Experimental

Epitalon (also known as Epithalon or Epithalone) is a synthetic tetrapeptide with the amino acid sequence Ala-Glu-Asp-Gly (AEDG), originally derived from epithalamin, a bovine pineal gland extract. Its primary mechanism of action involves activation of telomerase enzyme activity, leading to telomere elongation in human somatic cells, as well as regulation of melatonin production and circadian rhythms. Over 25 years of research has demonstrated geroprotective effects in multiple animal models, including increased lifespan (11-16% in fruit flies, 12-13% maximum lifespan extension in mice), improved biomarkers of aging, and inhibition of spontaneous tumor development. Limited human clinical trials have shown positive results in treating retinitis pigmentosa and reducing cardiovascular mortality in elderly patients with coronary disease. However, Epitalon remains an experimental research compound with no FDA or EMA approval for therapeutic use. Its regulatory status is that of an investigational peptide, not approved for clinical application in the United States or Europe, though it has been extensively studied in Russian research institutions for decades.

FGL (Fibroblast Growth Loop) is a synthetic 15-amino acid peptide derived from the second fibronectin type III module of Neural Cell Adhesion Molecule (NCAM) that functions as an NCAM mimetic by binding to and activating fibroblast growth factor receptor 1 (FGFR1). This peptide has demonstrated extensive neuroprotective, neurotrophic, and anti-inflammatory effects in preclinical studies, including mobilization of neural stem cells, enhancement of synaptic plasticity, and protection against ischemic and amyloid-beta-induced neuronal damage. FGL has advanced to early-stage human clinical trials for neurodegenerative diseases, showing favorable safety and tolerability profiles in Phase I studies with intranasal administration.

TB-500 (Thymosin Beta-4) is a naturally occurring 43-amino acid peptide that functions as the major G-actin-sequestering molecule in mammalian cells. It plays crucial roles in tissue repair, wound healing, and cellular regeneration by regulating cell migration, proliferation, and differentiation. The peptide has demonstrated significant therapeutic potential in multiple clinical applications including dermal wound healing, corneal injuries, dry eye disease, and cardiac tissue repair following myocardial infarction. Phase I and Phase II clinical trials have established its safety profile at various dosing regimens, though it remains unapproved by regulatory agencies. TB-500 is sold on the gray market as a research chemical and is prohibited in competitive sports by the World Anti-Doping Agency due to its performance-enhancing and tissue regeneration properties.

Follistatin-344 is a naturally occurring glycoprotein that functions as a potent myostatin inhibitor, primarily investigated for muscle growth and therapeutic applications in muscular dystrophy. It works by binding to and neutralizing myostatin and activin, growth factors that normally limit muscle development. The peptide consists of 344 amino acids and undergoes post-translational modification to generate the circulating FS-315 isoform. Preclinical research in mice, pigs, and non-human primates has demonstrated pronounced increases in muscle mass and strength following a single AAV1-mediated gene delivery. Clinical trials are underway for Becker and Duchenne muscular dystrophy, with early results showing improved ambulation without serious adverse effects. Beyond muscle growth, emerging research suggests potential applications in diabetes (promoting pancreatic beta-cell proliferation), bone health (supporting osteogenesis), and metabolic disorders. The peptide remains experimental with limited human safety data available.

Delta Sleep-Inducing Peptide (DSIP) is a naturally occurring nonapeptide (Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu) with molecular weight 848.824 Da, first isolated from rabbit cerebral venous blood in 1974. It functions as a neuromodulatory peptide found in the hypothalamus, limbic system, pituitary, and peripheral organs, crossing the blood-brain barrier easily without enzymatic degradation. DSIP's primary mechanisms involve modulation of sleep architecture, neurotransmitter regulation (serotonin, dopamine, glutamate), stress response via the HPA axis, and potential interaction with NMDA receptors and adrenergic pathways. Clinical applications have focused on chronic insomnia, stress-related disorders, pain management, and substance withdrawal symptoms, though exact mechanisms remain incompletely characterized. Despite 50 years of research, DSIP is not FDA-approved or regulated by major health authorities worldwide, remaining available only as a research compound. It exists in an unregulated gray market, with most commercially available forms being research-grade material not intended for human use, and the FDA has flagged it for potential immunogenicity risks.

