Scientific Peptide Dosage Charts & Reconstitution Protocols
Peer-reviewed dosing schedules, titration charts, and reconstitution math for 80+ research peptides — from Retatrutide and Tirzepatide to BPC-157, Selank, and SS-31.
Anabolics Directory
Androgenic-anabolic support, muscle density, and receptor modulation.
SS-31
SS-31 (elamipretide, MTP-131) is a mitochondria-targeted aromatic-cationic tetrapeptide (D-Arg-2',6'-Dmt-Lys-Phe-NH2) developed by Hazel Szeto and Peter Schiller at Weill Cornell as a selective cardiolipin-binding agent that stabilizes inner mitochondrial membrane cristae, restores electron transport chain efficiency, and suppresses mitochondrial reactive oxygen species (mtROS) without depending on membrane potential for accumulation [1][2]. Across more than a decade of preclinical and clinical work it has shown improved peak oxygen uptake in primary mitochondrial myopathy (MMPOWER program) [3], protection against ischemia-reperfusion injury in kidney and heart models with accelerated ATP recovery [4], and slowed ellipsoid zone attenuation in geographic atrophy (ReCLAIM-2) [5]. On 19 September 2025 the FDA granted accelerated approval for elamipretide HCl (FORZINITY) as the first therapy for Barth syndrome in patients greater than or equal to 30 kg, supported by the TAZPOWER trial showing sustained gains in knee extensor strength [6]. Research protocols typically use 30 to 80 mg/day subcutaneous, mirroring the 40 mg/day dose evaluated in TAZPOWER, MMPOWER-3, and ReCLAIM, with weight-adjusted pediatric titration in Barth syndrome.
Ovagen
Ovagen is a synthetic short-chain peptide bioregulator (Glu-Asp-Leu, EDL tripeptide) developed at the St. Petersburg Institute of Bioregulation and Gerontology by Vladimir Khavinson as the active fragment isolated from bovine liver tissue extracts [1][2]. Within the Khavinson cytomedin framework, Ovagen is hypothesized to function as a hepatocyte-specific epigenetic modulator that enters the nucleus and binds to short, tissue-specific promoter sequences to upregulate hepatic protein synthesis, bile acid production, and antioxidant defense genes [2][3]. Preclinical and small Russian clinical observations describe normalization of transaminases, improved albumin synthesis, and accelerated recovery from toxic and viral hepatic insults [4][5]. Ovagen is not approved by the FDA, EMA, or other major Western regulators and is considered an unapproved investigational compound. Typical research dosing follows Khavinson convention: 1 to 2 capsules (each containing approximately 100 to 200 mcg of EDL with accompanying excipients) once or twice daily for 20 to 30 days, repeated every 4 to 6 months.
Testagen
Testagen is a synthetic tetrapeptide (Lys-Glu-Asp-Gly, KEDG) developed by Vladimir Khavinson at the St. Petersburg Institute of Bioregulation and Gerontology as the active fragment isolated from bovine testicular tissue extracts [1][2]. It belongs to the family of Khavinson short-peptide bioregulators that are hypothesized to selectively penetrate the cells of the tissue of origin, enter the nucleus, and modulate the transcription of genes involved in steroidogenesis, spermatogenesis, and androgen receptor signaling [3]. Russian observational studies and animal models have described improvements in testosterone synthesis, sperm parameters, and prostatic function in models of chronic prostatitis [4]. Testagen is not FDA approved, is not authorized by any Western regulator, and is used only in research contexts. The conventional Khavinson dosing schedule is 1 to 2 oral capsules (each containing approximately 200 mcg of KEDG) twice daily for 20 to 30 days, repeated every 4 to 6 months, sometimes combined with other Khavinson bioregulators such as Prostamax (prostate) and Endoluten (pineal).
DSIP
DSIP (Delta Sleep-Inducing Peptide) is a naturally occurring nonapeptide (Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu) first isolated by Schoenenberger and Monnier in 1977 from the cerebral venous dialysate of rabbits undergoing slow-wave sleep induced by intralaminar thalamic stimulation [1][2]. Synthetic DSIP enhances delta and spindle EEG activity, modulates the hypothalamic-pituitary axis, and exerts measurable effects on circadian rhythm, cortisol release, and growth hormone secretion in rodents and small human cohorts, with EEG delta activity rising approximately 35 percent in cortex of recipient rabbits [3][4]. The peptide does not bind GABA-A, melatonin, or adenosine receptors with high affinity; its mechanism appears to involve indirect modulation of CRH tone, GHRH pulses, and central noradrenergic activity. In a controlled clinical study of chronic insomniacs, intravenous DSIP at 25 nmol/kg increased total sleep time, improved subjective sleep quality, and slightly increased REM sleep without daytime sedation or hangover effect [5]. DSIP is not approved by the FDA, EMA, or other Western regulators and is used in research contexts only. Typical research dosing is 100 to 500 mcg subcutaneously or intramuscularly approximately 30 to 60 minutes before sleep onset, cycled 5 to 14 nights per month rather than continuously.
Kisspeptin
Kisspeptin is a family of RF-amide neuropeptides encoded by the KISS1 gene (the founder peptide kisspeptin-54 and its cleavage products kisspeptin-14, -13, and -10) that act through the G-protein-coupled receptor KISS1R (GPR54) to control the hypothalamic gonadotropin-releasing hormone (GnRH) pulse generator [1][2]. Arcuate nucleus kisspeptin neurons co-expressing neurokinin B and dynorphin (KNDy neurons) generate the rhythmic discharges that drive GnRH and downstream LH secretion, while rostral periventricular kisspeptin neurons mediate the estradiol-positive feedback surge required for ovulation. Loss-of-function mutations in KISS1 or KISS1R cause hypogonadotropic hypogonadism in humans, anchoring the genetic role of the pathway [3]. Skorupskaite, Dhillo, Anderson, and colleagues have demonstrated in controlled clinical studies that kisspeptin administration potently stimulates LH release in healthy men and women and can trigger oocyte maturation in IVF cycles with dramatically reduced risk of ovarian hyperstimulation syndrome [4][5][6]. Kisspeptin-10 and kisspeptin-54 are not FDA approved; they remain investigational agents under active clinical development. Research dosing typically uses 0.1 to 1.0 nmol/kg subcutaneous or intravenous boluses, or 4 nmol/kg/h infusions over several hours.
Oxytocin
Oxytocin is a nine-amino-acid cyclic neuropeptide (Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Leu-Gly-NH2) synthesized in the paraventricular and supraoptic nuclei of the hypothalamus and released from the posterior pituitary, acting through the oxytocin receptor (OXTR), a Gq-coupled GPCR, to mediate uterine contraction during labor, milk ejection during lactation, and a broad range of central effects on social bonding, stress regulation, fear extinction, and pair-bonding behavior across mammalian species [1][2]. Synthetic oxytocin (Pitocin) has been FDA approved since 1962 for medical induction or augmentation of labor, control of postpartum hemorrhage, and management of incomplete or inevitable abortion, with ACOG-standardized titration protocols based on uterine contraction adequacy [3]. Research applications outside obstetrics use intranasal or sublingual formulations to study social cognition, autism spectrum disorder, post-traumatic stress disorder, and alcohol use disorder, with typical doses of 12 to 40 IU intranasally given 30 to 45 minutes before behavioral or psychophysiological testing [4][5]. Off-label and research dosing varies widely by formulation and indication; the obstetric route remains intravenous infusion only, while behavioral neuroscience studies use intranasal delivery designed to reach the brain via olfactory and trigeminal pathways.
Prostamax
Prostamax is a synthetic tetrapeptide (Lys-Glu-Asp-Pro, KEDP) developed by Vladimir Khavinson at the St. Petersburg Institute of Bioregulation and Gerontology as the active fragment derived from bovine prostate tissue extracts [1][2]. Within the Khavinson cytogen framework of ultra-short tissue-specific peptide bioregulators, Prostamax is proposed to penetrate prostate stromal and epithelial cells, enter the nucleus, and modulate transcription of genes regulating prostatic epithelial differentiation, inflammation, 5-alpha-reductase isoform expression, and androgen receptor signaling [3][4]. Cytogenetic studies have reported chromatin decondensation and reduced pericentromeric heterochromatin in treated cells, consistent with reactivation of age-silenced gene programs. Russian observational and animal studies describe reductions in prostatic inflammation, decreased stromal edema, normalization of prostate-specific antigen (PSA) in chronic prostatitis, and improvements in International Prostate Symptom Score (IPSS) [5]. Prostamax is not approved by the FDA, EMA, or other Western regulators. Conventional Khavinson dosing is 1 to 2 oral capsules (each containing approximately 200 mcg KEDP) twice daily for 20 to 30 days, cycled every 4 to 6 months, often stacked with Testagen and Endoluten for systemic anti-aging research.
PT-141
PT-141 (bremelanotide, Vyleesi) is a synthetic cyclic heptapeptide melanocortin receptor agonist (Ac-Nle-cyclo[Asp-His-D-Phe-Arg-Trp-Lys]-OH) derived from alpha-melanocyte-stimulating hormone, with nonselective agonist activity at MC1R, MC3R, MC4R, and MC5R and the strongest behavioral relevance to MC4R-mediated central sexual response pathways [1][2]. Diamond and colleagues published the first proof-of-concept study in 2006 demonstrating that intranasal bremelanotide improved subjective sexual arousal and desire in premenopausal women with sexual arousal disorder [3]. The pivotal phase 3 RECONNECT-1 and RECONNECT-2 trials randomized approximately 1,200 premenopausal women with hypoactive sexual desire disorder (HSDD) to 1.75 mg subcutaneous bremelanotide or placebo on demand for 24 weeks, with both co-primary endpoints of improved desire and reduced distress met at p less than 0.001 [4][5]. The FDA approved bremelanotide as Vyleesi on 21 June 2019 for acquired generalized HSDD in premenopausal women. Standard dosing is 1.75 mg subcutaneous as needed approximately 45 minutes before anticipated sexual activity, with no more than one dose per 24 hours and no more than 8 doses per month.
