Healing & Recovery Peptide Dosage Protocols
Healing and recovery peptides trigger angiogenesis, cell migration, and ECM remodeling. The flagship compounds are BPC-157 (gastric protective pentadecapeptide) and TB-500 (Thymosin Beta-4 fragment).
16 protocols indexed
Teduglutide
Teduglutide (brand names Gattex in the US and Revestive in the EU) is a recombinant 33-amino-acid analog of human glucagon-like peptide-2 (GLP-2) and a selective GLP-2 receptor agonist developed to treat short bowel syndrome (SBS) in patients who depend on parenteral nutrition or intravenous support. It is produced in Escherichia coli and differs from native GLP-2 by a single amino-acid substitution (alanine to glycine at position 2) that resists dipeptidyl peptidase-4 (DPP-4) cleavage, extending the biological half-life from roughly 7 minutes for native GLP-2 to about 2-3 hours. By binding intestinal GLP-2 receptors, teduglutide triggers release of IGF-1, keratinocyte growth factor and nitric oxide, increasing villus height, crypt depth and mucosal absorptive surface while slowing gastric emptying and acid secretion, all of which improve fluid and nutrient absorption. The standard Teduglutide dosage is 0.05 mg/kg injected subcutaneously once daily (about 3.5 mg/day for a 70 kg adult), reduced by half to 0.025 mg/kg in moderate-to-severe renal impairment. In the pivotal 24-week STEPS trial, 63% of teduglutide-treated patients achieved a 20% or greater reduction in parenteral support versus 30% on placebo. Teduglutide is a prescription biologic, FDA-approved (Gattex, December 2012; expanded to children 1 year and older in 2019) and EMA-approved (Revestive, August 2012). This page is an educational reconstitution and dosing reference, not medical advice.
Open Protocolarrow_forwardVasoactive Intestinal PeptideVIP
VIP (vasoactive intestinal peptide; the synthetic form is marketed as aviptadil, RLF-100/ZYESAMI) is a 28-amino-acid neuropeptide of the secretin/glucagon superfamily encoded by the VIP gene. It signals through the class II G-protein-coupled receptors VPAC1 and VPAC2, raising intracellular cAMP to drive vasodilation, bronchodilation, smooth-muscle relaxation, and a broadly anti-inflammatory, pro-regulatory immune shift. Native VIP has an extremely short plasma half-life of roughly 1-2 minutes because it is rapidly cleaved by DPP-4 and neutral endopeptidase, which is why therapeutic use relies on frequent intranasal dosing or continuous intravenous infusion rather than a single shot. The most widely cited VIP dosage is 50 mcg per intranasal spray, used one to four times daily, in Ritchie Shoemaker's open-label CIRS (chronic inflammatory response syndrome) protocol. As aviptadil, VIP has been studied by inhalation (about 100-200 mcg/day) for pulmonary arterial hypertension and by escalating IV infusion for COVID-19 acute respiratory failure, where the large randomized TESICO trial found no mortality benefit. VIP/aviptadil is not approved by the FDA or EMA for any indication; it holds only orphan-drug designations and remains investigational, with CIRS use being off-label compounded therapy. The reconstitution, half-life, and protocol figures on this page are an educational reference, not medical advice.
Open Protocolarrow_forwardTight-Junction RegulatorLarazotide acetate
Larazotide acetate (AT-1001, INN-202) is a synthetic single-chain octapeptide (Gly-Gly-Val-Leu-Val-Gln-Pro-Gly) derived from the zonula occludens toxin of Vibrio cholerae and developed as a first-in-class tight-junction regulator, or zonulin antagonist, for celiac disease. Rather than suppressing the immune system, it acts locally at the apical surface of the small-intestinal epithelium to blunt zonulin-driven opening of the paracellular tight junctions, reducing the leak of gluten peptides across the gut barrier. Because it is minimally absorbed into the bloodstream, it has no meaningful systemic exposure and is taken by mouth as a delayed-release capsule before meals. In the pivotal Phase 2b trial, the most-studied and only statistically effective Larazotide acetate dosage was 0.5 mg three times daily before meals; counter-intuitively, the higher 1 mg and 2 mg arms performed no better than placebo, producing an inverted dose-response curve. The headline dosing range across the program runs from 0.5 mg to 8 mg three times daily, but 0.5 mg before each meal is the figure carried forward into Phase 3. Despite a clean safety record over more than 15 years of study, the Phase 3 CeDLara trial was discontinued for futility in June 2022, and larazotide acetate has never been approved by the FDA or EMA. It remains an investigational, research-and-educational compound only.
Open Protocolarrow_forwardSemi-synthetic GlycosaminoglycanPentosan Polysulfate Sodium
Pentosan Polysulfate Sodium (PPS; brand names Elmiron, Cartrophen, Zydax, and the historical anticoagulant SP-54) is a semi-synthetic, heparin-like glycosaminoglycan made by sulfate-esterifying xylan extracted from beechwood hemicellulose, giving an average molecular weight of roughly 4,000-6,000 daltons [1]. It is the only oral drug FDA-approved (since 1996) for the bladder pain of interstitial cystitis, where it is thought to rebuild the protective glycosaminoglycan (GAG) layer lining the urothelium; in cartilage it behaves as a candidate disease-modifying osteoarthritis drug by stimulating proteoglycan and hyaluronan synthesis while inhibiting degradative enzymes [2][3]. The standard clinical Pentosan Polysulfate Sodium dosage is 100 mg by mouth three times daily (300 mg/day) [1]. The injectable, subcutaneous protocol modeled on this page mirrors the off-label/investigational joint-health regimen of about 2 mg/kg once weekly studied in knee osteoarthritis and now advancing through Phase 3 trials [4][6]. Oral bioavailability is very low (about 6% of a radiolabeled dose, under 1% as intact drug), most of a dose is excreted unchanged in feces, and the plasma half-life of total radioactivity is roughly 20-27 hours [1]. PPS carries heparin-like bleeding risk and, with prolonged high cumulative exposure, a documented risk of pigmentary maculopathy [7]. The figures here are educational, not medical advice.
