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.
7 protocols indexed
Follistatin-344
Follistatin-344 (FS-344) is a research-grade recombinant form of follistatin, a secreted glycoprotein in the TGF-β superfamily that acts as a high-affinity antagonist of myostatin (GDF-8) and activin A. The name refers to the 344-amino-acid precursor transcript, which after signal-peptide cleavage matures into the circulating 315-residue isoform (FST-315). By trapping myostatin and blocking it from engaging the ActRIIB receptor, follistatin lifts the brake on muscle protein synthesis and satellite-cell proliferation [1][2]. In transgenic and gene-therapy models this produces dramatic hypertrophy, up to a quadrupling of muscle mass in mice and durable strength gains in primates [3][6]. The most discussed Follistatin-344 dosage in research and community protocols is 100-200 mcg per day subcutaneously, with some sources citing up to 300 mcg/day, typically run in short 2-4 week cycles. It is essential to note that every controlled efficacy study used AAV-delivered gene therapy injected directly into muscle, not an exogenous subcutaneous peptide; the injected-protein route has no controlled human validation, and follistatin's circulating half-life is short. Follistatin-344 is NOT approved by the FDA or EMA for any indication, is not a dietary supplement, and is prohibited in sport by WADA as a myostatin-affecting agent. The reconstitution and dosing figures here are an educational reference for this muscle/performance research compound class, not medical advice.
Open Protocolarrow_forwardMyostatin Inhibitor (ActRIIB-Fc)ACE-031
ACE-031 (ramatercept, ActRIIB-Fc) is an investigational soluble activin type IIB receptor fusion protein: the extracellular ligand-binding domain of human ActRIIB joined to a human IgG1 Fc fragment. It belongs to the myostatin/activin inhibitor class and works as a circulating "ligand trap," sequestering myostatin (GDF-8), activin A and B, GDF-11 and related TGF-beta superfamily proteins before they can signal through their native receptors and restrain skeletal muscle growth. In every published human study it was given by subcutaneous injection, so the ACE-031 dosage discussed in trials is weight-based: 0.02 to 3 mg/kg subcutaneously every 2 to 4 weeks, with measurable gains in lean mass (+3.3%) and thigh muscle volume (+5.1%) seen only at the top 3 mg/kg single dose in healthy postmenopausal women. The elimination half-life is roughly 10 to 15 days. ACE-031 was developed by Acceleron Pharma with Shire as a Duchenne muscular dystrophy therapy, but the program was placed on clinical hold in 2011 and permanently discontinued in 2013 after vascular bleeding side effects (nosebleeds, gum bleeding, skin telangiectasia) linked to off-target inhibition of BMP9/BMP10. ACE-031 is not approved by the FDA or EMA, is prohibited in sport by WADA, and the figures here are an educational reconstitution reference only, not medical advice.
Open Protocolarrow_forwardIGF-1 AnalogIGF-1 DES
IGF-1 DES (DES(1-3)IGF-1) is a 67-amino-acid truncated analogue of insulin-like growth factor-1, created by removing the N-terminal tripeptide Gly-Pro-Glu from the 70-residue parent molecule. It is a naturally occurring IGF-1 fragment first isolated from bovine colostrum and later found in fetal and adult brain tissue, not a purely synthetic construct. The deletion sharply reduces binding to the insulin-like growth factor binding proteins (IGFBPs) while preserving full agonist activity at the type 1 IGF receptor (IGF-1R), which makes the free peptide roughly ten-fold more potent than native IGF-1 in IGFBP-rich systems. Unlike long-acting analogues such as IGF-1 LR3, IGF-1 DES has a very short circulating half-life (about 20-30 minutes), so it is used as a fast, locally acting research growth factor rather than a sustained systemic agent. The headline IGF-1 DES dosage discussed in research and community contexts is 20-100 mcg per injection on training days, often split bilaterally near worked muscle groups. There are no human clinical trials; the animal literature documents anabolic, anti-catabolic, and tissue-protective effects. IGF-1 DES is not approved by the FDA or EMA for any indication and is supplied strictly as a research chemical, so all figures here are educational and not medical advice.