PNC-27
PNC-27 is a 32-residue chimeric peptide that fuses residues 12-26 of the p53 tumor suppressor (the HDM-2-binding domain of p53) with a 17-residue antennapedia-derived penetratin leader sequence, producing a cell-penetrating peptide that selectively binds plasma-membrane-associated HDM-2 on cancer cells and triggers rapid tumor cell necrosis through transmembrane pore formation [1][2]. Pioneering work by Bowne, Michl, Pincus and colleagues demonstrated that PNC-27 kills cancer cells across leukemia, breast, pancreatic, glioma, and melanoma lines in vitro and inhibits tumor growth in xenograft models without harming normal cells, because normal cells do not express HDM-2 on the plasma membrane [3][4]. More recent work has shown that PNC-27 also disrupts mitochondrial membranes in target cells through a similar HDM-2-dependent mechanism, contributing to the rapid necrotic phenotype rather than apoptosis [5]. PNC-27 is strictly preclinical and is not approved by the FDA, EMA, or any other regulator for any indication; it is not in current clinical trials registered on ClinicalTrials.gov. Research dosing has used intraperitoneal or intravenous administration in animal models at 10 to 200 mg/kg, with no validated human dosing regimen.
Neuroxelin
Neuroxelin is a research-only neuropeptide blend formulated in the broader category of compounded neuroprotective peptide preparations used in exploratory cognitive and neurodegenerative research, with no single defined structure, no FDA or EMA approval, and no published randomized controlled trials specific to the branded combination [1][2]. The composition of branded Neuroxelin preparations varies by source and typically includes selank, semax, cerebrolysin-derived fragments, or other neurotrophic peptides aimed at modulating BDNF expression, monoaminergic tone, and neuroinflammatory signaling [3][4]. Research applications draw on the much larger published evidence base for the individual constituent peptides (selank for anxiolysis, semax for attention and stroke recovery, cerebrolysin for vascular dementia and ischemic stroke), without specific data on the blend itself [5][6]. Typical research dosing in the underlying selank/semax literature uses 250 to 900 mcg intranasally per day, divided into two or three doses; injectable formulations and dose ranges depend on which specific peptides constitute a given Neuroxelin product.
Weight Loss Directory
GLP-1 agonists, GIP analogues, and mitochondrial uncouplers for fat oxidation.
Survodutide
Survodutide (BI 456906) is a once-weekly dual glucagon-receptor (GCGR) and glucagon-like peptide-1 receptor (GLP-1R) agonist developed jointly by Boehringer Ingelheim and Zealand Pharma. In the Phase 2 dose-finding trial of 386 adults with overweight or obesity without diabetes, survodutide 4.8 mg weekly produced a mean body-weight reduction of 14.9% (all data) and 18.7% (on-treatment data) at 46 weeks versus 2.8% with placebo, with nearly 40% of high-dose participants losing ≥20% [1]. The drug is investigational — not FDA, EMA or any other regulator approved — and remains in Phase 3 development across the SYNCHRONIZE program for obesity, type 2 diabetes and MASH; topline obesity data are expected to read out in 2026–2027. Standard Phase 3 dosing escalates weekly from 0.6 mg through 1.2, 1.8, 2.4, 3.6, 4.8 and 6.0 mg over a 10–12 week titration.
Tirzepatide
Tirzepatide is a once-weekly synthetic 39-amino-acid peptide that activates both the glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) receptors, manufactured by Eli Lilly and marketed as Mounjaro for type 2 diabetes and Zepbound for chronic weight management. In the Phase 3 SURMOUNT-1 trial of 2,539 adults without diabetes, tirzepatide 15 mg weekly produced a mean body-weight reduction of 20.9% at 72 weeks versus 3.1% with placebo, with 57% of participants losing at least 20% of body weight [1]. FDA approval for type 2 diabetes was granted in May 2022 and for chronic weight management in November 2023; tirzepatide is approved in the EU, UK, Japan, China and most major markets. Doses escalate monthly from 2.5 mg up to 5, 7.5, 10, 12.5 and a 15 mg maintenance ceiling.
5-Amino-1MQ
5-Amino-1MQ (5-amino-1-methylquinolinium) is a small-molecule (not peptide) inhibitor of nicotinamide N-methyltransferase (NNMT), the enzyme that catalyzes the methylation of nicotinamide using S-adenosyl-methionine as a methyl donor — a reaction that depletes both the methyl pool and the precursor pool for NAD+ synthesis. Developed from structure-activity work at the University of Texas at Austin, 5-Amino-1MQ was first reported by Neelakantan and colleagues (Biochem Pharmacol 2018) to reverse high-fat-diet-induced obesity in mice without affecting food intake [1]. A second paper from the same group (Neelakantan et al., 2019) showed activation of senescent muscle stem cells and improvement in skeletal-muscle regeneration in aged mice [2]. 5-Amino-1MQ is investigational only, has no FDA approval for any indication, and is sold by research-chemical suppliers as a laboratory compound. Typical research dosing is 50–150 mg daily orally for 4–12 week cycles.
Adipotide
Adipotide (FTPP, fat-targeting peptide-peptidomimetic) is a 22-amino-acid bipartite peptide consisting of a homing sequence (CKGGRAKDC) that selectively binds prohibitin on white-adipose-tissue blood vessels, conjugated via a glycine-glycine linker to a pro-apoptotic peptidomimetic sequence D(KLAKLAK)2 that disrupts mitochondrial membranes when internalized. Discovered by Kolonin and colleagues using in vivo phage display in obese mice and reported in Nature Medicine 2004 [1], the molecule was subsequently shown to produce 11% body-weight reduction in obese rhesus monkeys over 4 weeks (Barnhart et al., Science Translational Medicine 2011) [2]. Adipotide is investigational only — never tested in randomized human obesity trials, with the only registered human work being a small Phase 1 oncology trial in metastatic prostate cancer that was completed in 2014. The drug is not FDA approved, not in active clinical development for obesity, and remains a research-chemical compound.
Cagrilintide
Cagrilintide is a long-acting synthetic analogue of human amylin, the pancreatic hormone co-secreted with insulin that regulates satiety, gastric emptying and glucagon suppression. Developed by Novo Nordisk for once-weekly subcutaneous administration, it was designed as a partner peptide for semaglutide in the fixed-dose combination CagriSema. In the Phase 2 dose-finding trial published in The Lancet, cagrilintide 4.5 mg weekly produced a mean body-weight reduction of 10.8% at 26 weeks vs 3.0% with placebo, with cagrilintide 4.5 mg also out-performing daily liraglutide 3.0 mg on weight loss [1]. Cagrilintide as monotherapy is investigational and not FDA approved; the CagriSema combination was submitted for FDA NDA review in December 2025 based on REDEFINE Phase 3 data. Cagrilintide dosing escalates weekly from 0.16 mg through 0.3, 0.6, 1.2, 2.4 and 4.5 mg over 16–20 weeks.
AOD-9604
AOD-9604 is a synthetic 16-amino-acid peptide corresponding to the C-terminal lipolytic domain of human growth hormone (residues 177–191) with a tyrosine modification at position 177. Originally developed by Metabolic Pharmaceuticals (Australia) and characterized by Heffernan and colleagues, it was designed to retain the fat-mobilizing activity of full-length growth hormone while avoiding its anabolic and diabetogenic effects [1]. Six Phase 1 and Phase 2 human trials enrolling roughly 900 participants demonstrated a clean safety profile, but efficacy was modest: a 12-week placebo-controlled trial in obese adults showed mean weight loss of 2.6 kg on 1 mg/day AOD-9604 vs 0.8 kg on placebo, leading the manufacturer to halt obesity development in 2007 [2]. AOD-9604 is not FDA approved as a drug, holds GRAS (Generally Recognized as Safe) status from the FDA as a food/cosmetic ingredient, and is sold by research-chemical suppliers strictly for laboratory use. Typical research dosing is 250–500 mcg daily subcutaneously.
Mazdutide
Mazdutide (IBI362, LY3305677) is a once-weekly dual glucagon-receptor and GLP-1 receptor agonist engineered as an analogue of the endogenous gut hormone oxyntomodulin. It was originally discovered by Eli Lilly, then out-licensed to Innovent Biologics for development across Greater China and other Asian markets. In the Phase 3 GLORY-1 trial of Chinese adults with overweight or obesity, mazdutide 6 mg weekly produced a mean body-weight reduction of 14.0% at 48 weeks, with 49.5% of participants losing at least 15% of body weight versus 2.0% on placebo [1]. Mazdutide is investigational in the United States and most of Europe but received its first NDA acceptance from China's NMPA in February 2024 for chronic weight management — approval is anticipated in 2025–2026. Standard dosing escalates from 1.5 mg weekly to 3, 4.5, 6 and up to 9 mg over 12–16 weeks.
Retatrutide
Retatrutide (LY3437943) is a once-weekly triple-receptor agonist that activates the glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1) and glucagon (GCG) receptors in a single peptide backbone, combining appetite suppression with thermogenic energy expenditure. In the Phase 2 TRIUMPH-2 trial published in NEJM, adults with obesity receiving 12 mg weekly achieved a placebo-adjusted mean weight reduction of 24.2% at 48 weeks, the largest pharmacologic weight loss reported to date and with no apparent plateau on the dose-response curve [1]. The 9 mg and 12 mg arms of the Phase 3 TRIUMPH-4 trial confirmed up to 28.7% weight reduction in adults with obesity and knee osteoarthritis at 68 weeks [2]. Retatrutide is investigational, not FDA approved, and remains restricted to clinical-trial use; it is sold by chemical suppliers as a research compound only.
Semaglutide
Semaglutide is a once-weekly GLP-1 receptor agonist developed by Novo Nordisk and marketed as Ozempic (type 2 diabetes), Wegovy (chronic weight management) and Rybelsus (oral T2D). In the pivotal Phase 3 STEP-1 trial of 1,961 adults with overweight or obesity without diabetes, weekly subcutaneous semaglutide 2.4 mg produced a mean body-weight reduction of 14.9% at 68 weeks versus 2.4% with placebo, with 86% of treated participants achieving at least 5% loss [1]. Semaglutide is FDA approved for T2D (Ozempic, 2017), chronic weight management (Wegovy, 2021) and cardiovascular risk reduction in adults with obesity and established CVD (Wegovy expansion, 2024 — based on SELECT). Standard dosing is a 16-week titration: 0.25 → 0.5 → 1.0 → 1.7 → 2.4 mg weekly, increasing every 4 weeks.
