis, including tryptophan, nicotinamide, nicotinic acid, nicotinamide riboside, and nicotinamide mononucleotide.(3) Once synthesized, research suggests it exerts over 500 enzymatic reactions and cellular processes(12) to aid metabolic activities. Essentially, it is suggested to act as a coenzyme in redox functions, converted to NADH (the energy-carrying form of NAD+), which may involve other metabolic pathways.

Overview

Researchers have suggested Nicotinamide Adenine Dinucleotide (NAD+) to act as a coenzyme, with three major classes of enzymes including:

Deacetylase enzymes in the sirtuin class (SIRTs)
\nPoly ADP ribose polymerase (PARPs) enzymes, and
\nCyclic ADP ribose synthetase (cADPRS)

Research suggests that each class of enzymes interacts with NAD+ in the following possible respects:

SIRTs may stimulate mitochondrial homeostasis, stem cell regeneration, loss of stem cells, and nerve degeneration.
\nPARPs, composed of 17 different enzymes, may act alongside NAD+ enzymes and synthesize poly ADP ribose polymers, which may lead to genome stability.
\ncADPRS include CD38 and CD157, which are considered to be key immunological cells. cADPRS appears to hydrolyze NAD+ and thereby may stimulate stem cell regeneration and DNA repair, which may be important for maintaining cell cycles.

Researchers suggest the above-mentioned enzymes to be NAD+ dependent enzymes, possibly acting based on the presence of Nicotinamide Adenine Dinucleotide (NAD). Researchers suggest that should all three enzymes be dependent on NAD+, they may potentially compete amongst themselves for bioavailability. It has been posited that the potential function of SIRTs, for instance, may lead to reduced PARPs activity and, thereby, potentially lead to weakened systems. Hence, it may be critical to maintain a balance between the availability and consumption of NAD+ to obtain optimal potential impact.(5)

Chemical Makeup

Molecular Formula: C21H27N7O14P2
\nMolecular Weight: 663.43 g/mol
\nOther Known Titles: nicotinamide adenine dinucleotide

Research and Clinical Studies
\nNAD+ Peptide and Productive Aging

Researchers suggest that NAD+ has two key intermediates: nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN). Studies have indicated that these intermediates may be potent agents for promoting ‘productive aging.’ In a study,(7) normal-aging mice were exposed to the NMN intermediate for 12 months. Following the study, the researchers suggested that NMN may promote NAD+ synthesis in the mice. Peptide exposure may have been the catalyst for the observed reduced weight gain, increased energy metabolism, enhanced physical activity, improved lipid profile, and other physiological impacts in the mice.

NAD+ Peptide and Neurodegenerative Activity

Scientists consider mitochondrial dysfunction to lead to various functional limitations in the electron transport chain and ATP (energy) synthesis, possibly resulting in various neurodegenerative diseases. A study(8) was conducted where aged mice were exposed to NMN, a NAD+ intermediate, for 3 to 12 months. The study’s main aim was to evaluate the potential impact of the peptide on mitochondrial respiratory processes, for which fluorescent NMN protein was presented to the mice models. After peptide introduction, the mitochondrial oxygen consumption rates in the nerve and brain cells of the mice were studied. Upon analysis, it was suggested that mitochondrial functions had been restored in the aged mice, suggesting that NMN may be immediately utilized by the cells to produce NAD+, exerting a possible positive impact.

NAD+ Peptide and DNA Repair After Ischemic Stress

The main aim of this study(11) was to determine the neuroprotective potential of Nicotinamide Adenine Dinucleotide against ischemic stress induced in mice. For this study, ischemic stress was induced in the neuronal cultures in rats via deprivation of oxygen and glucose for about 2 hours. NAD+ was directly replenished into the culture medium before or after the induced ischemic stress. After 72 hours of introducing NAD+ into the cultures, it was reported by the researchers that the DNA base excision repair activity (DNA BER), cell viability, and oxidative DNA damage repair appeared to be significantly improved, irrespective of whether Nicotinamide Adenine Dinucleotide was added before or after inducing the ischemic stress.

Indeed, NAD+ appears crucial for DNA integrity, with studies focusing on the enzyme poly(ADP-ribose) polymerase (PAR polymerase or PARP), which might depend on NAD+ for activating DNA repair. In the event of DNA damage, it is thought that PARP might be triggered, potentially attaching itself to the DNA’s damaged parts. Researchers suggest that PARP might utilize NAD+ molecules to add ADP-ribose units to itself and other proteins in a process known as PARylation, potentially aiding in the attraction and activation of other DNA repair proteins and thereby assisting in repairing DNA damage.(15) This PARylation may lead to the formation of PAR chains, which might signal the DNA repair systems to identify and address DNA damage. PARP is also considered to have a role in detecting and mending single-strand DNA breaks. If NAD+ is confirmed as a necessary cofactor, PARP may be important in preserving genomic stability by initiating DNA repair mechanisms. However, this activity could also reduce NAD+ levels within cells, potentially affecting other NAD+-dependent processes like energy production and cellular signaling. It has been noted that DNA damage may cause a rapid increase in PAR synthesis, possibly using up significant amounts of NAD+. Consequently, researchers are exploring the idea that NAD+ depletion, triggered by PAR polymerase activation, might influence the NAD+/SIRT1 pathway, potentially affecting mitochondrial function, ROS production, DNA repair, and cell survival.(16) Consequently, the reintroduction of NAD+ in such settings may compensate for this and may be posited to support the process of DNA repair and cell survival.

NAD+ Peptide and the Liver, Kidney

Upon introducing experimental mice with the NAD+ peptide and stimulating an increase in Nicotinamide Adenine Dinucleotide levels up to normal concentrations, researchers suggested the peptide exhibited positive potential in preventing obesity and alcoholic hepatitis while possibly improving glucose homeostasis and overall liver function. When aged mice kidney cells were supplemented with NAD+, the results indicated that adding the peptide possibly promoted SIRTs activity, which exhibited neuroprotective potential against glucose-induced kidney cell hypertrophy. Furthermore, when presented with NMN, NAD+ intermediate, it appeared to promote neuroprotective impact against cisplatin-induced kidney injury.(12)

NAD+ Peptide and Skeletal Function

Upon presenting aged mice with NMN daily for 7 days, researchers suggested that the peptide possibly increased ATP production, reduced inflammation, and elevated mitochondrial functions.(13) The researchers considered this may have been due to the role that NAD+ appears to play in cellular respiration and energy production, specifically acting as a helper molecule in redox reactions, which may be vital to converting nutrients into energy. This process, known as cellular respiration, is thought to allow cells to produce usable energy through a series of steps, and NAD+ is believed to play a key role in two specific phases: glycolysis and the citric acid cycle (or Krebs cycle). In glycolysis, the initial breakdown of glucose into pyruvate is suggested to be produced by a small amount of ATP and NADH. Here, NAD+ is thought to accept electrons and a hydrogen ion from glucose, turning into NADH. This transformation might allow NADH to transport these high-energy electrons to a later stage of energy production. Following glycolysis, pyruvate is further broken down in the citric acid cycle, potentially releasing more energy. NAD+ is implicated in various reactions during this cycle, possibly accepting electrons and hydrogen ions to form NADH. These crucial steps are considered to happen directly within the mitochondria. The NADH formed during both glycolysis and the citric acid cycle is presumed to carry high-energy electrons to the electron transport chain, the last step of cellular respiration. At this stage, NADH may give up its electrons, creating an electrochemical gradient and a chain reaction that drives protons across the mitochondrial membrane. This action appears to lead to the combination of electrons and protons with oxygen to produce water, and the energy released during this process may be used to generate ATP through oxidative phosphorylation. As NADH relinquishes its electrons, it may be transformed back into NAD+, ready to assist in another glycolysis and citric acid cycle. This regeneration of NAD+ is considered to be crucial for the ongoing production of ATP, thus maintaining the cell’s energy supply.

NAD+ Peptide and Cardiac Functions

Researchers have suggested Nicotinamide Adenine Dinucleotide deficiency may lead to reduced SIRT activity, which may in turn cause reduced energy production and aortic constriction. When mice were exposed to NMN 30 minutes prior to induced-ischemia, the peptide reportedly produced a cardioprotective function against ischemic injury.(14)

NAD+ peptide is available for research and laboratory purposes only. Please review and adhere to our before ordering.