Mazdutide is a first-in-class once-weekly dual agonist of both glucagon-like peptide-1 (GLP-1) and glucagon receptors, designed as a long-acting synthetic oxyntomodulin analog. It has been approved in China for chronic weight management in adults with obesity or overweight and is being investigated for type 2 diabetes treatment. Through its dual mechanism, mazdutide promotes insulin secretion and appetite suppression via GLP-1 receptor activation while increasing energy expenditure, enhancing fatty acid oxidation, and reducing liver fat through glucagon receptor activation. Phase 3 clinical trials have demonstrated superior efficacy compared to existing GLP-1 agonists, achieving up to 14% body weight reduction at 48 weeks, exceptional liver fat reduction (up to 80.2%), and multiple cardiometabolic benefits including improvements in blood glucose, lipids, blood pressure, and liver enzymes.

MOTS-c (Mitochondrial Open Reading Frame of the 12S rRNA Type-C) is a 16-amino-acid peptide encoded within the mitochondrial genome's 12S ribosomal RNA region, discovered in 2015 by researchers at the University of Southern California. This mitochondrial-derived peptide functions as a signaling molecule that translocates to the cell nucleus during metabolic stress, where it regulates nuclear gene expression through AMPK-dependent mechanisms. Primary research has focused on its roles in metabolic regulation, exercise performance, aging, insulin resistance, obesity, cardiovascular health, and bone metabolism. MOTS-c levels naturally decline with age in plasma, though skeletal muscle expression may increase compensatorily. The peptide is not approved by the FDA or other regulatory agencies for clinical use and remains an investigational compound available only in research settings. It is prohibited by the World Anti-Doping Agency (WADA) under metabolic modulators. Currently, MOTS-c is only available through research suppliers and is not approved for human therapeutic use outside of clinical trials.

Thymosin Alpha-1 is a 28-amino acid immunomodulatory peptide naturally occurring in the thymus gland that has been extensively studied for its ability to enhance and restore immune function. The peptide acts through Toll-like receptors in dendritic cells, promoting T-cell differentiation and maturation, activating natural killer cells, and modulating cytokine production. With over 4,400 subjects enrolled in clinical trials across the United States, Europe, and China, Thymosin Alpha-1 has demonstrated efficacy in treating chronic hepatitis B and C, cancer immunotherapy, sepsis, COVID-19, and as a vaccine adjuvant. The synthetic form, thymalfasin (Zadaxin), has received regulatory approval in over 30 countries for conditions including hepatitis B, hepatocellular carcinoma, and malignant melanoma. However, it is not FDA-approved in the United States, though it received orphan drug designation. Clinical experience involving over 11,000 subjects across more than 30 trials demonstrates a favorable safety profile with only minor, transient side effects, primarily mild injection site reactions. The peptide is typically administered subcutaneously at doses of 0.8-6.4 mg twice weekly.

KPV is a tripeptide consisting of lysine-proline-valine, derived from the C-terminal sequence of alpha-melanocyte stimulating hormone (α-MSH). This short peptide exhibits potent anti-inflammatory properties without the pigmentation effects associated with full-length α-MSH. [1][2] The peptide functions by modulating inflammatory pathways, particularly through inhibition of pro-inflammatory cytokines and regulation of NF-κB signaling. Research has demonstrated its ability to reduce inflammation in various tissue types, with particular interest in gastrointestinal applications for inflammatory bowel disease. [3][4] KPV can be administered orally, topically, or via injection, with each route showing different tissue targeting properties. The oral route appears particularly promising for gut-targeted anti-inflammatory effects, while topical application may benefit skin conditions. Research remains largely preclinical, with human clinical trials still limited. [5][6]

FOX-04-DRI (Proxofim) is a synthetic 46-amino acid cell-penetrating peptide composed of D-amino acids (D-retro-inverso configuration) designed to selectively eliminate senescent cells by disrupting the FOXO4-p53 protein interaction. By perturbing this critical survival mechanism, the peptide causes p53 nuclear exclusion and triggers selective apoptosis specifically in senescent cells while sparing healthy cells, demonstrating an 11.73-fold selectivity difference. Preclinical studies in aged and accelerated-aging mouse models have shown restoration of tissue homeostasis, improved renal and mitochondrial function, fur density restoration, enhanced physical fitness, and neutralization of chemotherapy-induced toxicity, positioning it as a promising senolytic agent for age-related diseases and healthspan extension.

PE-22-28 is a synthetic 7-amino acid peptide (sequence: GVSWGLR) derived from the analysis of spadin blood degradation products, designed as a potent and selective TREK-1 (TWIK-related potassium channel) inhibitor with antidepressant and neuroprotective properties. This shortened analog demonstrates superior pharmacological characteristics compared to its parent compound spadin, exhibiting an IC50 of 0.12 nM for TREK-1 inhibition (versus 40-60 nM for spadin) and an extended duration of action up to 23 hours (compared to 7 hours for spadin). Preclinical research indicates PE-22-28's potential for treating depression, post-stroke depression, traumatic brain injury, and ischemic stroke through mechanisms involving enhanced neurogenesis, synaptogenesis, and modulation of serotonergic pathways. While showing promising results in animal models with rapid onset of antidepressant effects and neuroprotective benefits, PE-22-28 remains strictly experimental with no approved human clinical applications.