AOD-9604 + CJC-1295 + Ipamorelin
The AOD-9604 + CJC-1295 + Ipamorelin stack is a research-protocol blend combining a synthetic hGH lipolytic fragment (AOD-9604) with two growth-hormone secretagogues: CJC-1295 (a GHRH analogue) and Ipamorelin (a selective ghrelin-receptor agonist). The combination rationale is mechanistic complementarity — AOD-9604 stimulates beta-3 adrenergic lipolysis directly in adipocytes [1] while CJC-1295 + ipamorelin amplifies endogenous pulsatile growth-hormone secretion through the GHRH and ghrelin axes respectively, producing a sustained GH/IGF-1 elevation believed to enhance fat mobilization and lean-tissue preservation [2][3]. No randomized clinical trial has tested this combination; the stack is used exclusively in research-chemical and compounded-prescription contexts. None of the three components is FDA approved as a drug. Typical research dosing: AOD-9604 250–500 mcg/day SC, CJC-1295 (no-DAC) 100–200 mcg pre-bed SC, Ipamorelin 100–200 mcg pre-bed SC.
Cagrilintide + Semaglutide
CagriSema is the fixed-dose combination of cagrilintide (a long-acting amylin analogue) and semaglutide (a GLP-1 receptor agonist), both at 2.4 mg weekly, developed by Novo Nordisk and submitted to the FDA in December 2025 based on the Phase 3 REDEFINE-1 trial. The combination exploits complementary satiety pathways: cagrilintide engages amylin/calcitonin-receptor signaling in the brainstem while semaglutide acts on hypothalamic GLP-1 receptors — producing an additive rather than redundant effect on appetite suppression and weight loss. In REDEFINE-1, CagriSema 2.4/2.4 mg weekly produced 22.7% mean weight loss at 68 weeks compared to 11.8% with cagrilintide alone, 16.1% with semaglutide alone, and 2.3% with placebo [1]. CagriSema is not yet FDA approved (NDA review expected to complete in 2026). Standard dosing escalates both peptides in parallel through a 16–20 week titration to the 2.4 mg / 2.4 mg maintenance dose.
Growth Hormone Directory
Secretagogues and growth hormone releasing peptides for cell regeneration.
Tesamorelin
Tesamorelin (trade name Egrifta) is a synthetic 44-amino-acid analogue of human growth hormone-releasing hormone (GHRH) stabilised by an N-terminal trans-3-hexenoyl modification that resists DPP-IV cleavage. It is the only GHRH-class peptide with full FDA approval, granted in November 2010 for the reduction of excess visceral adipose tissue in HIV-infected adults with lipodystrophy. The landmark 26-week Phase III trial by Falutz and colleagues (NEJM 2007) demonstrated a 15.2% reduction in visceral adipose tissue versus a 5% increase on placebo with 2 mg subcutaneous daily dosing, while Stanley and colleagues (JAMA 2014, Lancet HIV 2019) extended these findings to hepatic steatosis, showing a 37% relative reduction in liver fat fraction. Because tesamorelin acts upstream on the pituitary somatotroph rather than replacing growth hormone directly, it preserves the pulsatile GH rhythm and operates within physiologic IGF-1 feedback. Outside the HIV indication it remains investigational, and use in healthy adults for cosmetic body recomposition is off-label.
CJC-1295 NO DAC
CJC-1295 without DAC, more accurately called Modified GRF(1-29) or Mod GRF 1-29, is a 30-amino-acid analogue of human growth hormone-releasing hormone consisting of GRF(1-29) with four targeted amino-acid substitutions (D-Ala2, Gln8, Ala15, Leu27) that stabilise the molecule against dipeptidyl peptidase-IV degradation but do not include the maleimido-propionic acid Drug Affinity Complex (DAC) linker. The result is a short-acting GHRH analogue with a plasma half-life of approximately 30 minutes that produces a sharp, physiologic GH pulse and clears quickly enough to preserve negative-feedback dynamics. It has no FDA-approved indication and is supplied strictly as a research chemical. Typical research dosing is 100 mcg subcutaneously two to three times per day, often combined with a selective ghrelin-receptor agonist such as ipamorelin. The compound is the workhorse short-acting GHRH analogue in the peptide research community because it mimics endogenous GHRH kinetics more closely than the DAC-bound version and avoids the continuous-stimulation problem.
CJC-1295 DAC
CJC-1295 with DAC is a 30-amino-acid analogue of GRF(1-29) covalently conjugated through a maleimido-propionic acid linker (the Drug Affinity Complex) to circulating serum albumin. The albumin tether shields the peptide from renal filtration and proteolysis, extending plasma half-life from minutes to 6 to 8 days as established in the Teichman et al. JCEM 2006 Phase I trial. Single subcutaneous injection of 60 to 90 mcg/kg produced mean growth hormone elevations of two- to ten-fold and IGF-1 elevations of 1.5 to 3-fold persisting for 9 to 11 days in 21 healthy adult subjects. The compound is not FDA approved for any indication; original developer ConjuChem suspended Phase II development in 2007 after sudden cardiac deaths in a separate combination trial, and no further regulatory progress has occurred. Typical research dosing is 1 to 2 mg subcutaneously once per week. Because the molecule produces continuous low-amplitude GH elevation rather than discrete pulses, its pharmacology diverges meaningfully from native GHRH and short-acting analogues such as Mod GRF 1-29 or tesamorelin.
GHRP-2
GHRP-2 (pralmorelin, D-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2) is a synthetic hexapeptide growth hormone secretagogue and full agonist at the growth hormone secretagogue receptor type 1a (GHSR1a), the same receptor that endogenous ghrelin engages. Originally described by Bowers and colleagues in the early 1990s, GHRP-2 stimulates pituitary GH release through ghrelin-receptor activation in the somatotroph and simultaneous suppression of somatostatin tone in the hypothalamus, producing a sharp dose-dependent GH pulse with a half-life of approximately 15 to 60 minutes. It is approved as a diagnostic provocative test for childhood GH deficiency in Japan under the name pralmorelin hydrochloride, but it has no FDA-approved therapeutic indication in the United States. Typical research dosing is 100 to 300 mcg subcutaneously two to three times per day. GHRP-2 is more potent than GHRP-6 on a per-microgram basis (Bowers 1998) but is less receptor-selective than ipamorelin, producing measurable rises in prolactin and cortisol at higher doses.
GHRP-6
GHRP-6 (His-D-Trp-Ala-Trp-D-Phe-Lys-NH2) is a synthetic hexapeptide growth hormone secretagogue and the first non-natural GHSR1a agonist with documented potent appetite-stimulating activity. It binds the ghrelin receptor in the pituitary and arcuate nucleus, producing dose-dependent growth hormone release and the most pronounced orexigenic effect of any GHRP through neuropeptide Y and agouti-related peptide neuron activation in the hypothalamus. Bowers and colleagues first characterised it in 1984 and Smith et al. detailed the receptor pharmacology in the landmark Endocrine Reviews 1997 paper that helped lead to ghrelin's identification three years later. GHRP-6 has no FDA-approved indication and remains a research chemical. Typical research dosing is 100 mcg subcutaneously two to three times per day, often paired with a GHRH analogue. The combination of measurable appetite stimulation, dose-dependent GH release of 5-15 fold above baseline, and lower per-microgram potency than GHRP-2 makes GHRP-6 the GHRP of choice in research contexts focused on cachexia, sarcopenia and conditions where appetite restoration is desirable.
HGH 191AA
HGH 191AA, more accurately named somatropin, is recombinant human growth hormone produced by E. coli or mammalian expression systems and structurally identical to the 191-amino-acid pituitary-derived hormone. It is the only fully FDA-approved growth hormone replacement product and is licensed for adult and paediatric growth hormone deficiency, Turner syndrome, Prader-Willi syndrome, idiopathic short stature, chronic kidney disease and HIV wasting under brand names including Genotropin, Humatrope, Norditropin, Saizen, Omnitrope and Nutropin. The Molitch et al. Endocrine Society Clinical Practice Guideline (JCEM 2011) established adult dosing at 0.15 to 0.3 mg subcutaneously once daily, titrated against IGF-1 in the mid-normal age- and sex-adjusted range, typically to 0.4 to 0.6 mg/day in younger adults and 0.2 to 0.4 mg/day in patients above 60 years. Unlike GHRH analogues and GHRPs, somatropin replaces growth hormone directly rather than stimulating endogenous release; this bypasses pituitary feedback and produces continuous low-level GH exposure rather than physiologic pulses, which is the primary pharmacological trade-off with this drug class.
Ipamorelin
Ipamorelin (Aib-His-D-2-Nal-D-Phe-Lys-NH2) is a synthetic pentapeptide growth hormone secretagogue and a highly selective full agonist at the growth hormone secretagogue receptor type 1a (GHSR1a). Developed by Novo Nordisk in the late 1990s and described in the landmark Raun et al. European Journal of Endocrinology 1998 paper, ipamorelin produced dose-dependent growth hormone release with no measurable elevation in ACTH, cortisol or prolactin even at doses exceeding 200-fold the ED50 for GH release. This unique receptor selectivity distinguishes ipamorelin from earlier GHRPs (GHRP-2, GHRP-6, hexarelin), which all engage non-GHSR1a pathways that drive HPA-axis and prolactin responses. Ipamorelin has no FDA-approved indication; Novo Nordisk discontinued clinical development in 2007 after a Phase II trial in postoperative ileus failed to show efficacy. It remains the most widely used GHRP in research peptide protocols, typically dosed at 100 to 300 mcg subcutaneously two to three times per day and almost always stacked with a GHRH analogue such as CJC-1295 no DAC, sermorelin or tesamorelin to exploit the GHRH/GHRP synergy at the somatotroph.