References:
\nSchultz, Michael B, and David A Sinclair. “Why NAD(+) Declines during Aging: It’s Destroyed.” Cell metabolism vol. 23,6 (2016): 965-966.
\nBraidy N, Liu Y. NAD+ therapy in age-related degenerative disorders: A benefit/risk analysis. Exp Gerontol. 2020 Apr;132:110831. doi: 10.1016/j.exger.2020.110831.
\nJohnson, Sean, and Shin-Ichiro Imai. “NAD + biosynthesis, aging, and disease.” F1000Research vol. 7 132. 1 Feb 2018.
\nBieganowski P, Brenner C. Discoveries of nicotinamide riboside as a nutrient and conserved NRK genes establish a Preiss-Handler independent route to NAD+ in fungi and humans. Cell. 2004 May 14;117(4):495-502.
\nFang, E. F., Lautrup, S., Hou, Y., Demarest, T. G., Croteau, D. L., Mattson, M. P., & Bohr, V. A. (2017). NAD+ in Aging: Molecular Mechanisms and Translational Implications. Trends in molecular medicine, 23(10), 899–916.
\nHarden, A; Young, WJ (24 October 1906). “The alcoholic ferment of yeast-juice Part II.–The coferment of yeast-juice”. Proceedings of the Royal Society of London. Series B, Containing Papers of a Biological Character. 78 (526): 369–375.
\nMills KF, Yoshida S, Stein LR, Grozio A, Kubota S, Sasaki Y, Redpath P, Migaud ME, Apte RS, Uchida K, Yoshino J, Imai SI. Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice. Cell Metab. 2016 Dec 13;24(6):795-806.
\nLong AN, Owens K, Schlappal AE, Kristian T, Fishman PS, Schuh RA. Effect of nicotinamide mononucleotide on brain mitochondrial respiratory deficits in an Alzheimer’s disease-relevant murine model. BMC Neurol. 2015 Mar 1;15:19.
\nSafety & Efficacy of Nicotinamide Riboside Supplementation for Improving Physiological Function in Middle-Aged and Older Adults.
\nBraidy N, Liu Y. NAD+ therapy in age-related degenerative disorders: A benefit/risk analysis. Exp Gerontol. 2020 Apr;132:110831.
\nWang S, Xing Z, Vosler PS, Yin H, Li W, Zhang F, Signore AP, Stetler RA, Gao Y, Chen J. Cellular NAD replenishment confers marked neuroprotection against ischemic cell death: role of enhanced DNA repair. Stroke. 2008 Sep;39(9):2587-95.
\nRajman, Luis et al. “Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence.” Cell metabolism vol. 27,3 (2018): 529-547.
\nHeer C, et al, Coronavirus infection and PARP expression dysregulate the NAD metabolome: An actionable component of innate immunity. Journal of Biological Chemistry. Volume 295, Issue 52, Dec 2020.
\nMehmel, Mario et al. “Nicotinamide Riboside-The Current State of Research and Therapeutic Uses.” Nutrients vol. 12,6 1616. 31 May. 2020, doi:10.3390/nu12061616
\nLeung A, Todorova T, Ando Y, Chang P. Poly(ADP-ribose) regulates post-transcriptional gene regulation in the cytoplasm. RNA Biol. 2012 May;9(5):542-8. doi: 10.4161/rna.19899. Epub 2012 May 1. PMID: 22531498; PMCID: PMC3495734.
\nCroteau DL, Fang EF, Nilsen H, Bohr VA. NAD+ in DNA repair and mitochondrial maintenance. Cell Cycle. 2017 Mar 19;16(6):491-492. doi: 10.1080/15384101.2017.1285631. Epub 2017 Feb 1. PMID: 28145802; PMCID: PMC5384578.

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MOTS-c Peptide

MOTS-c (mitochondrial open-reading-frame of the 12S rRNA-c) peptide is a novel mitochondria-derived peptide. It is a short peptide composed of 16 amino acids, expressed in tissues and plasma, indicating a cell-specific and hormonal role.(1) With the potential to work both as a cell-specific compound and as a hormone, this peptide possibly acts by stimulating the AMP-activated protein kinase (AMPK) pathway. Only two mitochondrial-derived peptides (MDPs) have been studied, Humanin and MOTS-c. When metabolic stress occurs in the organism, the peptide is believed to translocate to the cellular nuclei and alter the gene expression. MOTS-c peptide may also be released extracellularly and is known as “mitochondrial hormone” or simply as “mitokine.” (2)(3)

Chemical Makeup(4)

Molecular Formula: C101H152N28O22S2
\nMolecular Weight: 2174.64 g/mol
\nOther Titles: Mitochondrial-derived peptide MOTS-c, Mitochondrial open reading frame of the 12S rRNA-c

Research and Clinical Studies

Animal research models have indicated multiple potential actions from MOTS-c peptide, including increased physical performance, regulated cellular and tissue metabolism, and myoblast adaptation.(2) Research suggests that these actions may primarily depend on age and age-related changes in MOTS-c expression. The researchers suggest MOTS-c levels and activity might decline, hinting at a role in the cell aging process and the development of age-related metabolic dysfunction. Furthermore, MOTS-c may interact with known aging regulators, such as NAD+ and sirtuins, suggesting its involvement in pathways potentially modulating the lifespan of the cell.(1) As per Joseph C Reynolds et al., “Mitochondria are chief metabolic organelles with strong implications in cell aging that also coordinate broad physiological functions, in part, using peptides that are encoded within their independent genome.”(4) The peptide endogenous expression has also been posited to be boosted via physical activity, potentially enhancing cellular metabolism.(5)

MOTS-c Peptide and Muscle Metabolism

With increasing age, skeletal muscles tend to gain insulin resistance, leading to decreased glucose uptake. Upon peptide exposure, skeletal muscles may be stimulated with an improved response toward AMPK activation. As a result, glucose transporter expression may increase, potentially improving skeletal muscle metabolism and enhancing skeletal muscle functioning and growth. Further, MOTS-c’s actions are posited to include targeting metabolic pathways such as the folate-methionine cycle and purine biosynthesis. This targeting may potentially lead to a modulation of cellular metabolism, including actions on glucose uptake and lipid utilization. The peptide’s impact might involve a shift in metabolic priorities within the cell, possibly affecting the balance between anabolic and catabolic processes. In systemic metabolism, MOTS-c is posited to function as a mitochondrial hormone, with circulating peptide levels appearing to affect metabolic functions in skeletal muscle and possibly adipose tissue. Its potential regulatory actions on glucose homeostasis and insulin action suggest a broader hormonal role in energy balance and nutrient sensing across different tissues.(1)

MOTS-c Peptide and Fat Cell Metabolism

Research has suggested that the peptide may potentially leave the mitochondrial site, translocate to cellular nuclei, and possibly alter gene expression. More specifically, the peptide may interact with a broad range of genes, particularly those with antioxidant response elements (ARE), hinting at a potential regulatory relationship with stress-responsive transcription factors like NRF2. Such findings suggest a genetically integrated system of mitonuclear communication, where both mitochondrial and nuclear genomes may encode factors that cross-regulate each other. This action, in turn, may alter glucose uptake restriction.(6) This hypothesis was first suggested from a study in which the experimental mice were given high-fat food, and only half were presented with the peptide. The researchers indicated that MOTS-c may potentially impact cellular metabolism by inhibiting the folate cycle directly tethered de novo purine biosynthesis, consequently leading to AMPK activation. Such actions hint at a broader role of the peptide in regulating insulin sensitivity and metabolic homeostasis, offering insights into its preventive potential against age-dependent and high-fat-induced insulin resistance and diet-induced obesity. The study presents supportive data to suggest that the peptide may stimulate glucose utilization, affect the methionine-folate cycle, and promote AMPK activation. These cellular actions suggest that MOTS-c might coordinate various metabolic processes, including glucose and lipid metabolism. Consequently, the murine models exposed to the peptide were lean and more energetic than the rest, further indicating that the peptide might prevent fat accumulation and induce glucose uptake via the AMPK pathway.(3)

MOTS-c Peptide and Bone

MOTS-c peptide has been suggested to regulate the transforming growth factor beta (TGF-beta)/SMAD pathway, which may profoundly affect bone tissues.(7) More specifically, MOTS-c’s actions may involve the upregulation of TGF-β/Smad pathway-related genes, including TGF-β1, TGF-β2, and Smad7, suggesting a pivotal role of this pathway in MOTS-c mediated osteogenic differentiation. This hypothesis is further supported when the osteogenic differentiation promoted by MOTS-c is reversed upon TGF-β1 knockdown, indicating that MOTS-c’s actions may be at least partly mediated through the TGF-β/Smad pathway. The peptide may also stimulate the expression of osteogenesis-related genes such as ALP, Bglap, and Runx2. Thus, this peptide may stimulate the SMAD pathway in the osteoblast cells, possibly improving bone density and strength. When studied in bone marrow cells, this compound appeared to trigger the differentiation of the stem cells, which may lead to bone tissue development.

