Peptide
Compound Profiles

TB-500 is a synthetic analogue of Thymosin Beta-4 (Tβ4), specifically the actin-binding domain fragment Ac-LKKTETQ. Tβ4 is an endogenous regulator of actin polymerization essential for cell migration, angiogenesis, and wound repair. Phase II clinical trials of full-length Tβ4 by RegeneRx (NCT01311518) demonstrated safety and improved healing outcomes in non-healing diabetic ulcers and dry eye disease [Sosne et al., 2013, Cornea]. TB-500 as the isolated fragment is studied primarily in preclinical and veterinary research settings, where it demonstrates comparable angiogenic and cytoprotective properties to the parent molecule.

Preclinical and human Tβ4 data indicate robust promotion of angiogenesis, cardiac tissue repair following ischemia, and acceleration of wound closure with minimal immunogenicity [Goldstein & Kleinman, 2015, Ann NY Acad Sci].

TB-500 sequesters G-actin monomers, modulating the G/F-actin equilibrium to promote lamellipodia formation and cell motility. It simultaneously upregulates Integrin-Linked Kinase (ILK) to activate the Akt/PI3K survival pathway, driving endothelial cell migration and neovascularization.

Ipamorelin (Aib-His-D-2-Nal-D-Phe-Lys-NH₂) is a synthetic pentapeptide growth hormone secretagogue developed by Novo Nordisk and later licensed to Helsinn Group. It acts as a selective agonist at the GHS-R1a (ghrelin receptor), stimulating pulsatile growth hormone release from the anterior pituitary with high receptor selectivity. Notably, at research doses ipamorelin does not significantly elevate cortisol or prolactin, distinguishing it from earlier-generation GHRPs [Raun et al., 1998, Eur J Endocrinol]. Helsinn's Phase II clinical program investigated ipamorelin for postoperative GI motility restoration.

Research data demonstrate selective, dose-dependent GH secretion with favorable selectivity over ACTH and cortisol pathways, supporting metabolic and body composition research without adrenal axis interference [Raun et al., 1998].

Ipamorelin binds selectively to GHS-R1a receptors in the hypothalamus and anterior pituitary, triggering IP3/DAG signaling and Ca²⁺ mobilization that drives GH vesicle exocytosis while synergizing with endogenous GHRH tone.

PT-141 (bremelanotide) is a cyclic heptapeptide melanocortin analogue originally derived from Melanotan II, developed by Palatin Technologies and approved by the FDA in June 2019 under the trade name Vyleesi for hypoactive sexual desire disorder (HSDD) in premenopausal women. Unlike phosphodiesterase inhibitors, it acts centrally via the melanocortin system rather than the vascular endothelium. The RECONNECT Phase III trials (n=1,267) demonstrated statistically significant improvements in satisfying sexual events and desire scores versus placebo [Simon et al., 2019, Obstet Gynecol].

PT-141 is the only CNS-targeted mechanism approved for female HSDD, addressing central desire pathways rather than peripheral vascular flow. Phase III data confirm durable efficacy with an as-needed dosing model [Simon et al., 2019].

Bremelanotide binds agonistically to MC3R and MC4R receptors within the hypothalamus and limbic system, activating cAMP-mediated cascades that modulate central dopaminergic and oxytocin pathways governing sexual motivation and arousal.

SS-31 (elamipretide, Bendavia) is a cell-permeable, mitochondria-targeting tetrapeptide (D-Arg-Dmt-Lys-Phe-NH₂) developed by Stealth BioTherapeutics. It selectively concentrates within the inner mitochondrial membrane by binding to cardiolipin, stabilizing electron transport chain complexes and reducing mitochondrial reactive oxygen species. A Phase II trial (EMBRACE-STEMI, n=118) demonstrated significant reduction in infarct size in acute MI patients receiving elamipretide during percutaneous coronary intervention [Chakrabarti et al., 2013, Circ Heart Fail].

SS-31 uniquely targets the mitochondrial inner membrane to preserve cristae architecture and ATP synthesis under ischemic stress, demonstrating cardioprotective and nephroprotective effects across multiple Phase II programs [Szeto, 2014, Pharm Res].

Elamipretide binds directly to cardiolipin on the inner mitochondrial membrane, preventing cytochrome c peroxidase activity and maintaining electron transport chain super-complex organization, thereby suppressing mitochondrial permeability transition pore opening and attenuating apoptotic signaling.