Bronchogen is a synthetic tetrapeptide bioregulator (Ala-Glu-Asp-Leu/AEDL) developed by Vladimir Khavinson for respiratory system support. This short peptide interacts directly with DNA and histone proteins to regulate gene expression in bronchial epithelium, promoting differentiation and functional activity of lung cells. Research demonstrates its ability to stabilize DNA, reduce inflammation, restore epithelial integrity, and enhance surfactant production in animal models of chronic obstructive pulmonary disease (COPD) and lung injury.

Thymalin is a polypeptide complex extracted from calf thymus tissue, developed by Prof. Vladimir Khavinson in the 1970s as an immunomodulatory bioregulator. It contains short peptides (KE, EW, EDP) that epigenetically regulate gene expression, stimulate hematopoietic stem cell differentiation into T-lymphocytes, and modulate inflammatory pathways. Extensive clinical research in Russia demonstrates geroprotective effects, with 2-4 fold mortality reduction in elderly populations and efficacy in treating immune dysfunction, viral infections, cancer support, and COVID-19.

Retatrutide (LY3437943) is a novel synthetic peptide that acts as a triple agonist at the glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), and glucagon receptors. This 39-amino acid peptide represents a significant advancement in obesity pharmacotherapy, demonstrating superior weight loss efficacy compared to existing dual agonists like tirzepatide and single agonists like semaglutide. Phase 2 clinical trials have shown up to 24.2% body weight reduction at 48 weeks with the 12 mg dose, making it one of the most effective weight loss therapeutics in development. The triple agonist mechanism combines appetite suppression and enhanced insulin secretion (via GIP and GLP-1) with increased energy expenditure (via glucagon receptor activation), while also showing promising results for metabolic dysfunction-associated steatotic liver disease (MASLD) and glycemic control in type 2 diabetes.

Cortagen is a synthetic tetrapeptide (Ala-Glu-Asp-Pro) derived from brain cortex polypeptide extract Cortexin, developed by Vladimir Khavinson as part of the peptide bioregulator family. It demonstrates neuroprotective properties through epigenetic gene regulation, promotes nerve regeneration, and crosses the blood-brain barrier to exert direct CNS effects. Research shows it increases nerve fiber growth rate by 27% and conduction velocity by 40%, while modulating gene expression across 110+ genes involved in neural repair, cardiovascular function, and cellular differentiation.

Pinealon (EDR) is a synthetic tripeptide bioregulator composed of glutamic acid, aspartic acid, and arginine (Glu-Asp-Arg) developed by Russian scientist Vladimir Khavinson. Originally isolated from the polypeptide neuroprotective drug Cortexin, it demonstrates potent neuroprotective properties through multiple mechanisms including ROS suppression, gene expression regulation, and epigenetic modulation. Pinealon has been extensively studied in Russian scientific literature for its effects on cognitive function, neuroplasticity, and cellular aging processes.

Vesugen (KED) is a synthetic tripeptide bioregulator consisting of lysine, glutamic acid, and aspartic acid (Lys-Glu-Asp), developed by Dr. Vladimir Khavinson for vascular health. Research demonstrates its ability to increase microvascular density in aged animals by 2.5-2.8 times and normalize endothelial cell function through epigenetic regulation of gene expression. Clinical studies in elderly patients show effectiveness in treating atherosclerosis, improving microcirculation, and protecting blood vessels from age-related dysfunction. The peptide acts as a geroprotector with vasoprotective properties, regulating expression of key proteins including Ki-67, SIRT1, endothelin-1, and connexin-37.

YK-11 is a synthetic steroidal selective androgen receptor modulator (SARM) structurally derived from dihydrotestosterone that exhibits both androgen receptor agonist activity and myostatin inhibition properties. It uniquely induces muscle differentiation by upregulating follistatin expression, a potent myostatin antagonist, leading to enhanced anabolic effects in skeletal muscle and bone tissue. YK-11 remains an experimental compound with no FDA approval, limited to in vitro and animal studies, with concerning safety profiles including neurotoxicity, hepatotoxicity, testosterone suppression, and cardiovascular risks. The compound is banned by WADA for athletic use and is not approved for human consumption in any jurisdiction.