MOTS-c Peptide and Cardiac Function

The peptide has not been suggested by researchers to directly influence cardiac function; instead, researchers posit that the peptide exerts potential on the endothelial cells that line the blood vessels inside. These endothelial tissues are considered to affect blood pressure and clotting. The researchers suspect a positive correlation exists between MOTS-c levels and microvascular and epicardial endothelial function. Such findings tentatively suggest MOTS-c as a potential biomarker for endothelial function, with the study revealing a nuanced relationship between MOTS-c levels and vascular reactivity. Further, the research suggested that when mice were exposed to MOTS-c, it appeared to improve the endothelial tissues’ functioning, thereby possibly facilitating dysfunction. The mechanistic basis for MOTS-c’s action on endothelial function remains speculative but may involve the activation of AMPK.(8)

MOTS-c Peptide and Cell Lifespan

Research has suggested that the peptide may be associated with enhanced longevity on a cellular level. The peptide typically contains glutamate residue, but when this is replaced by lysine, the new compound may exert a functional change. Scientists so far are aware that the functionality of the glutamate and lysine groups are vastly different, but how this specific structural change affects peptide functionality is yet to be understood. Noriyuki Fuku et al. suggests that there is “a biological link between MOTS-c and extended lifespan through the putative endocrine action of this mitokine. Further mechanistic research is needed to determine the functional signiﬁcance of polymorphism and the potential inﬂuence of MOTS-c in the […] aging process.” (9)

The peptide is available for research and laboratory purposes only. Please review and adhere to our before ordering.

References:
\nLee C, Kim KH, Cohen P. MOTS-c: A novel mitochondrial-derived peptide regulating muscle and fat metabolism. Free Radic Biol Med. 2016 Nov;100:182-187. doi: 10.1016/j.freeradbiomed.2016.05.015. Epub 2016 May 20. PMID: 27216708; PMCID: PMC5116416.
\nMohtashami Z, Singh MK, Salimiaghdam N, Ozgul M, Kenney MC. Most Recent Mitochondrial Derived Peptide in Human Aging and Age-Related Diseases. Int J Mol Sci. 2022 Oct 9;23(19):11991. . PMID: 36233287; PMCID: PMC9570330.
\nLee C, Zeng J, Drew BG, Sallam T, Martin-Montalvo A, Wan J, Kim SJ, Mehta H, Hevener AL, de Cabo R, Cohen P. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metab. 2015 Mar 3;21(3):443-54. . PMID: 25738459; PMCID: PMC4350682.
\nLu H, Wei M, Zhai Y, Li Q, Ye Z, Wang L, Luo W, Chen J, Lu Z. MOTS-c peptide regulates adipose homeostasis to prevent ovariectomy-induced metabolic dysfunction. J Mol Med (Berl). 2019 Apr;97(4):473-485. doi: 10.1007/s00109-018-01738-w. Epub 2019 Feb 6. PMID: 30725119.
\nReynolds JC, Lai RW, Woodhead JST, Joly JH, Mitchell CJ, Cameron-Smith D, Lu R, Cohen P, Graham NA, Benayoun BA, Merry TL, Lee C. MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nat Commun. 2021 Jan 20;12(1):470.
\nKim KH, Son JM, Benayoun BA, Lee C. The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress. Cell Metab. 2018 Sep 4;28(3):516-524.e7. doi: 10.1016/j.cmet.2018.06.008. Epub 2018 Jul 5. PMID: 29983246; PMCID: PMC6185997.
\nHu BT, Chen WZ. MOTS-c improves osteoporosis by promoting osteogenic differentiation of bone marrow mesenchymal stem cells via TGF-β/Smad pathway. Eur Rev Med Pharmacol Sci. 2018 Nov;22(21):7156-7163. doi: 10.26355/eurrev_201811_16247. PMID: 30468456.
\nQin Q, Delrio S, Wan J, Jay Widmer R, Cohen P, Lerman LO, Lerman A. Downregulation of circulating MOTS-c levels in patients with coronary endothelial dysfunction. Int J Cardiol. 2018 Mar 1;254:23-27. doi: 10.1016/j.ijcard.2017.12.001. Epub 2017 Dec 6. PMID: 29242099.
\nNoriyuki Fuku el al., The mitochondrial-derived peptide: A player in exceptional longevity?, .

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GHK-Cu Peptide

GHK-Cu is a naturally occurring complex molecule composed of a tripeptide called GHK (made up of glycine, histidine, and lysine amino acids) bound to a copper ion. The copper ion appears to stabilize and deliver GHK to cells. Research suggests that GHK-Cu may play a potentially essential role in restoring damaged tissues, wound repair, and may support immune response. These hypotheses have sprung from it’s perceived potential to stimulate the production of collagen, elastin, and glycosaminoglycans, crucial intercellular matrix components.

In addition to its potential on the intercellular matrix, GHK-Cu may also have antioxidant and anti-inflammatory characteristics that may protect cells from damage caused by free radicals.

Chemical Makeup

Molecular Formula: C14H23CuN6O4
\nMolecular Weight: 340.38 g/mol
\nOther Known Titles: Cu-GHK, Copper tripeptide-1, 6BJQ43T1I9

Research and Clinical Studies
\nGHK-Cu and Collagen Synthesis

Studies suggest that GHK-Cu may stimulate collagen synthesis and induce in situ tissue recovery. The researchers suggest that these actions may be due to “the presence of a GHK triplet in the alpha 2(I) chain of type I collagen”.(1) More specifically, the tripeptide sequence composed of glycine, histidine, and lysine, abbreviated as Gly-His-Lys, may be derived during the breakdown of collagen through hydrolysis. This breakdown is typically associated with the disintegration of collagen fibers, frequently resulting from either tissue damage or the natural degradation process. It is proposed that this specific peptide sequence may have a significant impact on cellular communication processes, specifically targeting fibroblasts. Fibroblasts are specialized cells deemed essential in producing new collagen fibers, vital components for structural support in various tissues.

The interaction between the Gly-His-Lys peptide and fibroblasts is believed to potentially initiate a cascade of biological events leading to the synthesis of collagen, thereby playing a potential role in the mechanisms of tissue repair and regeneration. This process of collagen synthesis by fibroblasts may be critical to contribute to the overall restoration and healing of damaged tissues. One study, lasted a month, reported that GHK-Cu might stimulate type 1 collagen production in clinical settings.(2) The scientists compared the potential of GHK-Cu to other peptides and vitamin C and vitamin A derivatives on photodamaged skin. The research primarily investigated the potential action of the peptide on dermal procollagen synthesis, keratinocyte proliferation, differentiation, and cutaneous inflammation. The peptide appeared to improve all indicators, and the researchers reported an apparent increase in skin thickness, elasticity, and hydration.

Another study explored the potential interaction between GHK-Cu and hyaluronic acid (HA) on collagen synthesis, particularly focusing on their potential collaborative actions in dermal fibroblasts and an ex-vivo skin model.(3) HA is portrayed as a significant component of skin cells, noted for its moisture-binding potential and actions on cell proliferation and inflammation, with different molecular weights (LMW and HMW) showing distinct biological activities. The experimental setup involved exposure of dermal fibroblasts with various combinations of GHK-Cu and HA, measuring the synthesis of collagen types I, IV, and VII. It was suggested that certain combinations, particularly at a GHK-Cu to LMW HA ratio of 1:9, appeared to have significantly boosted the synthesis of collagen IV—more so than when either compound was studied independently. This suggests a potential synergistic action between GHK-Cu and HA, specifically in enhancing collagen IV levels. The synergy might arise from the combined action of GHK-Cu in stimulating glycosaminoglycan production, promoting collagen synthesis, and HA’s role in reducing collagen degradation by scavenging reactive oxygen species and inhibiting matrix metalloproteinases. The research highlights that the molecular weight of HA and the ratio of GHK-Cu to HA may be crucial in maximizing this action, with optimal results observed at specific ratios. Further studies employing an ex-vivo skin model supported these findings, suggesting a notable increase in collagen IV synthesis at the dermal-epidermal junction when exposed to the optimized GHK-Cu and LMW HA mixture. This action was visually corroborated through increased fluorescence intensity in immunofluorescence assays, indicating higher collagen IV content.

GHK-Cu and Wound Infection

Both animal and clinical studies have hypothesized that GHK-Cu may reduce inflammation and the risk of infection in wounds. One murine study investigated the potential of GHK-Cu on ischemic open wounds.(4) The researchers reported, “On days 6, 10, and 13, tripeptide-copper complex-treated wounds contained significantly lower concentrations of TNF-alpha and MMP-2 and MMP-9 than control wounds.” Tumor necrosis factor-alpha (TNF-alpha), a cytokine involved in systemic inflammation, along with matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) — enzymes that break down extracellular matrix proteins — might potentially influence both the inflammatory processes and the remodeling of tissues. This suggests that GHK-Cu, a copper complex recognized for its healing capacities, might have a role in reducing inflammation and preventing tissue breakdown in models of ischemic wounds, where blood flow restriction potentially causes tissue damage.

A clinical trial that involved GHK-Cu in addition to standard wound care also reported an apparently reduced risk of infection compared to standard processes alone.(5) The study was conducted on models of diabetic neuropathic ulcers, and the rate of infections was only 7% in the GHK-Cu models compared to 34% in the control models.