Open Protocolarrow_forwardMuscle Peptide BioregulatorGotratix
Gotratix (also sold as Muscle Cytomax and labeled A-18) is an oral skeletal-muscle peptide bioregulator from the Khavinson "Cytomax" family, developed within Vladimir Khavinson's peptide-regulation program at the St. Petersburg Institute of Bioregulation and Gerontology. Its active ingredient is peptide complex A-18, a low-molecular-weight peptide fraction extracted from the triceps muscle of young calves (under 11 months). Like other Khavinson bioregulators, it is hypothesized to act not as a hormone but as a tissue-specific signal that enters the cell nucleus and modulates expression of muscle genes governing protein synthesis, satellite-cell activity, and mitochondrial function [1][2]. Manufacturers market it to support muscle recovery, reduce fatigue under heavy training, and counter age-related muscle loss, though no peer-reviewed human trials of Gotratix itself have been published. The typical Gotratix dosage reported on product labels is about 10 mg of active peptide per capsule, 1-2 capsules once or twice daily (roughly 10-40 mg/day, commonly around 20 mg/day) taken orally with meals across a 30-day course, repeated every 4-6 months. Gotratix is not approved by the FDA or EMA; it is sold abroad as a dietary supplement and is treated in many jurisdictions as a research/educational compound only. Because this site standardizes on injectable math, the subcutaneous reconstitution figures below are an educational reference for an orally dosed product, not a clinically validated route. Nothing here is medical advice.
Open Protocolarrow_forwardAnti-ActRII AntibodyBimagrumab
Bimagrumab (BYM338) is an investigational, fully human anti-activin type II receptor (anti-ActRII) IgG1 monoclonal antibody. By competitively binding ActRIIB (KD approximately 1.7 pM) and ActRIIA, it blocks myostatin, activin A, and GDF11, inhibiting Smad2/3 signaling to drive skeletal-muscle hypertrophy while producing a striking loss of body fat. The established Bimagrumab dosage in clinical trials is 10 mg/kg administered as an intravenous infusion once every 4 weeks, capped at 1200 mg per dose; dose-finding studies also used 1, 3, and 10 mg/kg monthly, and the first inclusion-body-myositis study used a single 30 mg/kg dose. This anti-ActRII monoclonal antibody was developed by Novartis and later advanced for obesity by Versanis Bio (acquired by Eli Lilly). In a phase 2 type 2 diabetes and obesity trial it cut total fat mass by about 20% while increasing lean mass and lowering HbA1c, and in the phase 2 BELIEVE trial it preserved muscle during semaglutide-driven weight loss. It has nonlinear, target-mediated pharmacokinetics with a concentration-dependent half-life (roughly 5 days up to about 19 days). Bimagrumab failed its primary functional endpoint in the phase 2b RESILIENT trial for sporadic inclusion body myositis. It is NOT approved by the FDA or EMA and remains investigational. Because it is a large protein given by IV infusion, the subcutaneous reconstitution protocol modeled here is an educational measurement reference only, not medical advice.
Open Protocolarrow_forwardMyostatin/Activin InhibitorFollistatin-315
Follistatin-315 (FS-315) is the major circulating isoform of follistatin, an autocrine/paracrine glycoprotein that acts as a high-affinity antagonist of TGF-beta superfamily ligands, most importantly myostatin (GDF-8) and activin A. FS-315 is the 315-amino-acid mature protein translated from the FST344 splice variant; cleavage of its 29-residue signal peptide yields the secreted form, whose acidic C-terminal tail masks the heparin-binding site so the molecule stays soluble in blood rather than tethering to cell-surface proteoglycans like the shorter FS-288 isoform [2][3]. By physically wrapping around myostatin and activin, follistatin blocks their engagement of activin type II receptors (ActRIIB) and the downstream Smad2/3 cascade that restrains muscle growth, which is why follistatin gene transfer drives skeletal-muscle hypertrophy in animals and improved walking distance in a small Becker muscular dystrophy gene-therapy trial [6][7][8]. There is no established injectable protein dose in humans: the only clinical follistatin data come from AAV1-FS344 gene therapy, not from injected recombinant peptide. The community Follistatin-315 dosage discussed in research circles is roughly 100-300 mcg per day subcutaneously in short cycles, a figure with no clinical validation. Recombinant FS-315 protein clears from circulation within hours, so it is poorly suited to standardized once-daily protein dosing. Follistatin-315 is not approved by the FDA or EMA for any indication and is sold strictly for laboratory research; the reconstitution and Follistatin-315 dosage figures here are an educational reference, not medical advice.
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_forward