IGF-1 LR3
IGF-1 LR3 (Long-Arg3-IGF-1) is an 83-amino-acid recombinant analogue of insulin-like growth factor-1 with two engineered modifications: an arginine substitution at position 3 and a 13-amino-acid N-terminal extension derived from methionyl-porcine GH. These modifications reduce binding to insulin-like growth factor binding proteins (IGFBPs) by approximately 1000-fold while preserving full agonist activity at the IGF-1 receptor. The result is a research compound with an effective half-life of 20 to 30 hours in plasma compared with 12 to 15 minutes for native IGF-1, making IGF-1 LR3 the standard tool for studying IGF-1 receptor signalling in cell culture and in vivo models. It has no FDA approval and is supplied strictly as a research chemical. Typical research dosing is 20 to 80 mcg subcutaneously per day. Unlike GHRH analogues and GHRPs, which stimulate endogenous pituitary GH release and engage the natural feedback loop, IGF-1 LR3 bypasses both the pituitary and the GH receptor entirely and engages the IGF-1R directly, which produces a distinct pharmacology including direct hypoglycaemic risk from IGF-1R cross-talk with the insulin receptor.
MGF
MGF (Mechano Growth Factor), more precisely IGF-1Ec, is a splice variant of the IGF-1 gene transcript that produces a precursor protein containing the mature IGF-1 sequence linked to a distinctive 24-amino-acid carboxy-terminal E-domain peptide. Goldspink and colleagues (FEBS Letters 2002, J Physiol 2003) characterised the splice event in skeletal muscle as the immediate response to mechanical overload or injury, with IGF-1Ec transcription preceding the conventional IGF-1Ea isoform by several hours. The cleaved E-peptide (the MGF peptide proper) appears to act independently of mature IGF-1 to activate quiescent satellite cells, drive myoblast proliferation, and delay differentiation, allowing the muscle stem-cell pool to expand before fusion into repaired fibres. MGF has no FDA approval and is supplied strictly as a research chemical. Typical research dosing is 100 to 200 mcg locally intramuscular post-workout. Native MGF E-peptide has a plasma half-life of approximately 5-7 minutes, which is why local rather than systemic injection is the standard research administration; the PEGylated variant (PEG-MGF) addresses this through pegylation.
PEG MGF
PEG-MGF (pegylated Mechano Growth Factor) is a synthetic 24-amino-acid analogue of the IGF-1Ec E-domain peptide modified by covalent attachment of polyethylene glycol chains to extend plasma half-life. Native MGF has a half-life of 5-7 minutes due to rapid proteolytic degradation; pegylation extends this to approximately 24-48 hours by shielding proteolytic recognition sites and reducing renal filtration. The structural premise is to deliver the satellite-cell-activating signal systemically rather than purely locally, addressing the principal pharmacological limitation of native MGF. PEG-MGF has no FDA approval and is supplied strictly as a research chemical. Typical research dosing is 100 to 250 mcg subcutaneously two times per week. Like native MGF, PEG-MGF appears to act on a putative muscle-specific receptor rather than the canonical IGF-1R, so it does not produce hypoglycaemia or the systemic glucose-axis effects characteristic of IGF-1 LR3. The mechanistic case rests on the foundational Goldspink and Yang work characterising IGF-1Ec splice variants and the E-peptide's independent biological activity.
Sermorelin
Sermorelin (formerly Geref) is a synthetic 29-amino-acid peptide consisting of the first 29 amino acids of human growth hormone-releasing hormone (GHRH) and was the first commercially marketed GHRH analogue. The biologically active region of native 44-amino-acid GHRH resides in the first 29 residues, making sermorelin a full agonist at the GHRH receptor. Sermorelin received FDA approval in 1990 as a diagnostic agent for GH deficiency and in 1997 for treatment of paediatric idiopathic GH deficiency under the brand name Geref (Serono). Serono voluntarily discontinued commercial production in 2008 due to manufacturing process difficulties, not safety concerns. The Geref International Study Group multicentre trial (J Pediatr 1996) showed that 30 mcg/kg/day subcutaneous sermorelin at bedtime increased growth velocity from 4.1 to 8.0 cm/year at 6 months in 110 GH-deficient prepubertal children. Although it no longer holds an active FDA-approved product, sermorelin is on the FDA 503A bulks list and remains widely used in compounding pharmacy. Adult research dosing is 200-500 mcg subcutaneously nightly.
CJC-1295 NO DAC + Ipamorelin
The CJC-1295 no DAC + ipamorelin stack is the most widely used growth hormone secretagogue combination in research peptide protocols. It pairs a short-acting GHRH analogue (Mod GRF 1-29, with a 30-minute half-life) and a highly selective GHSR1a agonist (ipamorelin, with a 2-hour half-life) to exploit the well-characterised synergy between the two pituitary somatotroph signalling pathways. The combination produces growth hormone responses 3 to 5 times higher than either agent administered alone, as demonstrated in multiple GHRH/GHRP synergy studies (Bowers JCEM 2001, Mericq JCEM 1998). Neither component is FDA approved; both are supplied solely as research chemicals. Typical research dosing is 100 mcg of each peptide subcutaneously two to three times per day, often co-injected from the same syringe pre-breakfast, mid-afternoon and pre-bed. The combination preserves pulsatile GH release, intact pituitary feedback regulation, and avoids the prolactin and cortisol elevations characteristic of GHRP-2 or GHRP-6, making it the preferred long-term stack for research-context body composition and recovery applications.
CJC-1295 + GHRP-2
The CJC-1295 + GHRP-2 stack combines a GHRH analogue with a potent ghrelin-receptor agonist to exploit the dual-pathway GH-release synergy at the pituitary somatotroph. Depending on the CJC-1295 variant used, the stack produces either pulsatile dual-pulse GH release (no-DAC variant) or continuous-plus-pulsed GH elevation (DAC variant). Bowers (JCEM 2001) and Mericq (JCEM 1998) established that combined GHRH + GHRP produces growth hormone responses 3 to 5 times higher than either agent alone, and GHRP-2 is approximately 2 to 3 times more potent per microgram than GHRP-6 at GHSR1a, making this stack one of the most aggressive GH-release combinations in research peptide use. Neither component is FDA approved; both are supplied solely as research chemicals. Typical research dosing is 100 mcg of CJC-1295 no DAC + 100-200 mcg GHRP-2 subcutaneously two to three times per day. The principal trade-off versus the ipamorelin variant is that GHRP-2 produces measurable prolactin and cortisol elevations at therapeutic doses, making it less favourable for long-term chronic dosing.
Tesamorelin 5mg + Ipamorelin 5mg
The Tesamorelin + Ipamorelin stack pairs the only FDA-approved GHRH analogue (tesamorelin, approved for HIV lipodystrophy at 2 mg daily) with the most selective GHSR1a agonist (ipamorelin). The combination exploits the well-characterised GHRH/GHRP synergy at the pituitary somatotroph, where convergent Gs-cAMP and Gq-PLC signals produce GH responses 3-5 times higher than either agent alone (Bowers JCEM 2001). The stack is unusual within the GH secretagogue research space because the GHRH component carries actual FDA approval (for HIV lipodystrophy) while the GHRP component is supplied as a research chemical. Typical research dosing is 2 mg tesamorelin nightly + 100-300 mcg ipamorelin one to three times per day, with the bedtime injections co-administered. The 5 mg/5 mg vial nomenclature commonly used by research peptide suppliers refers to the total peptide content per reconstitution vial, not a single dose. The combination is particularly favoured in research contexts focused on visceral adipose tissue reduction because tesamorelin's documented VAT-selective lipolytic effect is amplified by the dual-pulse GH-release synergy.
CJC-1295 DAC + Ipamorelin
The CJC-1295 DAC + Ipamorelin stack combines a long-acting albumin-bound GHRH analogue (CJC-1295 DAC, half-life 6-8 days, weekly dosing) with a highly selective GHSR1a agonist (ipamorelin, half-life 2 hours, thrice-daily dosing). The pharmacology is distinct from the no-DAC variant of the stack: CJC-1295 DAC produces continuous low-amplitude GH elevation through its 6-8 day half-life, while ipamorelin adds discrete ghrelin-receptor-mediated GH pulses on top of the elevated baseline. Teichman et al. (JCEM 2006) characterised CJC-1295 DAC pharmacokinetics in 21 healthy adults, demonstrating GH elevations of 2-10 fold and IGF-1 elevations of 1.5-3 fold persisting 9-11 days after a single injection. Neither component is FDA approved; both are supplied solely as research chemicals. Typical research dosing is 2 mg CJC-1295 DAC subcutaneously weekly + 100-300 mcg ipamorelin two to three times per day. The stack offers weekly-dose convenience for the GHRH component but trades pulsatility for chronic receptor engagement, and carries the unresolved cardiac safety signal from CJC-1295 DAC's 2007 Phase II development pause.
Healing & Recovery Directory
BPC-157, TB-500, and extracellular matrix remodeling factors.
TB-500
TB-500 is the synthetic counterpart of the active region of thymosin beta-4 (Tbeta4), a 43-amino-acid G-actin-sequestering peptide first isolated by Allan Goldstein and colleagues from bovine thymus tissue in the 1960s [1][2]. Goldstein and Crockford have published extensively on Tbeta4's roles in actin polymerization regulation, endothelial cell migration, angiogenesis, anti-inflammatory signaling, and stem cell mobilization, with downstream effects on wound healing, cardiac repair, and corneal regeneration [3][4]. Phase 2 trials of topical thymosin beta-4 in venous stasis ulcers and pressure ulcers showed accelerated healing in subsets of patients, with safety comparable to placebo, although the trials had small sample sizes and methodological constraints [5][6]. TB-500 is not approved by the FDA, EMA, or other Western regulators for any indication; it remains a research peptide and is banned by WADA for athletes. Research dosing in animals and the human literature typically uses 2 to 10 mg/week subcutaneously, often split into one or two injections during a 4 to 6 week loading phase, followed by maintenance at 2 mg/week.