GHK-Cu and Wound Healing

Studies in rabbits report that GHK-Cu has been tested regarding its potential in wound healing and laser exposure at different intensities.(6) The results were compared to control wounds without intervention. Wounds were observed daily, and biopsies were taken weekly for four weeks to evaluate the inflammation rate and neovascularization. The GHK-Cu and high-intensity laser groups appeared to have a shorter average time for healing and greater neutrophil and vessel counts. There was an apparently shorter median time for the first observable granulation tissue and an apparently faster filling of an open wound with granulation tissue compared to the control group. Granular tissue is composed of newly formed connective tissue and minuscule blood vessels that appear on wound surfaces as part of the healing process. It is suggested that there might be a link between the emergence of this tissue and heightened activity of antioxidant enzymes. These enzymes are proteins that assist in shielding cells from the harmful action of oxidative stress, a process where cell components are damaged due to the presence of unstable molecules known as free radicals. Furthermore, there is a potential enhancement in vascular development observed in these scenarios. This vascular development is considered vital for transporting essential nutrients and oxygen to the damaged area, thereby facilitating the repair of tissue.

The previously mentioned study on rats with open ischemic wounds also reported an apparent decrease in wound area of the GHK-Cu group that was greater compared to the control group on days 3 to 5, 6 to 9, and 11 to 13.(4)

Similarly, the clinical study on models of diabetic neuropathic ulcers reported that GHK-Cu, combined with standard wound care, appeared more impactful for wound closure than standard care alone.(5) The apparent closure rate was three times faster than standard care. The researchers also suggested that “The enhancement of wound closure was more pronounced (median of 89.2% compared with -10.3% for vehicle; p < 0.01) in larger (greater than 100 mm(2) initial area at study entry) plantar ulcers caused by the failure of this size of ulcer to respond adequately to standardized wound care.”

In research involving both standard murine models and those adapted to mimic diabetic conditions, wound dressings composed of collagen and infused with GHK were observed to potentially enhance wound healing.(7) The observations suggest that by the conclusion of the third week, wounds exposed to dressings containing biotinylated GHK (a tripeptide with skin regenerative properties) nearly achieved full closure, registering at 99.39%. This is potentially a significant enhancement compared to the 69.49% closure rate observed with control dressings lacking this modification. Further analysis indicated that the wounds exposed to GHK might have shown elevated levels of glutathione and ascorbic acid. These are considered critical antioxidants for their potential roles in facilitating tissue repair by protecting cells from oxidative stress. There was also a tentative observation of increased epithelialization, a process essential for the regeneration of the skin’s outer layer, in these experimental conditions. Apart from the enhanced activity of fibroblasts, which are pivotal in collagen synthesis, tissue repair, and regeneration, there was also noted a potential rise in mast cell activation. Mast cells are important for mediating inflammatory responses, which are deemed crucial during the initial phases of wound healing.

GHK-Cu and Active Radicals

Photodamage of tissues such as the skin involves the formation of reactive oxygen species (ROS), reactive nitrogen species (RNS), and reactive carbonyl species (RCS), which may induce damage to proteins, DNA, and lipids. Studies suggest that the amino acid sequence in GHK-Cu may have anti-RCS potential against radicals such as 4-hydroxynoneal, acrolein, malondialdehyde, and others.(8) Furthermore, it may potentially prevent protein glycation. Moreover, researchers have suggested that GHK-Cu may have potential action in reducing iron release from ferritin. Ferritin is a lipid peroxidation catalyst, and GHK-Cu may help to reduce the formation of iron complexes in damaged tissues and thus decrease inflammation. One study suggested an 87% decrease in iron release with the help of GHK-Cu to lower oxidation in damaged tissues.(9)

GHK-Cu may also reduce the production of reactive oxygen species and inflammatory cytokines while increasing the activity of antioxidant enzymes. This was proposed by an animal study investigating the potential of GHK-Cu on lipopolysaccharide-induced lung inflammation in mice.(10) The peptide was suggested to suppress the activation of NF-κB and p38 MAPK signaling pathways associated with inflammation. This might potentially lead to reduced infiltration of inflammatory cells in the lungs of mice with lung damage and lower levels of TNF-1 and IL-6 production to minimize damage.

Further studies also suggest that the amino-acid sequence of GHK-Cu may have an antioxidative potential on ROS, such as hydroxyl radicals, and it may be even stronger than generic antioxidative peptides.(12)

GHK-Cu and Wrinkles in Skin Tissue Models

GHK-Cu has been suggested to host potential for improving experimental models of disturbed skin topography, such as wrinkles and fine lines. One study posited that a GHK-Cu possibly reduces visible bioindicators, improving skin laxity, and clarity. The peptide apparently also reduced the depth of wrinkles while potentially increasing skin density and thickness after 12 weeks of experimentation in skin cell models with varying degrees of photodamage.(13)

Another investigation focused on the actions of GHK-Cu compared to a control compound and vitamin K. Over a period of 12 weeks, the GHK-Cu ostensibly performed better than the controls in reducing epidermal wrinkles. The peptide may also have increased skin density and thickness.(14)

In a separate 12-week study in mild to advanced photodamage, GHK-Cu seemingly improved skin attributes such as laxity, clarity, and firmness. This peptide was also associated with a reduction in coarse wrinkles, and mottled pigmentation. Additionally, the peptide apparently stimulated dermal keratinocyte proliferation, as evidenced by histological analysis of biopsies.(15)

GHK-Cu peptide is available for research and laboratory purposes only. Please review and adhere to our before ordering.

References
\nMaquart, F. X., Pickart, L., Laurent, M., Gillery, P., Monboisse, J. C., & Borel, J. P. (1988). Stimulation of collagen synthesis in fibroblast cultures by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+. FEBS letters, 238(2), 343–346.
\nAbdulghani, A. A., Sherr, A., Shirin, S., Solodkina, G., Tapia, E. M., Wolf, B., & Gottlieb, A. B. (1998). Effects of creams containing vitamin C, a copper-binding peptide cream and melatonin compared with tretinoin on the ultrastructure of normal skin-A pilot clinical, histologic, and ultrastructural study. Disease Management and Clinical Outcomes, 4(1), 136-141.
\nJiang F, Wu Y, Liu Z, Hong M, Huang Y. Synergy of GHK-Cu and hyaluronic acid on collagen IV upregulation via fibroblast and ex-vivo skin tests. J Cosmet Dermatol. 2023 Sep;22(9):2598-2604. doi: 10.1111/jocd.15763. Epub 2023 Apr 16. PMID: 37062921.
\nCanapp, S. O., Jr, Farese, J. P., Schultz, G. S., Gowda, S., Ishak, A. M., Swaim, S. F., Vangilder, J., Lee-Ambrose, L., & Martin, F. G. (2003). The effect of tripeptide-copper complex on healing of ischemic open wounds. Veterinary surgery : VS, 32(6), 515–523.
\nMulder, G. D., Patt, L. M., Sanders, L., Rosenstock, J., Altman, M. I., Hanley, M. E., & Duncan, G. W. (1994). Enhanced healing of ulcers in patients with diabetes by treatment with glycyl-l-histidyl-l-lysine copper. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society, 2(4), 259–269.
\nGul, N. Y., Topal, A., Cangul, I. T., & Yanik, K. (2008). The effects of tripeptide copper complex and helium-neon laser on wound healing in rabbits. Veterinary dermatology, 19(1), 7–14.
\nAlven, S., Peter, S., Mbese, Z., & Aderibigbe, B. A. (2022). Polymer-Based Wound Dressing Materials Loaded with Bioactive Agents: Potential Materials for the Treatment of Diabetic Wounds. Polymers, 14(4), 724.
\nCebrián, J., Messeguer, A., Facino, R. M., & García Antón, J. M. (2005). New anti-RNS and -RCS products for cosmetic treatment. International journal of cosmetic science, 27(5), 271–278.
\nMiller, D. M., DeSilva, D., Pickart, L., & Aust, S. D. (1990). Effects of glycyl-histidyl-lysyl chelated Cu(II) on ferritin dependent lipid peroxidation. Advances in experimental medicine and biology, 264, 79–84.
\nPark, J. R., Lee, H., Kim, S. I., & Yang, S. R. (2016). The tri-peptide GHK-Cu complex ameliorates lipopolysaccharide-induced acute lung injury in mice. Oncotarget, 7(36), 58405–58417.
\nZhang, Q., Yan, L., Lu, J., & Zhou, X. (2022). Glycyl-L-histidyl-L-lysine-Cu2+ attenuates cigarette smoke-induced pulmonary emphysema and inflammation by reducing oxidative stress pathway. Frontiers in molecular biosciences, 9, 925700.
\nSakuma, S., Ishimura, M., Yuba, Y., Itoh, Y., & Fujimoto, Y. (2018). The peptide glycyl-ʟ-histidyl-ʟ-lysine is an endogenous antioxidant in living organisms, possibly by diminishing hydroxyl and peroxyl radicals. International journal of physiology, pathophysiology and pharmacology, 10(3), 132–138.
\nLeyden J., Stephens T., Finkey M., Appa Y., Barkovic S. Skin care benefits of copper peptide containing facial cream. Proceedings of the American Academy of Dermatology Meeting; February 2002; New York, NY, USA.
\nLeyden J., Stephens T., Finkey M., Barkovic S. Skin Care Benefits of Copper Peptide Containing Eye Creams. University of Pennsylvania; 2002.
\nFinkley M., Appa Y., Bhandarkar S. Copper peptide and skin. In: Elsner P., Maibach H., editors. Cosmeceuticals and Active Cosmetics: Drugs vs. Cosmetics. New York, NY, USA: Marcel Dekker; 2005. pp. 549–563.