Epithalon (Ala-Glu-Asp-Gly) is a synthetic tetrapeptide analogue of epithalamin, a polypeptide extract isolated from the pineal gland, developed by the St. Petersburg Institute of Bioregulation and Gerontology. The compound is studied primarily for its ability to activate telomerase (hTERT) in somatic cells, with in vitro research documenting increased telomere length and extended cellular division capacity [Khavinson et al., 2003, Bull Exp Biol Med]. Longitudinal observational cohort studies in elderly Russian populations reported reduced all-cause mortality, though these data lack the rigor of randomized controlled trial designs.

In vitro and observational research models suggest telomere elongation, restoration of disrupted circadian melatonin secretion, and antioxidant activity. Cohort data indicate potential reduction in age-related pathology incidence [Anisimov et al., 2006, Bull Exp Biol Med].

Epithalon upregulates telomerase reverse transcriptase (hTERT) gene expression, enabling elongation of telomeres in aged cells and delaying replicative senescence. It also normalizes pineal melatonin secretion rhythmicity by modulating hypothalamic-pituitary signaling.

MOTS-c is a 16-amino acid mitochondria-derived peptide encoded by the mitochondrial genome, discovered by Lee et al. in 2015. It functions as a retrograde mitochondrial signal, translocating to the nucleus under metabolic stress to regulate gene expression programs governing glucose and lipid homeostasis. Preclinical research demonstrated that exogenous MOTS-c administration reversed diet-induced insulin resistance in murine models and extended lifespan in aged mice [Lee et al., 2015, Cell Metab; Reynolds et al., 2021, Nat Aging].

Research models document robust insulin sensitization, suppression of obesity-associated inflammation, and exercise-mimetic metabolic effects. MOTS-c also demonstrates neuroprotective properties in rodent Alzheimer's models [Yin et al., 2023, Aging Cell].

MOTS-c activates AMPK via AICAR accumulation from the folate cycle, suppressing the pentose phosphate pathway and redirecting carbon flux toward oxidative metabolism. Nuclear translocation under stress enables direct transcriptional regulation of antioxidant response element genes via interaction with NRF2 co-factors.

CJC-1295 is a synthetic 30-amino acid analogue of growth hormone-releasing hormone (GHRH) that, in its DAC form, covalently binds serum albumin to extend half-life to approximately 6–8 days. Ipamorelin acts via the independent GHS-R1a receptor pathway. Their combination is widely employed in research protocols because the two peptides act through orthogonal, synergistic mechanisms to amplify pulsatile GH release beyond what either achieves alone. CJC-1295 Phase II data demonstrated dose-dependent increases in serum GH (2–10-fold) and IGF-1 levels in healthy adults [Teichman et al., 2006, J Clin Endocrinol Metab].

The combination produces supraphysiologic pulsatile GH release with enhanced IGF-1 elevation, supporting research into body composition, recovery, and metabolic parameters while preserving natural GH rhythmicity [Teichman et al., 2006].

CJC-1295 binds and activates GHRH-R on somatotroph cells, stimulating cAMP/PKA-mediated GH gene transcription. Ipamorelin simultaneously activates GHS-R1a via IP3/Ca²⁺ signaling. The two pathways converge to produce supra-additive GH pulse amplitude.

GLOW is a proprietary multi-peptide blend formulated for dermal research use, typically combining GHK-Cu (copper tripeptide-1), BPC-157, and TB-500 or related fragments in a topical or injectable vehicle. The formulation targets synergistic collagen stimulation, angiogenesis, and skin barrier restoration. While GHK-Cu has an extensive independent literature base documenting dermal collagen I/III upregulation [Pickart et al., 2015, J Aging Res], the specific GLOW blend as a combined formulation has not been evaluated in published peer-reviewed clinical trials.

Component peptides collectively support collagen synthesis, epidermal regeneration, and microvascular perfusion of dermal tissue.

GHK-Cu upregulates TGF-β and decorin to stimulate collagen I/III synthesis; BPC-157 activates FAK-paxillin and VEGFR2 for angiogenesis; TB-500 modulates G-actin sequestration and ILK/Akt to drive keratinocyte and fibroblast migration.

KLOW is a proprietary peptide research stack formulated for musculoskeletal repair applications, typically encompassing BPC-157 and TB-500 as primary components alongside supporting peptides targeting collagen biosynthesis and anti-inflammatory signaling in joint and tendon tissue. Component peptides have established independent preclinical evidence bases for tendon and ligament repair, with BPC-157 demonstrating accelerated Achilles tendon healing in rodent transection models [Pevec et al., 2010, J Orthop Res].

The research rationale centers on synergistic soft-tissue repair: BPC-157 drives tendon fibroblast proliferation and vascularization, while TB-500 accelerates cell migration and reduces inflammatory cytokine burden at injury sites.