5-Amino-1MQ (5-amino-1-methylquinolinium) is a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), an enzyme that plays a critical role in cellular energy metabolism and NAD+ regulation. By inhibiting NNMT, 5-Amino-1MQ increases intracellular NAD+ levels and S-adenosylmethionine (SAM) availability, leading to enhanced energy expenditure, reduced fat accumulation, and improved metabolic function in preclinical models. This compound has demonstrated significant potential for treating obesity, metabolic syndrome, and age-related muscle decline in animal studies, though no human clinical trials have been published to date.

PNC-27 is a 32-residue synthetic anticancer peptide combining p53 residues 12-26 (HDM-2 binding domain) with a cell-penetrating penetratin sequence. It selectively kills cancer cells by binding to HDM-2 protein expressed in cancer cell membranes, inducing transmembrane pore formation and necrosis while sparing normal cells. Extensive preclinical research demonstrates efficacy against multiple cancer types including leukemia, ovarian, pancreatic, breast, and cervical cancers.

Humanin is a 24-amino acid mitochondrial-derived peptide (MDP) encoded by a small open reading frame within the mitochondrial 16S ribosomal RNA gene (MT-RNR2). First discovered in 2001 as a neuroprotective factor, humanin belongs to the novel class of mitochondria-derived peptides and represents the first peptide identified to be encoded by mitochondrial DNA. The peptide can be translated both in the mitochondrial matrix (producing a 21-amino acid variant) and the cytosol (producing the full 24-amino acid peptide), with both forms being biologically active. Humanin functions as a signaling molecule with cytoprotective and antiapoptotic properties, exerting beneficial effects across multiple organ systems including the brain, heart, skeletal muscle, and vascular tissues. Research has demonstrated humanin's role as a regulator of both lifespan and healthspan, with levels naturally declining with age and in various disease states including Alzheimer's disease, diabetes, and cardiovascular disorders. The peptide exerts its effects through multiple mechanisms including binding to cell surface receptors (FPRL1/2 and trimeric CNTFR-α/gp130/WSX-1 complex), intracellular protein interactions (BAX, IGFBP3), and modulation of key signaling pathways (STAT3, AMPK, ERK1/2). The highly potent S14G-humanin analog (HNG) shows 1000-fold greater biological activity than native humanin. While extensive preclinical evidence supports humanin's therapeutic potential for age-related diseases, neurodegenerative disorders, metabolic dysfunction, and cardiovascular conditions, the peptide remains investigational with no completed human clinical trials for therapeutic applications. Humanin is not approved by the FDA or other regulatory agencies for clinical use.

Cagrilintide is a long-acting, acylated amylin analogue that functions as a non-selective agonist of amylin receptors (AMY1R, AMY2R, AMY3R) and the calcitonin receptor (CTR). Developed by Novo Nordisk, it is designed for once-weekly subcutaneous administration with a half-life of approximately 8 days, addressing obesity and type 2 diabetes through appetite suppression, delayed gastric emptying, and glucagon inhibition. Clinical trials have demonstrated remarkable weight loss efficacy, particularly when combined with semaglutide (branded as CagriSema), with the REDEFINE 1 trial showing 60% of participants achieving at least 20% body weight reduction. Cagrilintide represents a significant advancement in obesity pharmacotherapy by leveraging the complementary mechanisms of amylin and GLP-1 receptor agonism.

Cardiogen is a synthetic tetrapeptide bioregulator (Ala-Glu-Asp-Arg) developed by Dr. Vladimir Khavinson in Russia during the 1980s-90s. It acts as a cardioprotective agent that regulates gene expression and protein synthesis in cardiac tissue, particularly targeting fibroblasts responsible for tissue repair. Studies demonstrate its ability to enhance cytoskeletal and nuclear matrix protein expression, reduce apoptosis through p53 modulation, and protect myocardial tissue following ischemic injury. While extensively studied in animal models, human clinical trials remain limited.

BPC-157 (Body Protection Compound-157) is a synthetic pentadecapeptide consisting of 15 amino acids (sequence: GEPPPGKPADDAGLV) derived from a protective protein found in human gastric juice. The peptide demonstrates pleiotropic biological activity through multiple mechanisms, including stimulation of vascular endothelial growth factor (VEGF) expression and VEGFR2 receptor activation, enhancement of growth hormone receptor expression, activation of the FAK-paxillin pathway for cell migration, and modulation of the nitric oxide system via Src-Caveolin-1-eNOS signaling. Preclinical research in animal models has shown consistent healing effects across diverse tissue types including tendons, ligaments, muscles, bones, gastrointestinal mucosa, and neural tissue. While BPC-157 was tested in Phase I clinical trials for inflammatory bowel disease (PL14736) by Pliva, Croatia, human clinical data remains extremely limited with only one small retrospective study in musculoskeletal pain. The FDA classified BPC-157 as a Category 2 bulk drug substance in 2023, prohibiting compounding due to insufficient safety evidence in humans. The World Anti-Doping Agency (WADA) and major sports organizations ban its use. Despite lack of FDA approval, the peptide is available through gray market channels and increasingly used by clinicians and athletes, raising significant safety and regulatory concerns.