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DSIP (Delta Sleep-Inducing Peptide)

Delta Sleep-Inducing Peptide, or DSIP, is a naturally-occurring peptide made of nine amino acids, isolated from the central nervous system of experimental models of electrically induced sleep. DSIP is posited to regulate the sleep cycle, as suggested by its name, but may also play a role in regulating various physiological processes. Suggested to induce delta sleep in test models, this neuropeptide also appears to impact electrophysiological activity and possibly regulate the neurotransmitter levels in the brain.(1)

DSIP peptide was first characterized and examined from 1963 to 1977 and has since been widely studied by scientists.(2) Initially regarded only for its potential as a sleep-including factor, DSIP was soon suggested to induce other potential actions, such as mitigating pain, sleep cycle regulation, and mitigating withdrawal.(3)

Mechanisms of Action

DSIP is believed to have the potential to modify the structure and quality of sleep by engaging with the central nervous system. It is thought that DSIP may potentially reduce the time it takes to fall asleep and enhance the overall quality of sleep by influencing the activity of various neurotransmitters within the brain. Despite these possibilities, scientific research has yet to definitively identify the primary mechanisms and pathways through which DSIP exerts its actions. However, it is hypothesized that DSIP may target several specific receptors, which are considered crucial in its function. These include:

N-methyl-D-aspartate (NMDA) receptors and gamma-aminobutyric acid (GABA) receptors: NMDA receptors are linked to glutamate, a vital neurotransmitter that facilitates brain excitation, while GABA receptors are associated with inhibitory neurotransmission, playing a significant role in calming the brain. Research conducted on murine models has suggested that DSIP might amplify GABA’s calming actions, which assists in reducing brain activity and helps individuals fall asleep more easily. Concurrently, murine studies suggest that DSIP may dampen some of the stimulatory impacts of NMDA receptors, thereby decreasing overall brain stimulation and further aiding in sleep promotion.(4)(5)
\nOpioid receptors: Further research indicates that DSIP might indirectly affect opioid receptors in the brain. This interaction is believed to influence the peptide’s ability to modulate sleep and alleviate withdrawal symptoms, highlighting its complex involvement in the brain’s signaling systems.(6)(7)
\nAlpha 1-adrenergic receptor: This receptor, apparently found in the pineal gland, has been another focus of DSIP research. An experimental study has suggested that DSIP’s modulation of the alpha 1-adrenergic receptor could be a mechanism through which it affects sleep patterns. This interaction also hints at DSIP’s potential role in managing stress tolerance, given the significant influence of alpha 1-adrenergic signaling in stress-related processes.(8)

These findings underline the complex and multifaceted ways in which DSIP might influence sleep and stress management, although more research is needed to understand its mechanisms of action.

Chemical Makeup

Molecular Formula: C35H48N10O15
\nMolecular Weight: 848.82 g/mol
\nOther Known Titles: DSIP nonapeptide; emideltide

Research and Clinical Studies
\nDSIP and Sleep Cycles

A study(9) was conducted on feline models to examine the potential action of DSIP on sleep patterns. The models were divided into two groups; one was a control, and the other was labeled as the DSIP group. The peptide was presented to the cats and was monitored for 8 hours. Results indicated that there appeared to be a significant increase in total sleep and slow wave sleep (SWS) in the DSIP group. The action of DSIP appeared to be immediate as the amount of SWS sleep elevated within the first hour following study initiation. This increase appeared to be maintained for 7 hours and then decreased in the eighth hour. SWS, often called deep sleep, is suggested as one of the core stages within sleep architecture, broadly categorized into non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep. The overall structure of sleep is typically cyclic, alternating between NREM and REM stages multiple times. Apparently, SWS falls under the NREM category and scientists detect it by its low-frequency, high-amplitude delta waves evident in electroencephalogram (EEG) recordings. Sleep begins with NREM sleep, subdivided into three stages: N1, N2, and N3. N1 and N2 are lighter stages of sleep, while N3, synonymous with SWS, is the deepest stage of sleep. Following the deep sleep stage, the cycle progresses into REM sleep, where brain activity increases and dreams occur.

A clinical study(10) has suggested that the peptide may lead to an immediate increase in sleep pressure and resulted in a 59% increase in sleep within two hours of initiating DSIP experimentation. The scientists also posited that the peptide may have enhanced sleep efficiency, potentially by shortening sleep onset.(10)

DSIP and Endocrine Regulation

DSIP has been posited to interact with certain hormonal messengers typically released during sleep. Examples may include the luteinizing hormone (LH), which is considered a crucial hormone in the regulation of reproductive hormones such as testosterone. In a study with murine models,(11) DSIP was examined for its potential actions on the endocrine system. Within 30 minutes, it was noted that the levels of LH appeared to be significantly elevated, whereas there was no perceived impact on another regulatory messenger called follicle-stimulating hormone (FSH).

Further studies have suggested that DSIP may lead to increased secretion of growth hormone, positing that the peptide may potentially act on the hypothalamus to regulate hormonal secretion. Utilizing ovariectomized murine models to exclude the actions of gonadal steroids, the research observed an apparent elevation in GH levels caused by DSIP. The potential involvement of a dopaminergic mechanism in this process was inferred from the blocking action of pimozide, a dopamine antagonist, on the DSIP-induced GH increase. Additionally, in vitro studies with pituitary cells suggest a similar increase in GH release upon exposure to DSIP, albeit with a notable decline at higher concentrations. This pattern hints at the complex nature of DSIP’s role in GH regulation, potentially linking it to sleep-induced GH release, given the peptide’s association with slow-wave sleep patterns and the apparent correlation of such sleep phases with GH secretion.(12)

DSIP and Stress Response

Researchers have investigated the potential action of DSIP on murine models subjected to experimentally induced stress.(13) The murine models were divided into six groups, where the control group was presented with a placebo and the rest with DSIP. The six groups included (i) control group, (ii) stress group, (iii) group with DSIP one hour before stress experiments, (iv) DSIP 24 hours before stress experiments, (v) DSIP one hour before the last stress experiment and (vi) DSIP 24 hours before the last stress experiment. This research primarily focused on assessing changes in substance P, beta-endorphin, and corticosterone levels, which are critical in understanding the stress response and potential modulatory impacts of DSIP. Initial findings highlighted that DSIP exposure might induce noticeable fluctuations in the levels of these markers, suggesting a possible stress-modulatory role. For instance, there was an initial decrease followed by a dramatic increase in beta-endorphin. This pattern suggests DSIP’s potential influence on the opioidergic system, possibly contributing to mechanisms of stress mitigation or adaptation. Regarding corticosterone levels, which directly indicate stress in murine models, a decrease was noted shortly after DSIP exposure. The study posits that DSIP’s actions on substance P, beta-endorphin, and corticosterone levels are part of a broader spectrum of biochemical changes, hinting that DSIP might initiate a series of molecular reactions contributing to its stress-modulatory actions.(13)

DSIP and Longevity

A study(14) was conducted on murine models, equally divided into DSIP and control groups. The researchers suggested that DSIP did not appear to influence food intake, however, it did apparently decrease the weight of the murine models. It appeared to decrease the chromosomal aberrations in the bone marrow by 23% and improve the life span by 24% compared to the control group. Moreover, DSIP also appeared to lead to a 2.5-fold decrease in the occurrence of malignancies.

Another study suggests that the apparent protective actions of DSIP may be due to the potential antioxidative properties of the peptide. The study(15) was conducted on murine models, and the researchers posited that DSIP may inhibit the levels of malonic dialdehyde in the models. Malonic dialdehyde is a byproduct of lipid peroxidation, and increased levels of malonic dialdehyde typically induce increased oxidative stress. This suggested that DSIP may prevent lipid peroxidation in the murine models, which may execute antioxidant properties. DSIP may also stimulate the endogenous antioxidant system, influencing various enzymatic levels. The researchers commented that “DSIP exerts stimulating influence upon the superoxid-dismutese, catalase, ceruloplasmin activities as well as the level of nonenzymatic antioxidants–urea and uric acids, because during organism aging the antioxidant defense systems are being suppressed. DSIP increases the volume of tissues and blood endogenous antioxidant defense system mainly by means of enzymatic antioxidant system, especially during later ontogenesis.”(15)

DSIP is available for research and laboratory purposes only. Please review and adhere to our before ordering.