BPC-157 activates VEGFR2 and FAK-paxillin signaling to drive angiogenesis and tendon fibroblast recruitment; TB-500 sequesters G-actin and upregulates ILK/Akt to enhance cellular motility and survival at sites of mechanical tissue damage.

Human Growth Hormone (somatropin) is an endogenous 191-amino acid single-chain polypeptide secreted by somatotroph cells of the anterior pituitary gland. Recombinant DNA-derived somatropin (rhGH) is FDA-approved for multiple indications including growth hormone deficiency (GHD) in adults and children, Turner syndrome, Prader-Willi syndrome, short bowel syndrome, and HIV-associated wasting. Landmark studies including the KIMS and HypoCCS databases have characterized the effects of rhGH replacement on body composition, lipid profiles, bone mineral density, and quality of life [Abs et al., 1999, J Clin Endocrinol Metab].

In GHD research populations, rhGH replacement restores lean body mass, reduces visceral adiposity, improves lipid profiles, and normalizes bone mineral density. IGF-1-mediated anabolic effects are central to its tissue-level actions [Carroll et al., 1998, J Clin Endocrinol Metab].

GH binds GHR homodimers to activate JAK2/STAT5b signaling, directly stimulating hepatic IGF-1 production. Peripheral GHR activation drives protein synthesis, lipolysis via hormone-sensitive lipase, and anti-insulin metabolic effects, while IGF-1 mediates most anabolic tissue-level actions through IGF1R/PI3K/Akt signaling.

Semax (ACTH(4-7)-Pro-Gly-Pro) is a synthetic heptapeptide derived from the adrenocorticotropic hormone (ACTH) fragment 4-10, developed by the Institute of Molecular Genetics of the Russian Academy of Sciences. It is approved in Russia and Ukraine for the treatment of stroke, transient ischemic attacks, and cognitive impairment. Semax markedly upregulates BDNF, NGF, and VEGF expression in hippocampal tissue and demonstrates robust neuroprotective activity in ischemia models [Dolotov et al., 2006, J Neurochem].

Research data document significant enhancement of working memory, attention, and learning in both healthy subjects and stroke recovery models, alongside potent neuroprotection against ischemic and oxidative neuronal injury [Shadrina et al., 2010, J Mol Neurosci].

Semax rapidly upregulates BDNF and TrkB signaling in hippocampal and prefrontal circuits, enhancing long-term potentiation and synaptic plasticity. It also inhibits enkephalin-degrading enzymes and suppresses NF-κB-mediated neuroinflammatory cascades following ischemic insult.

Selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) is a synthetic heptapeptide anxiolytic analogue of the endogenous immunopeptide tuftsin, approved in Russia for the treatment of generalized anxiety disorder (GAD) and neurasthenia. Selank demonstrates anxiolytic efficacy comparable to benzodiazepines in clinical trials without sedation, tolerance, or withdrawal concerns, while also exhibiting nootropic and immunomodulatory properties [Semenova et al., 2010, Bull Exp Biol Med].

Clinical research data indicate significant anxiolysis, improvement in memory consolidation, and enhanced stress resilience without the tolerance, dependence, or cognitive impairment associated with benzodiazepine receptor agonists [Semenova et al., 2010].

Selank modulates GABAergic tone through allosteric interaction with GABA-A receptor complexes and inhibits enkephalin-degrading enzymes, potentiating endogenous enkephalin. It also upregulates BDNF expression and modulates IL-6 and interferon signaling in neuroimmune circuits.

Retatrutide (LY3437943) is a once-weekly injectable triple hormone receptor agonist developed by Eli Lilly that simultaneously activates receptors for GIP, GLP-1, and glucagon. A landmark Phase II trial (n=338) demonstrated up to 24.2% mean body weight reduction at 48 weeks at the 12 mg dose, representing the highest weight loss observed with any pharmacologic agent to date in a clinical trial setting [Jastreboff et al., 2023, NEJM]. The glucagon receptor component contributes to enhanced energy expenditure beyond GLP-1 agonism alone.

Phase II data document unprecedented pharmacological weight reduction (~24% body weight), significant improvements in HbA1c, fasting glucose, lipid profiles, and blood pressure [Jastreboff et al., 2023, NEJM].

Retatrutide activates GIPR to enhance insulin secretion and improve adipocyte metabolism; GLP-1R to suppress appetite and delay gastric emptying; and GCGR to increase energy expenditure through brown adipose tissue thermogenesis.