JBSNF-000088 (6-methoxynicotinamide) is a potent and orally active small molecule inhibitor of nicotinamide N-methyltransferase (NNMT), though commonly marketed in peptide research circles. It demonstrates IC50 values of 1.8 µM, 2.8 µM, and 5.0 µM for human, monkey, and mouse NNMT respectively. In preclinical studies, JBSNF-000088 has shown significant efficacy in reducing body weight, improving insulin sensitivity, normalizing glucose tolerance, and potentially reversing EGFR-TKI resistance in non-small cell lung cancer. The compound functions as a slow-turnover substrate analog that modulates the NAD+ salvage pathway, influencing energy metabolism and sirtuin activity.

Small Humanin-Like Peptides (SHLPs 1-6) are a family of mitochondrial-derived peptides encoded by the 16S ribosomal RNA region of mitochondrial DNA, each comprising 24-38 amino acids. These microproteins function as age-dependent regulators of cellular metabolism, apoptosis, insulin sensitivity, and inflammatory responses. SHLP2 and SHLP3 exhibit cytoprotective effects by enhancing mitochondrial function and reducing oxidative stress, while SHLP6 demonstrates opposing pro-apoptotic activity. Emerging research indicates these peptides play crucial roles in metabolic disorders, neurodegenerative diseases, and aging-related pathologies, with SHLP2 showing particular promise as a therapeutic target for obesity, diabetes, macular degeneration, and Parkinson's disease.

Cerebrolysin is a parenterally administered neuropeptide preparation derived from purified porcine brain proteins through controlled enzymatic digestion. Composed of low molecular weight peptides (25%) and free amino acids (75%), it contains over 14,000 identified peptides corresponding to more than 1,600 porcine neuronal proteins. Cerebrolysin exhibits pharmacodynamic properties similar to endogenous neurotrophic factors, demonstrating neuroprotective and neurorestorative effects across multiple neurological conditions. The preparation has been extensively studied in clinical trials for acute ischemic stroke, traumatic brain injury, Alzheimer's disease, vascular dementia, and amyotrophic lateral sclerosis. While approved in over 50 countries including Austria, China, Germany, Russia, and South Korea, it remains unapproved by the FDA in the United States. Clinical evidence suggests potential benefits for cognitive function, neurological recovery, and functional outcomes, though results vary across different meta-analyses and patient populations.

ACE-031 (ramatercept) is a recombinant fusion protein consisting of the extracellular domain of activin receptor type IIB (ActRIIB) fused to human IgG1-Fc, designed to function as a myostatin inhibitor and ligand trap. By binding to myostatin, GDF-11, and activins, ACE-031 blocks these negative regulators of muscle growth from interacting with endogenous ActRIIB receptors, thereby promoting muscle hypertrophy and increased lean body mass. Originally developed by Acceleron Pharma in collaboration with Shire for treating Duchenne muscular dystrophy and other muscle-wasting conditions, the drug demonstrated promising pharmacodynamic effects on muscle mass and function in clinical trials but was discontinued in 2013 due to safety concerns including epistaxis (nosebleeds) and telangiectasias (dilated blood vessels). Despite the termination of clinical development, ACE-031 remains an important proof-of-concept demonstrating the therapeutic potential and challenges of targeting the myostatin/activin signaling pathway for muscle wasting disorders.

PT-141 (Bremelanotide) is a synthetic cyclic heptapeptide analogue of alpha-melanocyte-stimulating hormone (α-MSH) developed as a melanocortin receptor agonist. Originally derived from Melanotan II in the 1990s by Palatin Technologies, bremelanotide was specifically developed to address sexual dysfunction after the parent compound unexpectedly caused sexual arousal in clinical trials for tanning. The peptide primarily activates melanocortin receptors MC3R and MC4R in the central nervous system, particularly in the hypothalamic regions involved in sexual response. After extensive clinical development including two large Phase 3 RECONNECT trials involving over 1,200 premenopausal women, bremelanotide received FDA approval in June 2019 for the treatment of acquired, generalized hypoactive sexual desire disorder (HSDD) in premenopausal women. It is marketed as Vyleesi and administered as a 1.75 mg subcutaneous injection at least 45 minutes before anticipated sexual activity. The FDA considers it a first-in-class medication, representing a novel non-hormonal approach to treating sexual dysfunction through central melanocortin pathway activation.

