Anabolics Peptide Dosage Protocols
Anabolic compounds in research settings target androgen receptor signaling, nitrogen retention, and skeletal muscle protein synthesis. This directory aggregates protocols, titration schedules, and reconstitution math for compounds investigated for lean mass research.
10 protocols indexed
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.
Open Protocolarrow_forwardResearch PeptideOvagen
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.
Open Protocolarrow_forwardResearch PeptideTestagen
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).
Open Protocolarrow_forwardNootropic & NeuropeptideDSIP
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.
Open Protocolarrow_forwardResearch PeptideKisspeptin
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.
Open Protocolarrow_forwardResearch PeptideOxytocin
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.
Open Protocolarrow_forwardResearch PeptideProstamax
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.
Open Protocolarrow_forwardMelanocortin / Tanning & LibidoPT-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.
Open Protocolarrow_forwardResearch PeptidePNC-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.
Open Protocolarrow_forwardTherapeutic BlendNeuroxelin
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.
Open Protocolarrow_forward