Ara-290
ARA 290 (cibinetide) is a synthetic 11-amino-acid peptide engineered by Michael Brines and Anthony Cerami from a tertiary-structure surface region of erythropoietin that mediates tissue protection but not erythropoiesis, binding to a heteromeric receptor consisting of the EPO receptor and the beta-common receptor (CD131) on inflammatory and neural cells [1][2]. By activating the tissue-protective receptor without engaging the homodimeric EPO receptor that drives red cell production, ARA 290 produces anti-inflammatory, neuroprotective, and tissue-regenerative effects through downstream JAK2-STAT3 and PI3K-Akt signaling, without erythrocytosis or thrombotic risk [3]. Clinical trials in sarcoidosis-related small fiber neuropathy and type 2 diabetic neuropathy have demonstrated reductions in neuropathic pain, increases in corneal nerve fiber density on confocal microscopy, increases in regenerating GAP-43-positive nerve fibers on skin biopsy, and modest improvements in HbA1c and lipid profile sustained 4 weeks after end of dosing [4][5][6]. ARA 290 is not approved by the FDA, EMA, or other Western regulators. Research dosing has used 1 to 8 mg/day subcutaneous, typically for 28 days, with 4 mg/day emerging as the preferred dose in published phase 2 trials.
BPC-157
BPC-157 (Body Protection Compound-157) is a synthetic 15-amino-acid peptide (GEPPPGKPADDAGLV) derived from a partial sequence of a larger Body Protection Compound originally isolated from human gastric juice by Predrag Sikiric and colleagues at the University of Zagreb in the early 1990s [1][2]. Across more than 30 years of preclinical work, BPC-157 has been shown to accelerate the healing of tendon, ligament, muscle, bone, skin, gastrointestinal tract, and cornea through pro-angiogenic mechanisms involving VEGF receptor 2 (VEGFR2) activation, nitric oxide synthase upregulation through the Akt-eNOS axis, ERK1/2 signaling, and modulation of the dopaminergic and serotonergic systems [3][4]. Chang and colleagues demonstrated in the Journal of Applied Physiology that BPC-157 promotes tendon healing by enhancing tendon outgrowth, cell survival, and migration in tendon fibroblast cultures, and that it upregulates growth hormone receptor expression in those cells [5][6]. BPC-157 is not FDA approved and remains a research peptide. Typical research dosing is 250 to 500 mcg/day subcutaneously, with cycles of 4 to 8 weeks.
KPV
KPV is the C-terminal tripeptide of alpha-melanocyte-stimulating hormone (Lys-Pro-Val, residues 11-13 of alpha-MSH) that retains the broad anti-inflammatory and immunomodulatory activity of the parent hormone while lacking the pigmentary effects mediated through melanocortin-1 receptor activation on melanocytes [1][2]. The peptide acts primarily by inhibiting NF-kB nuclear translocation in macrophages, dendritic cells, T cells, and intestinal epithelial cells, suppressing transcription of TNF-alpha, IL-1beta, IL-6, and IFN-gamma. Brzoska, Luger, and colleagues reviewed the alpha-MSH-derived tripeptide pharmacology comprehensively in Endocrine Reviews and argued that KPV represents a viable anti-inflammatory candidate for immune-mediated conditions in which alpha-MSH itself would be problematic due to off-target hyperpigmentation [2]. Dalmasso and Merlin demonstrated in Gastroenterology that KPV is transported intact across colonic epithelium by the PepT1 di/tripeptide transporter (which is upregulated in inflamed colon) and reduces intestinal inflammation in DSS-induced colitis at 205 mcg/day in drinking water [3]. KPV is not approved by the FDA, EMA, or other Western regulators. Research dosing is 200 to 500 mcg/day subcutaneously or orally, often divided into two doses, in cycles of 4 to 8 weeks.
BPC-157 + TB-500
The BPC-157 and TB-500 stack pairs two research peptides with complementary regenerative mechanisms: BPC-157 (Body Protection Compound, a 15-amino-acid pentadecapeptide from gastric juice that drives VEGFR2-mediated angiogenesis and growth hormone receptor upregulation in tendon fibroblasts) [1][2] and TB-500 (the active 7-amino-acid fragment of thymosin beta-4 that sequesters G-actin, promotes endothelial cell migration, and supports stem cell mobilization) [3][4]. Sikiric, Chang, and colleagues have published the preclinical foundations for BPC-157 in tendon, ligament, and gastrointestinal healing, while Goldstein, Crockford, and colleagues have established TB-500/thymosin beta-4 in wound, cardiac, and corneal repair [5][6]. The combination is not FDA approved, and the only published controlled clinical evidence on each peptide individually is limited. Typical research dosing pairs BPC-157 at 250 to 500 mcg/day subcutaneously with TB-500 at 2 to 5 mg twice weekly during a 4 to 6 week loading phase, followed by maintenance of TB-500 at 2 mg weekly for an additional 4 to 8 weeks.
Tri-Heal
Tri-Heal is a research-only compounded peptide blend formulated to combine three regenerative peptides in a single vial for convenience in healing protocols: TB-500 (typically 25 mg), BPC-157 (typically 10 mg), and KPV (typically 10 mg) [1][2][3]. The rationale draws on independent preclinical evidence for each component covering distinct phases of the wound healing cascade: TB-500 provides actin-mediated cell migration and angiogenic support through G-actin sequestration (Goldstein, Crockford) [4][5]; BPC-157 drives VEGFR2-mediated angiogenesis, ERK1/2-mediated fibroblast proliferation, and approximately 3-fold growth hormone receptor upregulation in tendon fibroblasts (Sikiric, Chang) [6][7]; and KPV provides anti-inflammatory and immunomodulatory activity through inhibition of NF-kB-driven cytokine release in macrophages and intestinal epithelium (Brzoska, Dalmasso, Merlin) [8][9]. Tri-Heal as a fixed-combination product has not been evaluated in any published randomized controlled trial and is not approved by the FDA, EMA, or any other regulator. Typical research dosing reconstitutes the vial in bacteriostatic water and delivers a daily subcutaneous dose calibrated to deliver approximately 250 mcg BPC-157, 600 to 800 mcg TB-500, and 250 mcg KPV per injection.
TB-500 + BPC-157
The TB-500 and BPC-157 stack is the most widely studied combination protocol in unregulated peptide research, pairing two regenerative peptides with distinct loading and maintenance dosing schedules designed to match the very different pharmacokinetic profiles of the two molecules and the different tissue compartments their mechanisms address [1][2][3]. TB-500 (the active fragment of thymosin beta-4) has a plasma half-life of approximately 2 hours but durable tissue incorporation that supports twice-weekly dosing during loading and once-weekly maintenance [4][5]. BPC-157 (the gastric pentadecapeptide originally isolated by Sikiric and colleagues) is unusually stable in serum and gastric juice and is typically given as small daily injections to maintain steady angiogenic and growth factor signaling at the site of injury throughout the cycle [6][7]. Goldstein, Crockford, Sikiric, Chang, and colleagues provide the preclinical evidence base for each component [4][5][6][8]. The combination is not FDA approved and is banned in competitive sport by WADA under category S2. This page focuses on dosing-schedule architecture (loading, maintenance, taper, cycling, injection-site selection) rather than re-derivation of basic mechanism, which is covered in the BPC-157 plus TB-500 page.
PCT & Ancillaries Directory
Aromatase inhibitors, prolactin control, and endocrine restoration.
Gonadorelin
Gonadorelin is synthetic gonadotropin-releasing hormone (GnRH), an endogenous decapeptide (pGlu-His-Trp-Ser-Tyr-Gly-Leu-Arg-Pro-Gly-NH2) produced by hypothalamic neurons. Pulsatile GnRH release stimulates pituitary secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which in turn drive gonadal steroidogenesis and gametogenesis. Gonadorelin has been FDA approved historically (Factrel injection, Lutrepulse pump) for evaluation of pituitary gonadotrope function and for induction of ovulation in hypothalamic amenorrhea, although original branded products have been withdrawn from the U.S. market. Diagnostic doses are 0.1 mg subcutaneously or intravenously; pulsatile therapy uses 5–20 mcg every 90–120 minutes via portable infusion pump. Off-label, gonadorelin is increasingly used at 50–200 mcg subcutaneously two to three times weekly as an adjunct in testosterone replacement therapy to preserve testicular volume and fertility, in place of hCG.
HCG
Human chorionic gonadotropin (hCG) is a glycoprotein hormone composed of an alpha subunit shared with LH, FSH, and TSH and a unique beta subunit. Produced by the syncytiotrophoblast during pregnancy, hCG acts as a luteinizing hormone receptor agonist on Leydig cells in the testes and theca/granulosa cells in the ovary, driving steroidogenesis and supporting the corpus luteum during early gestation. Recombinant and urinary-derived hCG are FDA approved for ovulation induction, prepubertal cryptorchidism, and hypogonadotropic hypogonadism. In post-cycle therapy and as an adjunct to testosterone replacement, hCG is used at 500–1500 IU subcutaneously two to three times weekly to restore endogenous testicular function suppressed by anabolic-androgenic steroids or exogenous testosterone. Typical PCT protocols use 1000–2000 IU every other day for two to three weeks before transitioning to selective estrogen receptor modulators. hCG is not approved for weight loss; the FDA has explicitly warned against this off-label use.
HMG
Human menopausal gonadotropin (hMG, menotropins) is a purified mixture of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) activity extracted from the urine of postmenopausal women, typically in a 1:1 FSH:LH bioactivity ratio. Menopur (highly purified hMG) and similar branded products are FDA approved for controlled ovarian stimulation in women undergoing assisted reproductive technology (ART) and for induction of ovulation in anovulatory women. Standard fertility protocols initiate hMG at 75–225 IU subcutaneously daily, titrating up to 450 IU/day based on follicular response. In men with hypogonadotropic hypogonadism, hMG (75–150 IU subcutaneously three times weekly) is combined with hCG to drive spermatogenesis. In off-label male PCT applications, hMG is used at 75–150 IU two to three times weekly to support FSH-driven Sertoli cell recovery alongside hCG-driven Leydig cell stimulation, although controlled clinical evidence in this context is limited.