References:
\nNational Center for Biotechnology Information. “PubChem Compound Summary for CID 3623358, Emideltide;delta Sleep Inducing Peptide” PubChem,
\nGraf MV, Kastin AJ. Delta-sleep-inducing peptide (DSIP): an update. Peptides. 1986 Nov-Dec;7(6):1165-87.
\nKovalzon VM, Strekalova TV. Delta sleep-inducing peptide (DSIP): a still unresolved riddle. J Neurochem. 2006 Apr;97(2):303-9.
\nGrigor’ev VV, Ivanova TA, Kustova EA, Petrova LN, Serkova TP, Bachurin SO. Effects of delta sleep-inducing peptide on pre- and postsynaptic glutamate and postsynaptic GABA receptors in neurons of the cortex, hippocampus, and cerebellum in rats. Bull Exp Biol Med. 2006 Aug;142(2):186-8. English, Russian. doi: 10.1007/s10517-006-0323-9. PMID: 17369935
\nSudakov KV, Umriukhin PE, Rayevsky KS. Delta-sleep inducing peptide and neuronal activity after glutamate microiontophoresis: the role of NMDA-receptors. Pathophysiology. 2004 Oct;11(2):81-86.
\nNakamura A, Nakashima M, Sakai K, Niwa M, Nozaki M, Shiomi H. Delta-sleep-inducing peptide (DSIP) stimulates the release of immunoreactive Met-enkephalin from rat lower brainstem slices in vitro. Brain Res. 1989 Feb 27;481(1):165-8. doi: 10.1016/0006-8993(89)90498-8. PMID: 2706459.
\nDick P, Grandjean ME, Tissot R. Successful treatment of withdrawal symptoms with delta sleep-inducing peptide, a neuropeptide with potential agonistic activity on opiate receptors. Neuropsychobiology. 1983;10(4):205-8. doi: 10.1159/000118012. PMID: 6328354.
\nGraf MV, Schoenenberger GA. Delta sleep-inducing peptide modulates the stimulation of rat pineal N-acetyltransferase activity by involving the alpha 1-adrenergic receptor. J Neurochem. 1987 Apr;48(4):1252-7. doi: 10.1111/j.1471-4159.1987.tb05654.x. PMID: 3029331.
\nSusić V, Masirević G, Totić S. The effects of delta-sleep-inducing peptide (DSIP) on wakefulness and sleep patterns in the cat. Brain Res. 1987 Jun 30;414(2):262-70.
\nSchneider-Helmert D, Gnirss F, Monnier M, Schenker J, Schoenenberger GA. Acute and delayed effects of DSIP (delta sleep-inducing peptide) on human sleep behavior. Int J Clin Pharmacol Ther Toxicol. 1981 Aug;19(8):341-5.
\nIyer KS, McCann SM. Delta sleep inducing peptide (DSIP) stimulates the release of LH but not FSH via a hypothalamic site of action in the rat. Brain Res Bull. 1987 Nov;19(5):535-8. doi: 10.1016/0361-9230(87)90069-4.
\nIyer KS, McCann SM. Delta sleep-inducing peptide (DSIP) stimulates growth hormone (GH) release in the rat by hypothalamic and pituitary actions. Peptides. 1987 Jan-Feb;8(1):45-8. doi: 10.1016/0196-9781(87)90163-x. PMID: 3575154.
\nSudakov KV, Coghlan JP, Kotov AV, Salieva RM, Polyntsev YuV, Koplik EV. Delta-sleep-inducing peptide sequels in the mechanisms of resistance to emotional stress. Ann N Y Acad Sci. 1995 Dec 29;771:240-51.
\nPopovich IG, Voitenkov BO, Anisimov VN, Ivanov VT, Mikhaleva II, Zabezhinski MA, Alimova IN, Baturin DA, Zavarzina NY, Rosenfeld SV, Semenchenko AV, Yashin AI. Effect of delta-sleep inducing peptide-containing preparation Deltaran on biomarkers of aging, life span and spontaneous tumor incidence in female SHR mice. Mech Ageing Dev. 2003 Jun;124(6).
\nBondarenko TI, Maĭboroda EA, Mikhaleva II, Prudchenko IA. [Mechanism of delta-sleep inducing peptide geroprotective activity]. Adv Gerontol. 2011;24(1):80-92. Russian.

",23,98,"https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/migrated-wc/ce1b9964-58eb-4e24-9a1a-c299489edd11/8ad43d5d8c815aee6bc46709.png",[697,156,157,158],[700,701,702,703],{"_124":708,"_153":154,"_155":695,"_141":142,"_134":-5},{"_124":707,"_153":174,"_155":434,"_141":142,"_134":-5},{"_124":705,"_153":172,"_155":706,"_141":142,"_134":-5},{"_124":704,"_153":383,"_155":696,"_141":142,"_134":-5},"06ce49b5-28cd-48f4-b9b0-646227594cca","1b32e1ee-d804-48ba-bc23-763ec33f9be5",73,"b038c47a-7448-469b-89b5-2ad43569ef8b","af9a4ee9-6224-480b-9dfa-b3257f2a0227","7c383571-4ca3-46dc-a1ac-a3b4a2907006","BPC 157","bpc-157","

BPC-157 – Peptide for Regeneration and Recovery
\nBPC-157 (Body Protection Compound-157) is a synthetic peptide derived from a gastroprotective protein naturally present in gastric juice. Consisting of 15 amino acids, BPC-157 has demonstrated exceptional tissue repair properties, support in musculoskeletal injuries, intestinal barrier support, and anti-inflammatory and neuroprotective effects in research models.

BPC-157 is a synthetic peptide with proven regenerative and gastroprotective properties. Ideal for recovery from musculoskeletal injuries, improving intestinal function, and protecting against inflammation. Buy online at the best price in Romania from Peptology.

It is part of the Recovery and Anabolic Peptides category.

What is BPC-157?

BPC-157 (Body Protection Compound) is a synthetic peptide derived from a gastroprotective protein naturally found in gastric juice. It is made up of 15 amino acids and has demonstrated exceptional properties for tissue repair, treatment of muscle and tendon injuries, improvement of the intestinal barrier and neuroprotection.

Main effects:

Accelerates the healing of tendons, muscles and ligaments

Helps in recovery from injuries

Regenerates the intestinal mucosa

Can reduce inflammation and pain

⚙️ How does BPC-157 work?

BPC-157 interacts with several regulatory molecules and promotes:

Angiogenesis (formation of new blood vessels)

Collagen synthesis and accelerated cell proliferation

Modulation of NO pathways and reduction of oxidative stress

Improved digestion and intestinal barrier function

Clinical studies and results
\nAlthough largely based on animal models, studies have shown:

Faster healing of tendons, muscles and tendon-muscle interfaces

Protection of the liver and intestinal tract from toxins and damage

Potential for neuroprotection and reduction of neurodegeneration

BPC-157 exhibits excellent tolerability and stability in the body, even when administered orally or injected.

Benefits of BPC-157
\n✔️ Accelerated recovery after injuries
\n✔️ Improved joint and tendon function
\n✔️ Regeneration of the intestinal wall
\n✔️ Relieves gastritis and ulcers
\n✔️ Possible neuroprotective effect
\n✔️ Anti-inflammatory effect

⚠️ Possible side effects
\nBPC-157 has a very high safety profile. No serious adverse reactions have been reported, either with injectable or oral administration. In rare cases, the following may occur:

Mild discomfort at the injection site

Transient fatigue

Nausea at higher doses

In case of prolonged use, monitoring and consultation with a specialist is recommended.

✅ Why choose BPC-157 from Peptology?
\nHigh quality research peptides with laboratory-confirmed origin
\nSterile packaging and guaranteed content
\nDetailed information, tables and instructions for easy and safe use
\nPart of the Recovery and Anabolic Peptides category

The product is intended for research purposes only!

",28,"https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/migrated-wc/ce1b9964-58eb-4e24-9a1a-c299489edd11/a45ffdf7478077bda3b0c9bf.png",[714,156,157,158],[717,718,719,720],{"_124":724,"_153":154,"_155":713,"_141":142,"_134":-5},{"_124":723,"_153":174,"_155":616,"_141":142,"_134":-5},{"_124":722,"_153":172,"_155":164,"_141":142,"_134":-5},{"_124":721,"_153":383,"_155":607,"_141":142,"_134":-5},"ed757cb9-e36c-4492-a873-568a67770592","0462d58a-1201-4f33-887f-d05511a977ff","ded20f74-67f1-4dcb-ba5b-7aa36c111f47","8837b476-26fb-43f7-bf70-5224f9718cc5","f0224172-8c5f-45cf-b084-0806afb6c95f","Semaglutide","semaglutide","

What is Semaglutide?
\nSemaglutide is a next-generation GLP-1 receptor agonist, initially used in the treatment of type 2 diabetes, but which has rapidly gained popularity among researchers and healthcare professionals due to its remarkable effects on weight loss. By mimicking the action of the natural hormone GLP-1 (glucagon-like peptide-1), semaglutide helps regulate blood sugar levels and control appetite, offering significant benefits for people with metabolic syndrome, obesity or insulin resistance.