Tirzepatide is a synthetic 39-amino acid dual GIP/GLP-1 receptor agonist developed by Eli Lilly, approved by the FDA in May 2022 as Mounjaro for type 2 diabetes and in November 2023 as Zepbound for chronic weight management. The SURPASS Phase III program (8 trials, >10,000 participants) demonstrated HbA1c reductions of 1.87–2.58% and body weight reductions of 7.5–11.0 kg versus placebo at 40 weeks [Dahl et al., 2022, Lancet Diabetes Endocrinol]. The SURMOUNT program confirmed 20.9% mean body weight reduction in obesity management.

SURPASS and SURMOUNT trial data confirm superior glycemic control, class-leading weight reduction (~21% body weight), and meaningful improvements in cardiometabolic risk factors including blood pressure, lipids, and hepatic steatosis markers [Jastreboff et al., 2022, NEJM].

Tirzepatide co-activates GIPR and GLP-1R, leveraging GIPR activity to enhance insulin sensitivity in adipose tissue and potentiate GLP-1R-mediated appetite suppression. Together these produce synergistic glycemic and weight outcomes exceeding selective GLP-1R agonism.

Nicotinamide adenine dinucleotide (NAD+) is an essential coenzyme present in all living cells, functioning as a central electron carrier in cellular energy metabolism and as a critical substrate for longevity-associated enzymes including sirtuins (SIRT1–7) and poly(ADP-ribose) polymerases (PARPs). NAD+ levels decline progressively with age in humans across multiple tissues [Rajman et al., 2018, Cell Metab]. Clinical trials of NAD+ precursors (NR and NMN) have demonstrated safe and effective restoration of whole-blood and tissue NAD+ levels in aging adults.

Research data document mitochondrial biogenesis, DNA repair enhancement via PARP activation, sirtuin-mediated epigenetic remodeling, and improved insulin sensitivity following NAD+ repletion in aged research subjects [Yoshino et al., 2021, Science].

NAD+ serves as the obligatory electron acceptor in glycolysis and the TCA cycle, while its oxidized form activates SIRT1/3 to deacetylate and regulate PGC-1α (mitochondrial biogenesis), FOXO transcription factors (stress resistance), and p53 (DNA repair).

Thymosin Alpha-1 (thymalfasin, Zadaxin) is a synthetic 28-amino acid peptide identical to the N-terminal fragment of prothymosin alpha, naturally secreted by thymic epithelial cells. It is approved in over 35 countries for treatment of hepatitis B, hepatitis C, and as an immune adjuvant in certain malignancies, and holds FDA Orphan Drug designation. Clinical evidence from hepatitis B trials demonstrated significant rates of sustained HBeAg seroconversion versus control [Chan et al., 2005, Hepatology].

Established clinical evidence supports immune reconstitution in immunocompromised patients, enhanced vaccine response, antiviral activity in chronic viral hepatitis, and adjuvant efficacy in oncology settings [Billich, 2002, Curr Opin Investig Drugs].

Tα1 activates TLR2 and TLR9 on dendritic cells and macrophages, triggering NF-κB-mediated cytokine production and maturation of antigen-presenting cells. It promotes differentiation of naïve T-cells into Th1-polarized effectors and enhances NK cell cytotoxicity.

GHK-Cu (Copper Tripeptide-1, Gly-His-Lys:Cu²⁺) is an endogenous copper-binding tripeptide naturally present in human plasma, saliva, and urine, with plasma concentrations declining markedly from ~200 ng/mL in young adults to ~80 ng/mL by age 60. It demonstrates upregulation of collagen I, III, and VI, elastin, decorin, and chondroitin sulfate in human fibroblast models [Pickart et al., 2015, J Aging Res]. Transcriptomic analyses reveal GHK-Cu modulates over 4,000 human genes associated with tissue remodeling, anti-inflammatory, and antioxidant pathways.

Research consistently documents stimulation of collagen and glycosaminoglycan synthesis, acceleration of wound healing, reduction of oxidative stress via SOD upregulation, and promotion of hair follicle cycling. Clinical cosmetic studies report measurable improvements in skin density, fine lines, and elasticity [Gorouhi & Maibach, 2009, Int J Cosmet Sci].

GHK-Cu upregulates TGF-β1/β2 signaling and VEGF expression to drive fibroblast collagen synthesis and angiogenesis. The Cu²⁺ ion activates copper-dependent enzymes including lysyl oxidase (collagen cross-linking) and SOD1 (antioxidant defense), while the GHK peptide moiety modulates Wnt/β-catenin and SPARC pathways.