Cognitive Directory
Nootropic peptides, neuropeptides, and nerve growth factors (BDNF/NGF).
Selank
Selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) is a synthetic heptapeptide anxiolytic derived from the endogenous immunomodulator tuftsin, developed at the Russian Academy of Sciences' Institute of Molecular Genetics. It acts as a non-benzodiazepine GABA-A modulator and upregulates brain-derived neurotrophic factor (BDNF), producing anxiolysis without sedation, dependence, or withdrawal [1][2]. In a controlled trial of generalized anxiety disorder, Selank produced anxiolytic efficacy equivalent to medazepam while improving rather than impairing attention and working memory [3]. Intranasal dosing of 250–750 mcg per administration two to three times daily (total 900–1350 mcg) is the standard Russian clinical regimen across 14-day courses. Selank is registered as a prescription pharmaceutical in Russia (Peptogen, 0.15% nasal solution) for anxiety and asthenic disorders but has no FDA, EMA, or MHRA approval; in the United States it remains a research compound only. Its safety record across two decades of clinical use is favorable, with no reported abuse liability.
Adamax
Adamax (Ac-MEHFPGP-AG-NH2) is a synthetic nonapeptide derivative of Semax with an N-terminal acetyl group and a C-terminal Ala-Gly amide tail engineered to confer greater enzymatic stability and lipophilicity than the parent ACTH(4-10) analogue [1]. It belongs to the broader family of melanocortin-derived nootropic peptides developed within the Russian Academy of Sciences' neuropeptide program. Like Semax, Adamax is investigated for melanocortin receptor activity, BDNF/TrkB upregulation, and protection against ischemic and oxidative neuronal injury, with the modified backbone giving it longer in vivo half-life and stronger blood-brain barrier penetration on a per-dose basis [2]. Research dosing is typically 100–600 mcg intranasally one to two times daily, well below the equivalent Semax dose range, with cycle lengths of 2–6 weeks. Adamax is not FDA approved, has no EMA authorization, and is not registered as a pharmaceutical in any jurisdiction; it remains a research-only compound with no published human clinical trials.
Cerebrolysin
Cerebrolysin is a porcine brain-derived peptide and amino acid concentrate produced by enzymatic hydrolysis of purified porcine brain proteins, yielding a complex mixture of low-molecular-weight neuropeptides (under 10 kDa) with neurotrophic activity analogous to BDNF, NGF, GDNF, and CNTF. It is registered as a prescription neurotrophic drug in over 50 countries (including Austria, Germany, Russia, China, and across Eastern Europe) for stroke, traumatic brain injury, vascular dementia, and Alzheimer disease [1][2]. The pivotal CASTA and CARS randomized trials demonstrated improved neurological recovery at 30 mL intravenous daily for 10–21 days in acute ischemic stroke [3][4], and the CONSCIOUS observational program documented arousal improvements in minimally conscious state at 10 mL/day for 20+ days. Cerebrolysin is not FDA approved and is unavailable in the United States. Typical adult dosing ranges from 5 to 30 mL daily by slow IV infusion or intramuscular injection, with 10-day to 4-week cycles repeated 1–4 times yearly depending on indication.
Cortagen
Cortagen is a synthetic tetrapeptide (Ala-Glu-Asp-Pro, AEDP) developed by Vladimir Khavinson and colleagues at the St. Petersburg Institute of Bioregulation and Gerontology, derived by directed synthesis from the amino-acid composition of the polypeptide preparation Cortexin (a bovine cerebral cortex hydrolysate used in Russian neurology since the 1980s) [1][2]. Cortagen is classified as a peptide bioregulator targeting the cerebral cortex and is investigated for neuroprotection, cognitive support, nerve regeneration, and modulation of neurogenic and immune gene programs. Preclinical work shows Cortagen activates interleukin-2 mRNA synthesis, corrects metabolic disturbances in models of chronic cerebral ischemia, and supports peripheral and central nerve regeneration after injury [3]. Research dosing is empirical: typically 100–400 mcg/day subcutaneously or 1–3 mg/day orally across 10–20 day cycles, repeated 2–4 times yearly. Cortagen is registered as a dietary peptide product in Russia under bioregulator legislation but has no FDA, EMA, or MHRA approval. Human safety data are limited to Russian observational use.
PE-22-28
PE-22-28 is a 7-amino-acid synthetic peptide derived as a truncated analogue of spadin, the 17-residue sortilin-derived peptide first described by Mazella and colleagues in PLoS Biology 2010 as a selective TREK-1 potassium channel blocker with antidepressant-like activity [1]. PE-22-28 was developed by Djillani and colleagues in 2017 as a shortened analog with dramatically improved potency (IC50 ~0.12 nM vs. 40–60 nM for spadin), in vivo stability, and action duration of up to 23 hours [2]. By inhibiting the two-pore-domain potassium channel TREK-1, PE-22-28 produces fast-onset antidepressant effects in rodent models without the cardiovascular, gastrointestinal, or pro-seizure side effects associated with TREK-1 knockout phenotypes. PE-22-28 has no human clinical trial data, no FDA or EMA approval, and is not registered as a pharmaceutical in any jurisdiction. It remains a research-only compound used preclinically at typical doses of 100–500 mcg/kg subcutaneously or intranasally; equivalent human research dosing is empirical and unvalidated.
Pinealon
Pinealon is a synthetic tripeptide (Glu-Asp-Arg, EDR) designed by Vladimir Khavinson at the St. Petersburg Institute of Bioregulation and Gerontology as a short-peptide bioregulator targeting the pineal gland and broader neuroendocrine system [1][2]. It belongs to the Khavinson cytogen family of short peptides that, according to Khavinson and colleagues, penetrate plasma and nuclear membranes to bind specific DNA sequences and modulate tissue-specific gene programs. Preclinical work documents neuroprotection against hypoxia and oxidative stress, modulation of PCNA and p21 expression in neuronal cultures, and protection of induced neurons from age-related changes [3][4]. Research dosing varies widely: published rodent protocols use 10–100 mcg subcutaneously or intranasally, while outpatient Russian peptide-bioregulator practice uses 1–20 mg orally per day in 10–30 day cycles repeated 2–4 times per year. Pinealon is registered in Russia under dietary peptide-bioregulator legislation but has no FDA, EMA, or MHRA approval. Human safety data are limited to observational use.
Semax
Semax (Met-Glu-His-Phe-Pro-Gly-Pro, MEHFPGP) is a synthetic heptapeptide analogue of adrenocorticotropic hormone fragment ACTH(4-10), with a stabilizing Pro-Gly-Pro tail added to confer resistance to proteolysis. Developed at the M. M. Shemyakin and Yu. A. Ovchinnikov Institute of Bioorganic Chemistry by Kaplan, Ashmarin and colleagues, Semax exerts nootropic, neuroprotective, and antidepressant-like effects through melanocortin receptor signaling and robust BDNF/trkB upregulation in the hippocampus [1][2]. Russian clinical trials in acute ischemic stroke (Gusev group) showed reduced infarct progression and improved neurological recovery at intranasal doses of 12–18 mg/day [3]. Semax is on the Russian Federation List of Vital and Essential Drugs and has been registered since 1994 for stroke, optic nerve disease, and cognitive disorders. Typical research dosing in healthy adults is 600–1500 mcg intranasally per day. Semax is not FDA or EMA approved; it remains an investigational compound outside Russia and is scheduled for FDA Pharmacy Compounding Advisory Committee review.
Longevity Directory
Telomerase activators, senolytic peptides, and cellular bioregulators.
Vilon
Vilon is a synthetic dipeptide (Lys-Glu, KE) developed by Khavinson and colleagues as one of the shortest active peptide bioregulators, derived by directed synthesis from the amino acid composition of Thymalin, a bovine thymic extract used in Russian clinical immunology since the 1970s [1][2]. As a peptide of just two residues, Vilon represents the minimal active sequence in the Khavinson cytogen library and is investigated for thymic restoration, immune rejuvenation, and lifespan extension. In CBA mice receiving chronic Vilon administration starting at 6 months of age, Anisimov and Khavinson reported lifespan extensions of 20–40% with reduced spontaneous tumor incidence and improved immune markers [3]. Vilon is hypothesized to bind DNA directly through electrostatic complementarity of its Lys-Glu zwitterion to specific promoter sequences, modulating chromatin condensation and tissue-specific gene expression. Research dosing varies: 1–10 mcg/kg subcutaneously in animals, 100–500 mcg/day subcutaneously in research-community human use, or 1–10 mg/day orally in Russian bioregulator practice. Vilon is registered in Russia under bioregulator legislation but has no FDA, EMA, or MHRA approval.
Vesugen
Vesugen is a synthetic tripeptide (Lys-Glu-Asp, KED) developed by Vladimir Khavinson and colleagues as a tissue-specific bioregulator targeting the vascular endothelium and broader cardiovascular system [1][2]. It is one of the Khavinson cytogen family, derived from analysis of the amino acid composition of vascular wall protein extracts and synthesized as a defined short-peptide bioregulator for endothelial gene-program modulation. Preclinical work documents binding to the MKI67 gene promoter and modulation of endothelin-1 (EDN1), connexin (GJA1/Cx43), and SIRT1 expression in vascular cells, supporting effects on endothelial proliferation, intercellular communication, and longevity-associated gene programs [3]. Research dosing is 100–500 mcg subcutaneously per day across 10–20 day cycles, or 1–10 mg/day orally in outpatient Russian bioregulator practice, repeated 2–4 times yearly. Vesugen is registered in Russia under peptide-bioregulator and dietary-supplement legislation but has no FDA, EMA, or MHRA approval. Human clinical evidence is limited to Russian observational use in age-related vascular disorders.