Thymulin is a zinc-dependent nonapeptide hormone exclusively produced by thymic epithelial cells that plays a critical role in T-cell differentiation and immune system regulation. First characterized by Bach and Dardenne in 1977, thymulin requires zinc in an equimolecular ratio for biological activity and has been extensively studied for its immunomodulatory, anti-inflammatory, and analgesic properties. Research demonstrates bidirectional communication between thymulin and the neuroendocrine system, with therapeutic applications ranging from age-related immune decline to autoimmune diseases and inflammatory pain conditions.

Calcitonin Gene-Related Peptide (CGRP) is a 37-amino acid neuropeptide primarily found in C and Aδ sensory nerve fibers arising from dorsal root and trigeminal ganglia, playing a critical role in migraine pathophysiology and pain signaling. CGRP functions as a highly potent vasodilator and is involved in neurogenic vasodilation, cardioprotection, neuroprotection, and tissue healing through complex neuroimmune interactions. The peptide's central role in migraine has led to the development of CGRP-targeted therapies, including monoclonal antibodies (erenumab, fremanezumab, galcanezumab, eptinezumab) and small-molecule antagonists (gepants), which represent the first disease-specific preventive treatments for migraine. While CGRP demonstrates protective effects in cardiovascular disease, stroke, wound healing, and potentially neurodegenerative disorders, therapeutic CGRP blockade has shown favorable safety profiles in clinical trials, though long-term effects in high-risk populations require further investigation.

Substance P (SP) is an 11-amino acid neuropeptide belonging to the tachykinin family, encoded by the TAC1 gene and acting primarily through the neurokinin-1 (NK1) receptor. It serves as a key neurotransmitter in pain transmission, a mediator of neurogenic inflammation, and a critical regulator of immune function and tissue repair. SP is synthesized in sensory neurons and released from C-fibers in response to noxious stimuli, playing multifaceted roles in nociception, cardiovascular regulation, wound healing, and immune modulation.

Dihexa (PNB-0408) is a small-molecule, orally active angiotensin IV analog developed at Washington State University that functions as a potent hepatocyte growth factor (HGF) mimetic. It binds with high affinity to HGF (Kd=65 pM) and potentiates its activity at the c-Met receptor, stimulating synaptogenesis and neurogenesis at picomolar concentrations. Preclinical research demonstrates that Dihexa is seven orders of magnitude more potent than brain-derived neurotrophic factor (BDNF) at promoting synaptic connectivity. The compound crosses the blood-brain barrier, making it highly bioavailable compared to native HGF. In animal models, Dihexa has shown remarkable efficacy in reversing cognitive deficits, restoring motor function in Parkinson's disease models, and protecting against neurodegeneration through activation of the PI3K/AKT signaling pathway. The prodrug fosgonimeton (ATH-1017) entered clinical trials for Alzheimer's and Parkinson's disease but failed Phase 2/3 trials in 2024. Despite promising preclinical data, no human studies of Dihexa itself have been published, and significant safety concerns exist regarding potential cancer risk from c-Met activation. Dihexa remains an experimental research compound without regulatory approval in any country.

P21 (also known as P021) is a synthetic tetrapeptide (Ac-DGGLAG-NH2) derived from the biologically active region of human ciliary neurotrophic factor (CNTF; amino acid residues 148-151). An adamantylated glycine is added to its C-terminal to enhance blood-brain barrier permeability and reduce degradation by exopeptidases. P21 promotes neurogenesis in the hippocampal dentate gyrus by competitively inhibiting the leukemia inhibitory factor (LIF) signaling pathway and increasing brain-derived neurotrophic factor (BDNF) expression. Preclinical studies demonstrate P21's ability to enhance learning, memory, and synaptic plasticity while reducing tau hyperphosphorylation and amyloid-beta pathology in Alzheimer's disease models. The compound exhibits favorable pharmacokinetics for oral administration with minimal adverse effects compared to full-length CNTF.

Vasoactive Intestinal Peptide (VIP) is a 28-amino acid neuropeptide that functions as both a potent anti-inflammatory agent and neuroprotective factor throughout the body. VIP operates through three G-protein-coupled receptors (VPAC1, VPAC2, and PAC1) to regulate immune homeostasis, modulate inflammatory responses, and protect neural tissue from degeneration. Clinical research has demonstrated VIP's therapeutic potential in treating chronic inflammatory response syndrome (CIRS), neurodegenerative diseases, autoimmune conditions, and inflammatory bowel disorders through its ability to suppress pro-inflammatory cytokines, promote regulatory T cells, and induce neuroprotective proteins.