Semaglutide works by stimulating insulin secretion in a glucose-dependent manner, inhibiting glucagon secretion and slowing gastric emptying. The result is a prolonged feeling of satiety and a significant reduction in caloric intake.

Semaglutide in the treatment of obesity and weight control

Semaglutide is one of the most studied peptides for weight management, with extensive clinical trials demonstrating its effectiveness in reducing body mass in overweight or obese patients. At higher doses (2.4 mg, under the trade name Wegovy®), it has shown average body weight reductions of up to 15-17% over 68 weeks.

In addition to weight loss, patients have reported improvements in:

Appetite control and cravings reduction

Glucose and HbA1c levels

Blood pressure and lipid profile

Quality of life and daily energy

How does Semaglutide work?

Semaglutide is administered subcutaneously, usually once a week, and acts on the endocrine system in several ways:

✅ Stimulates insulin secretion when blood sugar is high

✅ Inhibits glucagon secretion

✅ Slows gastric emptying

✅ Reduces appetite and increases satiety

✅ Supports weight loss and improves insulin sensitivity

Clinical results and studies
\nSemaglutide has been the subject of several phase III studies (STEP program), which have confirmed its effectiveness in weight loss and diabetes control. In a study published in The New England Journal of Medicine, patients who used semaglutide lost an average of 14.9% of their body weight compared to 2.4% in the placebo group.

In another study (STEP 4), 88% of participants who continued treatment lost at least 5% of their weight, and 70% lost more than 10%.

Semaglutide and type 2 diabetes
\nSemaglutide is approved for the treatment of type 2 diabetes under the brand name Ozempic®. It offers:

Reduction of HbA1c by up to 1.5-1.8%

Superior glycemic control compared to other oral therapies

Possibility of reducing or discontinuing other antidiabetic drugs

Reduced risk of cardiovascular complications

Possible side effects
\nLike any peptide with pharmacological action, semaglutide can cause side effects, especially in the initial phases of use:

Nausea (most common, usually disappears over time)

Vomiting

Constipation or diarrhea

Fatigue, mild headaches

Rarely: pancreatitis or more severe gastrointestinal problems

It is recommended to start with a low dose and increase gradually to minimize gastric discomfort. The product is intended for laboratory research purposes only.

Why choose Semaglutide from Peptology?

✔️ High purity lyophilized peptide

✔️ Publicly available lab tests

✔️ 5mg version for flexible dosing

✔️ Fast shipping to Romania and EU

✔️ Dedicated customer and researcher support

⚠️ LEGAL NOTICE

All products are intended for scientific research or in vitro analysis only. They are not intended for human use or administration to animals.

Want to learn more about our peptides? Discover additional categories:

Peptides for weight management

Peptides for energy and vitality

Peptides for hormonal balance

Injectable peptides vs. spray

How to choose the right peptide for research

",95,"https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/74da1df4-fe57-423b-b171-8c3632af364d.png",[742],[733,734,735,736],{"_124":741,"_153":174,"_155":413,"_141":142,"_134":-5},{"_124":740,"_153":172,"_155":684,"_141":142,"_134":-5},{"_124":738,"_153":606,"_155":739,"_141":142,"_134":-5},{"_124":737,"_153":383,"_155":729,"_141":142,"_134":-5},"e1e95c75-e0a0-481c-9d37-6ec5e8f02da9","538ee544-0dd8-4765-bc40-905395b5721d",85,"bf7c2dbf-4e96-45df-83d1-e3bf3787e981","b7e90f53-1274-4d85-b9f8-5b1fdbfe37ea","https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/gallery/60b8c042-e9ef-4883-a86d-19f1c8ef9592.png","f0b8b4cf-1aab-4e8f-b256-51d1bbb72bff","TB500(Thymosin B4 Acetate)","

TB500 – peptide for accelerated regeneration and joint and muscle recovery
\nTB500 (Thymosin Beta-4) is a peptide involved in cell migration, tissue repair and inflammation regulation. It supports the formation of new blood vessels (angiogenesis) and accelerates the healing of damaged tissues, especially in muscles, joints, tendons and skin.

TB500 5mg/10mg is a powerful repair and regeneration peptide, used in research to accelerate the healing of tissues, joints and muscles. With prolonged action and good tolerability, it is an ideal choice for models targeting athletes and active people. Buy online at a great price in Romania from Peptology.

It is part of the Recovery and anabolic peptides category.

What is TB500?
\nPeptide TB500 is a peptide involved in cell migration, repair and inflammation. Promotes the formation of new blood vessels (angiogenesis) and accelerates the repair of damaged tissues, especially in muscles, tendons and skin.

✔️ Supports regeneration
\n✔️ Stimulates cell motility
\n✔️ Improves recovery from injuries
\n✔️ Has the potential for chronic inflammation

⚙️ How does TB500 work?
\nTB500 works by:

Increasing actin migration – helps cells move towards damaged tissue
\nAngiogenesis – promotes the formation of new blood vessels
\nAnti-inflammatory effect – especially useful for chronic injuries
\nRapid healing of muscles, joints and tissues

Clinical studies
\nTB500 is successfully used for:

Sports injuries and tendon ruptures

Osteoarthritis and joint pain

Heart and muscle tissue regeneration

Improvement of inflammatory autoimmune conditions

TB500 Benefits
\n✔️ Accelerated muscle and joint recovery
\n✔️ Increased flexibility and mobility
\n✔️ Reduced inflammation and swelling
\n✔️ Promotes cell growth and repair
\n✔️ Convenient subcutaneous or intramuscular injection

⚠️ Possible side effects
\nTB500 is well tolerated, but in rare cases the following may occur:

Mild discomfort at the injection site

Headache or fatigue

Slightly increased appetite

Drowsiness in the first few days

With proper use and storage, the risk of side effects is minimal.

✅ Why choose TB500 from PEPTIDESHEALTHS?
\nHigh-quality research peptides with laboratory-confirmed origin
\nSterile packaging and guaranteed content
\nDetailed information, tables and instructions for easy and safe use
\nPart of the Recovery and Anabolic Peptides category, ideal for regeneration protocols and sports medicine

The product is intended for research purposes only!

",71,195,"https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/42a307aa-7e8c-4f90-acfd-f9bae019bc37.png",[758],[751,752,753],{"_124":757,"_153":154,"_155":746,"_141":142,"_134":-5},{"_124":755,"_153":174,"_155":756,"_141":142,"_134":-5},{"_124":754,"_153":172,"_155":747,"_141":142,"_134":-5},"c61e1320-fc9d-4a11-82e9-fdd566c29e4f","6677e348-c52e-4dd1-a8f5-20040c32d9a9",105,"c2f842f6-682d-4ccb-8db6-dd41da85dad4","https://szphcbeamjelkdqjjewe.supabase.co/storage/v1/object/public/product-images/cca3aedd-3640-47c0-97a2-80d01f38be95/gallery/35c7371d-901e-412e-926c-bea56574edc7.png","31b1efad-bd0e-4279-b109-5fc7f1b07bfd","Sermorelin Acetate","sermorelin-acetate","

Sermorelin Peptide

Sermorelin is a 29 amino acid peptide, the shortest synthetically developed peptide that may potentially induce biological activity at the receptors for the growth hormone-releasing hormone (GHRH).(2) Sermorelin polypeptide is an analog of the GHRH factor consisting of GHRH (1-29 acid)-amide. Due to this structural and functional mimicry, Sermorelin has been studied across multiple branches of scientific research involving growth hormone deficiency models.(3)

It was in the early 1980s that the action of Sermorelin, classified as a growth hormone-releasing fragment GHRF (1-29) amide, was first explored. Several research studies were conducted on rats where exogenous GHRF (1-29) amide was introduced in conscious and anesthetized rats. It was observed that the presence of GHRF appeared to stimulate the pituitary gland and promote growth. Following this theory, Sermorelin and similar compounds have become the subject of further research in growth hormone deficiency models.(4)

Overview

Sermorelin is suggested to be a growth hormone analog constituting the first 29 amino acids out of the usual 44 amino acids found in growth hormone-releasing hormone (GHRH). Researchers posit that Sermorelin binds with the GHRH receptors found on the pituitary gland and suggest further that the synthetic peptide may stimulate secretion of growth hormone (hGH). Thus, Sermorelin is believed to maintain the fundamental function of GHRH, possibly stimulating the GHRH receptors in the pituitary gland and leading to sporadic release of growth hormone despite its reduced amino acid sequence. This mechanism is thought to result in increased levels of insulin-like growth factor-1 (IGF-1), primarily recognized for its role in the anabolic actions of growth hormone. The estimated half-life of Sermorelin is around 11 to 12 minutes.