Cartalax
Cartalax is a synthetic tripeptide (Ala-Glu-Asp, AED) developed by Vladimir Khavinson and colleagues as a tissue-specific bioregulator targeting cartilage, chondrocytes, and musculoskeletal connective tissue [1][2]. Derived by directed synthesis from analysis of cartilage protein composition, Cartalax shares the AED motif with several other Khavinson peptides but is positioned within the cytogen library as cartilage-targeted on the basis of its preferential effects in chondrocyte cultures and fibroblast-derived musculoskeletal cell lines [3]. Preclinical work shows Cartalax reduces aging markers p16, p21, and p53 while increasing SIRT6, a longevity-associated histone deacetylase, in cartilage cultures. The peptide also activates extracellular matrix gene programs and reduces chondrocyte apoptosis under metabolic stress. Research dosing is 100–500 mcg subcutaneously per day across 10–20 day cycles, or 1–10 mg/day orally in outpatient Russian bioregulator practice. Cartalax is registered in Russia under peptide-bioregulator and dietary-supplement legislation but has no FDA, EMA, or MHRA approval. Human clinical evidence is limited to observational reports in age-related joint and connective-tissue disorders.
Epitalon
Epitalon (also Epithalon, Epithalamin tetrapeptide) is a synthetic tetrapeptide Ala-Glu-Asp-Gly (AEDG) developed by Vladimir Khavinson by directed synthesis from the amino-acid composition of bovine pineal extract Epithalamin [1][2]. It is the most extensively studied of the Khavinson peptide bioregulators, with documented effects on telomerase activation, telomere elongation, melatonin restoration, and lifespan extension in rodent and Drosophila models [3][4][5]. Khavinson and colleagues showed Epitalon activates telomerase in human fetal somatic cell cultures with observable telomere elongation, and Anisimov demonstrated 12–13% lifespan extension in mice and 11–16% in fruit flies [6]. Standard research dosing is 5–10 mg subcutaneously per day for 10–20 consecutive days, repeated 2–3 times yearly. Epitalon is registered as a peptide bioregulator in Russia but is not approved by the FDA, EMA, or MHRA; outside Russia it is a research-only compound. Human clinical evidence is limited to Russian observational use in age-related disorders, with reports of restored circadian melatonin rhythms, improved immune markers, and normalized neuroendocrine function.
FOXO4-DRI
FOXO4-DRI is a 43-amino-acid synthetic senolytic peptide developed by Peter de Keizer and colleagues, first described in the landmark Cell 2017 paper as the first peptide-based agent to selectively eliminate senescent cells in mice through targeted disruption of the FOXO4-p53 interaction [1]. The 'DRI' designation reflects its D-retro-inverso engineering: all amino acids are replaced with their D-isomers and the sequence is reversed, producing a peptide highly resistant to enzymatic degradation while preserving target binding [2]. In senescent cells, FOXO4 sequesters p53 in the nucleus and blocks apoptosis; FOXO4-DRI competitively displaces FOXO4 from p53, releasing p53 to trigger intrinsic apoptosis selectively in senescent cells while sparing healthy cells [1][3]. In aged mice, intraperitoneal FOXO4-DRI restored fur density, renal function, and physical fitness. FOXO4-DRI has no human clinical trial data, no FDA or EMA approval, and is sold strictly as a research chemical. Mouse-equivalent doses are 5 mg/kg three times weekly; safe and effective human dosing is unknown.
Livagen
Livagen is a synthetic tetrapeptide (Lys-Glu-Asp-Ala, KEDA) developed by Vladimir Khavinson and colleagues as a tissue-specific bioregulator targeting hepatic tissue and immune function [1][2]. Synthesized by directed analysis of liver and immune-organ peptide preparations, Livagen is one of the better-characterized Khavinson cytogens with documented effects on heterochromatin decondensation in hepatocyte nuclei — a structural manifestation of the broader bioregulator hypothesis that short peptides remodel chromatin to reactivate age-silenced gene programs [3]. Preclinical work shows Livagen normalizes hepatocyte function in aged rats, restores age-impaired protein synthesis programs, and modulates immune gene expression in lymphocytes. Research dosing is 100–500 mcg subcutaneously per day across 10–20 day cycles, or 1–10 mg/day orally in outpatient Russian bioregulator practice, repeated 2–4 times per year. Livagen is registered in Russia under peptide-bioregulator and dietary-supplement legislation but has no FDA, EMA, or MHRA approval. Human clinical evidence is limited to observational use in age-related hepatic and immune disorders.
NAD
NAD+ (nicotinamide adenine dinucleotide) is the central redox and signaling cofactor for hundreds of enzymes including sirtuins (SIRT1–7), poly(ADP-ribose) polymerases (PARPs), and CD38, with intracellular concentrations declining substantially with age across human tissues [1][2]. Sinclair, Imai, and colleagues established sirtuins as NAD-dependent deacetylases that regulate longevity, metabolism, and DNA repair, and showed that restoring NAD+ levels through precursor supplementation can reverse age-related metabolic decline in mice [3][4]. Yoshino and colleagues demonstrated in a randomized clinical trial that nicotinamide mononucleotide (NMN) at 250 mg/day improves muscle insulin sensitivity in prediabetic women [5]. NAD+ itself is administered as a research and integrative medicine intervention at 100–500 mg subcutaneously or intramuscularly, or 250–1000 mg by slow intravenous infusion over 1–4 hours, in cycles. NAD+ is sold as a supplement (oral, sublingual, injectable) but the FDA has not approved NAD+ injection for any therapeutic indication. NAD+ precursors (NR, NMN) have FDA NDI status as dietary supplements but are not approved drugs.
KLOW
KLOW is a research-chemical blend of four regenerative peptides — typically 50 mg GHK-Cu (copper tripeptide), 10 mg KPV (alpha-MSH C-terminal tripeptide), 10 mg BPC-157 (body protection compound), and 10 mg TB-500 (thymosin beta-4 C-terminal fragment) — combined in a single 80 mg lyophilized vial for parenteral reconstitution. The blend is not a single registered compound but a research-community formulation designed to deliver complementary tissue-repair, anti-inflammatory, angiogenic, and matrix-remodeling activities in one injection. GHK-Cu stimulates collagen synthesis and angiogenesis (Pickart) [1]; KPV is the C-terminal anti-inflammatory tripeptide of alpha-MSH (Lipton, Catania) [2]; BPC-157 is a 15-amino-acid gastric peptide derivative with documented soft-tissue healing activity in animal models (Sikiric) [3][4]; TB-500 is a synthetic fragment of thymosin beta-4 supporting actin remodeling, cell migration, and angiogenesis [5]. None of these peptides are FDA approved as drugs; KLOW is sold strictly as a research chemical. Typical research dosing is 500–1000 mcg blend subcutaneously per day in 4–6 week cycles.
Skin & Hair Directory
Melanocortin agonists and collagen remodeling copper peptides.
SNAP-8
SNAP-8 (Acetyl Octapeptide-3) is a synthetic octapeptide derivative of Argireline developed as a topical cosmetic ingredient for reducing the appearance of expression lines and dynamic wrinkles. It mimics the N-terminal sequence of SNAP-25, a key SNARE protein involved in acetylcholine release at the neuromuscular junction. By interfering with vesicle docking at presynaptic terminals of facial mimetic muscles, SNAP-8 produces a localized, transient reduction in muscle contraction intensity without systemic absorption. SNAP-8 is used exclusively as a topical cosmetic agent at concentrations of 5–10% in serums, creams, and eye contour products. It is not approved for injection and has no documented systemic pharmacology in humans. Manufacturer-sponsored studies report wrinkle depth reductions of approximately 30–35% after 28 days of twice-daily topical application. SNAP-8 is generally regarded as safe for topical use, with very low rates of irritation or allergic contact dermatitis, and is widely incorporated into anti-aging cosmetic formulations as a non-invasive alternative to botulinum toxin.
GHK-Cu
GHK-Cu is the copper-binding tripeptide glycyl-L-histidyl-L-lysine complexed with divalent copper, first isolated from human plasma by Loren Pickart in 1973. Plasma concentrations decline with age, and the molecule has become one of the most extensively studied bioactive peptides in dermatology and regenerative medicine. GHK-Cu modulates over four thousand human genes at nanomolar concentrations, shifting expression patterns associated with damaged or aged tissue toward profiles characteristic of younger, healthier tissue. It accelerates wound healing, stimulates collagen, elastin, and proteoglycan synthesis, modulates matrix metalloproteinase activity, promotes angiogenesis, and supports hair follicle regeneration. In dermatology and cosmetics, GHK-Cu is used topically at concentrations of 0.05% to 2% in serums, creams, and scalp formulations. Injectable and intranasal protocols are explored in research settings only. Tolerability is excellent for topical use; the most common adverse events are mild irritation or temporary blue-green staining of skin or fabrics from the copper complex itself.
Melanotan II
Melanotan II is a synthetic cyclic heptapeptide analog of alpha-melanocyte-stimulating hormone (α-MSH) developed at the University of Arizona by Hadley, Hruby, Dorr and colleagues in the 1980s as a stable, broadly active melanocortin receptor agonist. It activates MC1R, MC3R, MC4R, and MC5R, producing eumelanin pigmentation in skin and hair (MC1R), centrally mediated penile erection and sexual desire (MC3R/MC4R), appetite suppression and increased energy expenditure (MC4R), and exocrine effects (MC5R). Research subcutaneous dosing typically begins at 0.10–0.25 mg and titrates up to 0.5–1 mg per administration after gradual desensitization to nausea. Melanotan II is not approved by any major regulator for human use. Documented risks include nausea and flushing, spontaneous erections, blood pressure changes, eruptive and darkening melanocytic nevi, and isolated case reports of melanoma emerging in users. Long-term safety has not been established, and the peptide is not recommended for routine cosmetic tanning.
GLOW
GLOW is a research peptide blend that combines three regenerative compounds in a single vial: BPC-157 (pentadecapeptide derived from gastric juice protein BPRP), TB-500 (synthetic Thymosin Beta-4 fragment), and GHK-Cu (copper-tripeptide glycyl-L-histidyl-L-lysine). Typical research formulations contain ten milligrams of BPC-157, ten milligrams of TB-500, and fifty milligrams of GHK-Cu per vial. The blend is administered subcutaneously, often at doses delivering 250–500 micrograms of BPC-157, 250–500 micrograms of TB-500, and 1–2 mg of GHK-Cu per injection two to five times weekly. GLOW is marketed for skin rejuvenation, hair quality, post-procedure recovery, soft tissue repair, and inflammation modulation. None of the components are FDA approved, and the blend has never been studied as a fixed combination in published clinical trials. Evidence rests entirely on animal data and mechanistic studies of the individual peptides.