Endoluten is a peptide bioregulator complex derived from pineal gland tissue, developed by Professor Vladimir Khavinson at the St. Petersburg Institute of Bioregulation and Gerontology. It contains short peptides (molecular weight <5000 Da) including the tetrapeptide AEDG (Ala-Glu-Asp-Gly), which regulates melatonin synthesis, circadian rhythms, and neuroendocrine function. Clinical and experimental studies demonstrate geroprotective effects including normalized hormonal function, improved cardiovascular and immune parameters, and significant mortality reduction in elderly populations over 6-8 year follow-up periods.

N-Acetyl Selank is an enhanced synthetic heptapeptide derived from the endogenous immune peptide tuftsin, featuring acetylation for improved stability and bioavailability. It functions as a potent anxiolytic and nootropic compound with demonstrated effects on GABAergic, dopaminergic, and serotonergic neurotransmission. Originally developed by the Institute of Molecular Genetics of the Russian Academy of Sciences and approved for anxiety disorder treatment in Russia, it exhibits neuroprotective, immunomodulatory, and cognitive-enhancing properties without the side effects typical of benzodiazepines.

Thymopentin (TP-5) is a synthetic pentapeptide corresponding to amino acids 32-36 of the thymic hormone thymopoietin, exhibiting the full biological activity of the natural hormone. This immunomodulatory agent has been studied extensively for its ability to enhance T-cell differentiation and maturation, increase IL-2 production, and modulate immune responses in various clinical conditions including cancer, HIV, autoimmune diseases, and immunodeficiency states. With the molecular formula C₃₀H₄₉N₉O₉ and CAS number 69558-55-0, thymopentin has demonstrated therapeutic potential in clinical trials for melanoma, atopic dermatitis, and age-related immune decline, though results have been mixed across different disease conditions.

RU-58841 (also known as PSK-3841 or HMR-3841) is a nonsteroidal anti-androgen compound originally developed by Roussel Uclaf in the 1980s for topical treatment of androgen-dependent conditions. The compound functions as a competitive androgen receptor antagonist with high affinity for androgen receptors in hair follicles and sebaceous glands. RU-58841 demonstrates a relative binding affinity of 5% compared to DHT and exhibits a notably short in vivo half-life of less than one hour, making it unsuitable for systemic use but ideal for topical application. The mechanism involves blocking dihydrotestosterone (DHT) from binding to androgen receptors in dermal papilla cells, thereby preventing follicular miniaturization characteristic of androgenetic alopecia. Preclinical studies in animal models demonstrated potent efficacy, with 60% reduction in sebaceous gland size in hamsters and significant hair regrowth in stumptailed macaques without systemic antiandrogenic effects. Human clinical trials conducted by ProStrakan (Phase I with 30 subjects and Phase IIa with 120 subjects) reportedly showed equivalent or better hair growth compared to finasteride after six months of treatment with 2.5% or 5% topical solutions applied once daily. However, these clinical trial results were never formally published in peer-reviewed journals, and development was discontinued following corporate acquisition. RU-58841 is not FDA-approved and no regulatory agency has authorized its use in humans. Despite lack of approval, the compound is available through research chemical suppliers and is used off-label by individuals seeking alternatives to approved treatments like finasteride and minoxidil.

Kisspeptin-10 (Kp-10) is a bioactive 10-amino acid peptide derived from the KISS1 gene, corresponding to amino acids 45-54 of metastin. It acts as a critical regulator of reproductive function through activation of the GPR54 receptor, stimulating the release of gonadotropin-releasing hormone (GnRH) and subsequently luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Originally discovered for its anti-metastatic properties in cancer, kisspeptin-10 has emerged as a key player in the hypothalamic-pituitary-gonadal axis. The peptide shows therapeutic potential for fertility disorders including PCOS, hypothalamic amenorrhea, and male hypogonadism. It is currently experimental with no FDA approval and is classified as a substantial safety risk for compounding pharmacy use.

LL-37 is the sole human member of the cathelicidin family of antimicrobial peptides, derived from the C-terminal fragment of the human cationic antimicrobial protein 18 (hCAP18). This 37-amino acid peptide was identified in the 1990s as a critical component of human innate immunity. LL-37 functions through multiple mechanisms including direct antimicrobial activity via membrane disruption, immunomodulation through regulation of inflammatory responses, chemotaxis of immune cells, lipopolysaccharide neutralization, and promotion of wound healing and angiogenesis. The peptide is expressed in epithelial tissues of the skin, gastrointestinal tract, respiratory tract, and in various leukocytes including neutrophils, monocytes, and lymphocytes. Its expression is regulated by vitamin D, bacterial components, cytokines, and tissue injury signals. Currently, LL-37 is not FDA-approved for therapeutic use and remains available only for research purposes, though phase 1 clinical trials have been completed for melanoma and exploratory studies conducted for COVID-19 and sepsis.