A major potential advantage of the peptide is that due to its apparent GHRH receptor specificity, it may not induce any significant change in the levels of other endocrine markers such as prolactin, insulin, cortisol, glucose, or thyroid hormones.(6)

Chemical Makeup

Molecular Formula: C149H246N44O42S
\nMolecular Weight: 3357.93 g/mol
\nOther Known Titles: GRF 1-29

Research and Clinical Studies
\nSermorelin and GHRH Receptors

Sermorelin is thought to interact with GHRH receptors through complex molecular mechanisms, possibly triggering various cellular signaling pathways. It is hypothesized that upon binding to the GHRH receptor, Sermorelin may alter the receptor’s structure, potentially initiating a series of intracellular signaling events.(12) Some researchers propose that Sermorelin might enhance the production of cyclic adenosine monophosphate (cAMP) in specific cells. This enhancement may occur through the activation of adenylate cyclase, which is suggested to convert ATP into cAMP. Higher levels of cAMP might lead to the activation of protein kinase A (PKA), a key enzyme in cellular signaling processes. PKA might phosphorylate various target proteins, thereby initiating further cellular responses. The potential activation of the GHRH receptor by Sermorelin, along with the ensuing cAMP-PKA signaling cascade, is thought to possibly promote the secretion and distribution of growth hormone (hGH) from somatotroph cells in the pituitary gland. The secreted hGH is also believed to contribute to the synthesis of insulin-like growth factor-1 (IGF-1).(12)

Sermorelin Peptide and Growth Velocity

Researchers reported positive results in the idiopathic GH deficiency when Sermorelin was presented to underdeveloped animal models. Increased growth and height velocity rate was observed within 12 months of consistent, continuous peptide presence. These elevated levels were reported to be sustained for an average of 36 months after continuous presence.(7)

Sermorelin Peptide and Anabolic Research Outcomes

Preliminary findings from one investigation indicate that Sermorelin may lead to an 82% enhancement in average growth hormone levels, with actions persisting for approximately two hours.(13) A separate study conducted over 16 weeks hypothesizes that Sermorelin might elevate growth hormone levels by as much as 107%, and increase IGF-1 levels by about 28%.(14) The research further suggests a possible increase in lean body mass of approximately 2.78 lbs (1.26 kg), with no significant change in fat mass. These actions are tentatively attributed to the peptide’s capacity to boost growth hormone levels, and in turn, IGF-1, which is considered a potential anabolic agent influencing growth hormone activity. The most noteworthy outcomes identified by the researchers include observations that there was “a gain of 1.26 ± 0.52 kg (P < 0.05) in LBM” and that “skin thickness increased significantly.”

Sermorelin Peptide and Lipodystrophy

Scientists carried out a controlled clinical study involving 31 HIV-positive subjects with lipodystrophy, to investigate the potential impact of Sermorelin.(8) All 31 subjects were divided into two groups, where one was presented with Sermorelin, and the other group with a placebo for 12 weeks. Following the study, it was suggested by the research team that growth hormone levels appeared significantly increased in Sermorelin subjects as compared to the ones given a placebo. Levels of insulin-like growth factor (IGF-1) had apparently increased – resulting in increased lean body mass in the peptide group. Abdominal visceral fat and the ratio of trunk to lower extremity fat were reported by the researchers to be significantly reduced. There was no other reported change in the glucose or insulin levels.(8)

Sermorelin Peptide and Cognition

In the early 2000s, clinical research studies were conducted with 89 subjects between 68 and 69 years of age to explore the correlation (if any) between tapering growth hormone release and impaired cognition. Scientists consider that with increasing age, levels of growth hormone naturally decline, which may result in reduced physiological functions, including cognition (i.e. ability to collect, process, and recollect information). Following the introduction of Sermorelin, it was observed that there was an apparent improved performance in the Wechsler Adult Intelligence Scale (WAIS) – i.e. improved IQ levels, picture arrangement tests, and verbal tests – amongst the test subjects.(9)

Sermorelin Peptide and Tumor Cells

A clinical study was designed where 1,018 glioma subjects were presented with over 4,000 compounds each, and following each presentation, a DRS was determined for all compounds, for each subject. Following the results of the study, it appeared that the Sermorelin compound reportedly induced the most sensitivity in the test subjects. Upon analysis, it was suggested by the researchers that this may be due to the potential of Sermorelin to block the tumor cell cycles, thereby possibly preventing tumor cell proliferation.(10)

Sermorelin Peptide and Hypogonadism

Initial research into the peptide suggested that Sermorelin might be impactful in increasing lean mass. One study sought to explore if Sermorelin had potential in hypogonadism (which is considered to stem from additional fat mass). Test models were divided into two groups where one group was presented with Sermorelin followed by GHRH 1-40, with a one week interval between the two compounds, whereas the other group was given the same combination in reverse order. Following the study, it was reported by the researchers that for both groups, the Sermorelin appeared to stimulate the release of FSH and LH, which might stimulate testosterone production.

This initial research spawned additional studies, including one clinical study that included 19 male subjects, 9 of whom were aged between 22 and 33 years of age, and 10 were aged between 60 and 78 years of age. The more elderly subjects were presented with one of two concentrations of Sermorelin for a period of 28 days, with an interval of 14 days in between the two instances. Testosterone levels in the elderly subjects reportedly increased after the presentation of Sermorelin; however, it should be noted that the levels were not statistically significant. Furthermore, researchers suggested that elevated levels of growth hormones, possibly induced by Sermorelin presence, appeared to be at peak during the night time, for all test subjects, as compared during the day.(11)

Sermorelin peptide is available for research and laboratory purposes only. Please review and adhere to our before ordering.

References:
\nGarcia JM, Merriam GR, Kargi AY. Growth Hormone in Aging. [Updated 2019 Oct 7]. In: Feingold KR, Anawalt B, Boyce A, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000.
\nPrakash, A, and K L Goa. “Sermorelin: a review of its use in the diagnosis and treatment of children with idiopathic growth hormone deficiency.” BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy vol. 12,2 (1999): 139-57.
\nNational Center for Biotechnology Information. “PubChem Compound Summary for CID 16129620, Sermorelin” PubChem
\nClark, R G, and I C Robinson. “Growth induced by pulsatile infusion of an amidated fragment of human growth hormone releasing factor in normal and GHRF-deficient rats.” Nature vol. 314,6008 (1985): 281-3.
\nDrugs at FDA: FDA Approved Drugs.
\nJunichi I. et al, Growth hormone secretagogues: history, mechanism of action, and clinical development, JSCM Rapid Communications Vol. 3 Issue 1, 09 February 2020.
\nPrakash, A, and K L Goa. “Sermorelin: a review of its use in the diagnosis and treatment of children with idiopathic growth hormone deficiency.” BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy vol. 12,2 (1999): 139-57.
\nKoutkia, Polyxeni et al. “Growth hormone-releasing hormone in HIV-infected men with lipodystrophy: a randomized controlled trial.” JAMA vol. 292,2 (2004): 210-8.
\nVitiello, Michael V et al. “Growth hormone releasing hormone improves the cognition of healthy older adults.” Neurobiology of aging vol. 27,2 (2006): 318-23.
\nChang, Yuanhao et al. “A potentially effective drug for patients with recurrent glioma: sermorelin.” Annals of translational medicine vol. 9,5 (2021): 406. doi:10.21037/atm-20-6561.
\nSinha, Deepankar K et al. “Beyond the androgen receptor: the role of growth hormone secretagogues in the modern management of body composition in hypogonadal males.” Translational andrology and urology vol. 9,Suppl 2 (2020): S149-S159. doi:10.21037/tau.2019.11.30.
\nZhou, F., Zhang, H., Cong, Z., Zhao, L. H., Zhou, Q., Mao, C., Cheng, X., Shen, D. D., Cai, X., Ma, C., Wang, Y., Dai, A., Zhou, Y., Sun, W., Zhao, F., Zhao, S., Jiang, H., Jiang, Y., Yang, D., Eric Xu, H., … Wang, M. W. (2020). Structural basis for activation of the growth hormone-releasing hormone receptor. Nature communications, 11(1), 5205.
\nVittone, J., Blackman, M. R., Busby-Whitehead, J., Tsiao, C., Stewart, K. J., Tobin, J., Stevens, T., Bellantoni, M. F., Rogers, M. A., Baumann, G., Roth, J., Harman, S. M., & Spencer, R. G. (1997). Effects of single nightly injections of growth hormone-releasing hormone (GHRH 1-29) in healthy elderly men. Metabolism: clinical and experimental, 46(1), 89–96.
\nKhorram, O., Laughlin, G. A., & Yen, S. S. (1997). Endocrine and metabolic effects of long-term administration of [Nle27]growth hormone-releasing hormone-(1-29)-NH2 in age-advanced men and women. The Journal of clinical endocrinology and metabolism, 82(5), 1472–1479.

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Popular peptides