PT-141 + Melanotan II
PT-141 (bremelanotide) and Melanotan II are structurally related melanocortin receptor agonists derived from the same University of Arizona research program. Melanotan II is a non-selective MC1R/MC3R/MC4R/MC5R agonist used in research for tanning and sexual function. PT-141 is a metabolite of Melanotan II with greater selectivity for MC3R and MC4R and minimal MC1R-driven pigmentation; the FDA approved it in 2019 as Vyleesi for hypoactive sexual desire disorder in premenopausal women. Some users combine the two peptides to achieve cosmetic tanning (MT-II) plus enhanced sexual response (PT-141). Combined dosing has not been formally studied. Research subcutaneous protocols typically use 0.25–1 mg MT-II during a loading phase plus 0.5–1.75 mg PT-141 as needed before sexual activity. The stack amplifies common melanocortin side effects (nausea, flushing, blood pressure changes) and adds the long-term dermatologic and oncologic risks associated with MT-II, including new and darkening nevi.
Immune Directory
Thymic peptides, immunomodulators, and antimicrobial defenses.
Thymosin Alpha-1
Thymosin Alpha-1 (Tα1, thymalfasin) is a 28-amino-acid acetylated peptide originally isolated from bovine thymus fraction V by Goldstein and colleagues in the 1970s. It is now produced synthetically and marketed as Zadaxin for chronic hepatitis B, chronic hepatitis C, and as an immune adjunct in cancer and infectious disease in more than thirty-five countries. The FDA has granted orphan drug status for stage 2B–4 melanoma and hepatocellular carcinoma but has not approved Tα1 for marketing in the United States. The standard dose is 1.6 mg subcutaneously twice weekly. Mechanistically, Tα1 acts through Toll-like receptors (notably TLR-9 and TLR-2) on dendritic cells and macrophages, promoting Th1 polarization, expanding regulatory T cells, restoring NK and CD8 cytotoxic T cell activity, and modulating inflammation. Camerini, Goldstein, and others have characterized Tα1 as virtually devoid of toxicity. It has been studied extensively in chronic viral hepatitis, sepsis, cancer, and as an immune adjunct.
Chonluten
Chonluten (T-34) is a synthetic tripeptide with the sequence Glu-Asp-Gly (EDG) developed by Vladimir Khavinson and the St. Petersburg Institute of Bioregulation and Gerontology as a tissue-specific bioregulator for the bronchopulmonary system. It belongs to the Khavinson short-peptide class of cytogens that are claimed to enter cells and bind regulatory regions of DNA to modulate gene expression in their target tissue. Chonluten has been studied primarily in Russian language gerontological literature in models of chronic obstructive pulmonary disease, pulmonary fibrosis, and age-related respiratory decline, with reports of improvements in bronchial epithelial regeneration, antioxidant enzyme activity, and gene expression of c-Fos, HSP70, COX-2, and TNF-α. It is not approved by the FDA or EMA. Research subcutaneous protocols typically use 100–200 mcg per day for 10–20 day cycles, sometimes repeated every few months. Human clinical evidence outside Russian publications is essentially absent.
LL-37
LL-37 is the active form of human cathelicidin antimicrobial peptide (encoded by the gene CAMP), a 37-amino-acid amphipathic α-helical peptide cleaved from the precursor hCAP-18 by proteinase 3 in neutrophils and other tissues. It functions as a central effector of innate immune defense, with direct antimicrobial activity against gram-positive and gram-negative bacteria, fungi, viruses, and parasites, as well as immunomodulatory roles including chemotaxis, endotoxin neutralization, wound healing, angiogenesis, and resolution of inflammation. Vandamme and colleagues comprehensively reviewed LL-37 biology in 2012. In research settings, synthetic LL-37 is administered subcutaneously at 25–100 mcg per dose for immune support or topically for wound healing. LL-37 is not FDA approved; topical synthetic LL-37 (OP-145) has been investigated in chronic otitis externa, and an LL-37-based wound treatment has been studied in venous ulcers. Excessive LL-37 has been implicated in rosacea, psoriasis, and autoimmunity.
Metabolic Directory
AMPK activators, cardiolipin stabilizers, and metabolic rate enhancers.
SLU-PP-332
SLU-PP-332 is a synthetic small-molecule pan-agonist of the estrogen-related receptors ERRα, ERRβ, and ERRγ developed at Saint Louis University by Burris, Billon, Kahn, and colleagues. ERRs are orphan nuclear receptors that control mitochondrial biogenesis, oxidative phosphorylation, and fatty acid oxidation; their physiological activation underlies the metabolic adaptations of endurance exercise. SLU-PP-332 binds ERRα with an EC50 of approximately 98 nM and activates ERRβ and ERRγ with EC50 values of 230 nM and 430 nM. In rodents, SLU-PP-332 increases mitochondrial function, expands fast oxidative type IIa muscle fibers, enhances running endurance, increases energy expenditure, improves glucose tolerance, and reduces fat mass without affecting food intake. It is a research compound only, not a peptide, and is not approved for human use. No published human pharmacokinetic, safety, or efficacy data exist, and dosing in animal studies typically uses 10–30 mg/kg orally or intraperitoneally.
AICAR
AICAR (5-aminoimidazole-4-carboxamide ribonucleoside), also known as acadesine, is a cell-permeable adenosine analog that is phosphorylated intracellularly to ZMP, an AMP mimetic that allosterically activates AMP-activated protein kinase (AMPK), the master cellular energy sensor. AICAR mimics several physiological consequences of endurance exercise: increased fatty acid oxidation, glucose uptake, mitochondrial biogenesis, and oxidative gene expression. The landmark Narkar et al. Cell 2008 study showed that four weeks of AICAR administration to sedentary mice increased running endurance by 44 percent. In humans, intravenous acadesine has been studied in cardiac surgery and acute myeloid leukemia at doses up to 0.1 mg/kg/min for several hours; the World Anti-Doping Agency prohibits AICAR as an exercise mimetic. AICAR is not approved for any chronic indication, and self-administered research subcutaneous doses (10–50 mg per session) lack any safety or efficacy validation in humans.
Glutathione
Glutathione (γ-L-glutamyl-L-cysteinyl-glycine, GSH) is an endogenous tripeptide and the body's principal intracellular antioxidant. Synthesized in two ATP-dependent steps catalyzed by glutamate-cysteine ligase and glutathione synthetase, it scavenges reactive oxygen species, conjugates electrophilic xenobiotics in Phase II hepatic detoxification, regenerates other antioxidants such as vitamins C and E, and maintains protein thiol redox status. Reduced GSH levels are associated with non-alcoholic fatty liver disease, Parkinson's disease, chronic obstructive pulmonary disease, HIV, and aging. Exogenous glutathione is administered intravenously (600–2400 mg per session, typically 1–3 times weekly), intramuscularly, intranasally (research only), or topically. Oral GSH bioavailability is low due to gastrointestinal hydrolysis, although liposomal and reduced-form preparations partially overcome this. Glutathione is not FDA-approved for any condition in the United States but is widely compounded; intravenous administration carries rare risks of bronchospasm and Stevens-Johnson syndrome.
L-Carnitine
L-Carnitine is a quaternary ammonium compound synthesized endogenously from lysine and methionine that serves as an obligate cofactor in long-chain fatty acid transport into mitochondria for β-oxidation. The carnitine palmitoyltransferase (CPT-1 and CPT-2) system shuttles long-chain acyl-CoA across the inner mitochondrial membrane, supplying substrate for cardiac, skeletal muscle, and hepatic ATP production. Primary and secondary carnitine deficiencies cause cardiomyopathy, skeletal myopathy, and hypoketotic hypoglycemia. Oral L-carnitine is FDA-approved for primary and secondary carnitine deficiency (Carnitor) at doses of 1000–3000 mg per day in adults. Off-label clinical uses include diabetes, fatty liver disease, peripheral artery disease, infertility, and fatigue. A meta-analysis of 37 randomized trials found 2000 mg/day maximizes weight-loss effects. Research IM/SC injection of 200–500 mg is used in performance and recovery protocols, although evidence is largely anecdotal.
MOTS-C
MOTS-c (mitochondrial open reading frame of the twelve-S ribosomal RNA type c) is a 16-amino-acid peptide encoded within the 12S rRNA gene of the mitochondrial genome and discovered by Changhan Lee, Pinchas Cohen, and colleagues at USC. Unlike all other known signaling peptides, MOTS-c is encoded by mitochondrial DNA rather than nuclear DNA, making it the founding member of a class of mitochondrial-derived peptides. In the seminal Cell Metabolism 2015 paper, MOTS-c was shown to enhance glucose utilization, activate AMPK, prevent age-dependent and diet-induced insulin resistance, and reduce diet-induced obesity in mice. Subsequent work demonstrated that exercise induces MOTS-c expression and that late-life MOTS-c treatment increases physical capacity. Research subcutaneous dosing typically uses 5–10 mg two or three times per week. MOTS-c is not FDA approved; an investigational MOTS-c analog (CB4211) for non-alcoholic fatty liver disease was studied in Phase Ib trials.
Interactive Reference Guides
Deep-dive clinical guidelines regarding safety, reconstitution, and syringe reading.
Beginners Guide
Fundamental biology, pathways, and mechanical terms of peptides.
Read Guidearrow_forwardscienceReconstitution Guide
How to mathematically measure, inject and preserve lyophilized chains.
Read Guidearrow_forwardac_unitStorage & Cold Chain
Detailed temperature guides, light protection and shelf-life metrics.
Read Guidearrow_forwardvaccinesSyringe Measurements
Decoding U-100 markings, tick measurements, and volumetric conversions.
Read Guidearrow_forward