N-Acetyl Semax Amidate is a modified and enhanced version of the Russian nootropic peptide Semax, incorporating both N-terminal acetylation and C-terminal amidation modifications. This dual modification dramatically improves pharmacokinetic properties compared to standard Semax, including enhanced metabolic stability, extended half-life (6-12 hours vs 2-4 hours), superior bioavailability, and increased resistance to enzymatic degradation. The peptide is based on Semax, a synthetic heptapeptide analog of ACTH(4-10) with the sequence Met-Glu-His-Phe-Pro-Gly-Pro. N-Acetyl Semax Amidate exhibits pronounced nootropic, neuroprotective, and neurotrophic properties through multiple mechanisms including upregulation of brain-derived neurotrophic factor (BDNF) expression, enhancement of dopamine and serotonin neurotransmission, melanocortin receptor modulation, and anti-inflammatory effects. While the parent compound Semax has extensive clinical research demonstrating efficacy in stroke recovery, cognitive enhancement, and neuroprotection, specific clinical trials on N-Acetyl Semax Amidate remain limited. The compound is primarily used as a research chemical and has not been evaluated or approved by regulatory agencies including the FDA, making it available only for research purposes in most countries outside Russia.

Pyrilutamide (also known as KX-826) is a novel, nonsteroidal, selective androgen receptor (AR) antagonist being developed as a topical treatment for androgenetic alopecia (male and female pattern hair loss). The compound functions as a high-affinity silent antagonist that competitively binds to androgen receptors in dermal papilla cells and hair follicles, preventing dihydrotestosterone (DHT) from activating these receptors and subsequently blocking the cascade of events that lead to hair follicle miniaturization. Mechanistically, pyrilutamide decreases androgen receptor protein levels and enhances Wnt/β-catenin signaling pathways crucial for hair growth, while also preventing the androgen-mediated secretion of paracrine inhibitory factors such as TGF-β1, IL-6, and DKK-1 that suppress hair follicle epithelial cell proliferation and induce apoptosis. Clinical development has progressed through multiple Phase II and Phase III trials in both China and the United States for male and female androgenetic alopecia. Phase II trials demonstrated promising results with the 0.5% solution applied twice daily showing increases in target area hair count (TAHC) of 10 hairs/cm² in U.S. males and 22.73 hairs/cm² in Chinese males after 24 weeks, with females showing an 11.39 hairs/cm² increase compared to placebo. However, the pivotal Phase III efficacy trial announced in November 2023 failed to meet its primary endpoint, showing no statistically significant difference in TAHC compared to placebo at 24 weeks, though the treatment did demonstrate significant increases in non-vellus TAHC compared to baseline and maintained an excellent safety profile. A separate long-term safety Phase III trial completed with more encouraging results, reporting that 53% of men and 48% of women experienced hair improvement after 52 weeks of twice-daily application of 0.5% pyrilutamide solution. Throughout all clinical trials, pyrilutamide has demonstrated a favorable safety profile with no serious adverse events (SAE) or adverse drug reactions (ADR) reported. Pyrilutamide is not currently FDA-approved and remains investigational, though it is available through research chemical suppliers for experimental use. The compound represents a new generation of topical antiandrogens designed to provide localized efficacy without the systemic side effects associated with oral antiandrogen therapies like finasteride.

AC-SDKP (N-Acetyl-Ser-Asp-Lys-Pro) is an endogenous tetrapeptide derived from thymosin β4 through enzymatic processing by meprin-α and prolyl oligopeptidase, subsequently degraded by the N-terminal domain of angiotensin-converting enzyme (ACE). This naturally occurring peptide functions as a negative regulator of hematopoietic stem cell differentiation and demonstrates potent anti-fibrotic, anti-inflammatory, and pro-angiogenic properties across multiple organ systems including the heart, kidneys, lungs, and liver. ACE inhibitors prevent AC-SDKP degradation, raising circulating levels approximately 5-fold, which contributes to their cardiovascular protective effects beyond traditional angiotensin II blockade. Extensive preclinical research over the past 20 years has established AC-SDKP's therapeutic potential for treating fibrotic diseases, with mechanisms involving TGF-β/Smad2 pathway suppression, inhibition of myofibroblast differentiation, and promotion of endothelial function.