Open Protocolarrow_forwardRelaxin RXFP1 Biased AgonistB7-33
B7-33 is a 27-amino-acid single-chain relaxin-2 (RXFP1) biased agonist derived from the B-chain (residues B7–B33) of human H2 relaxin, engineered as a smaller, cheaper alternative to the two-chain hormone serelaxin. Two native cysteines are replaced with serine so the peptide stays linear and non-aggregating (CAS 1818415-56-3, molecular weight ~2,986 Da). Mechanistically it is a functionally selective ("biased") agonist of relaxin family peptide receptor 1 (RXFP1): it preferentially drives the anti-fibrotic pERK1/2–matrix-metalloproteinase pathway, partly through RXFP1–angiotensin II type-2 receptor heterodimers, while largely sparing the cAMP signalling linked to relaxin's vascular and proliferative effects [1]. In rodent models of cardiac, pulmonary and vascular fibrosis it matched native relaxin's anti-scarring potency without promoting tumour growth [1][3][4]. There is no validated human B7-33 dosage; the most-cited preclinical regimen is roughly 0.25 mg/kg/day subcutaneously, or 0.25 mg/kg twice daily after myocardial infarction, usually delivered by osmotic minipump because the peptide's in-vitro serum half-life is only about 6 minutes [3][5]. This single-chain relaxin mimetic is not approved by the FDA or EMA, has never entered human clinical trials, and is sold strictly for laboratory research. The subcutaneous reconstitution and B7-33 dosage figures on this page are an educational reference, not medical advice.
Open Protocolarrow_forwardGLP-2 Receptor AgonistApraglutide
Apraglutide (development code FE 203799) is a synthetic, long-acting glucagon-like peptide-2 (GLP-2) receptor agonist developed as a gut-trophic therapy for short bowel syndrome with intestinal failure (SBS-IF). It is a tetrasubstituted analog of human GLP-2, written as [Gly2, Nle10, D-Phe11, Leu16]hGLP-2(1-33)-NH2, whose four amino-acid changes confer resistance to dipeptidyl peptidase-4 (DPP-4) degradation, very low systemic clearance, and high plasma-protein binding. These properties give it a far longer half-life than native GLP-2 or daily-dosed teduglutide and enable true once-weekly subcutaneous administration [1][2]. The headline Apraglutide dosage studied across the phase 1-3 program is 5 mg subcutaneously once weekly for adults weighing at least 50 kg, with 2.5 mg once weekly for those under 50 kg [3][5]. By activating intestinal GLP-2 receptors on subepithelial myofibroblasts and enteric neurons, apraglutide promotes mucosal growth, increases villus height and absorptive surface area, slows gastric emptying, and improves fluid, sodium, and energy absorption, reducing dependence on parenteral support. In the phase 3 STARS trial of 164 adults, once-weekly apraglutide reduced weekly parenteral-support volume by 25.5% versus 12.5% with placebo at week 24 [5]. As a GLP-2 receptor agonist peptide, apraglutide remains investigational: it is NOT approved by the FDA or EMA, and in 2025 the FDA requested a confirmatory phase 3 trial before approval [7]. All figures here are educational, not medical advice.
Open Protocolarrow_forwardGLP-2 Receptor AgonistGlepaglutide
Glepaglutide (developmental code ZP1848) is a long-acting glucagon-like peptide-2 (GLP-2) receptor agonist, a synthetic analogue of the 33-amino-acid human gut hormone GLP-2, developed by Zealand Pharma to treat short bowel syndrome (SBS) with intestinal failure. By activating GLP-2 receptors on intestinal subepithelial cells and enteric neurons it drives mucosal growth, slows gastric emptying and increases intestinal blood flow, improving the absorption of fluid and nutrients so patients can reduce their dependence on parenteral (intravenous) support. Its defining feature is protraction: amino-acid modifications and a self-assembling subcutaneous depot give an effective half-life of roughly 88 hours, enabling once- or twice-weekly injection rather than the daily dosing required by the approved GLP-2 analogue teduglutide. The most-studied Glepaglutide dosage is 10 mg injected subcutaneously, given twice weekly in the Phase 3 trial that met its primary endpoint (a 5.13 L/week reduction in parenteral support volume versus 2.85 L/week on placebo); a 10 mg once-weekly regimen was also evaluated. Common side effects are gastrointestinal (nausea, abdominal pain and distension, vomiting), stoma complications, fluid retention and injection-site reactions, and the GLP-2 class carries monitoring requirements for intestinal polyps and biliary or pancreatic disease. Regulatory status: glepaglutide holds FDA orphan-drug designation but is NOT approved, the FDA issued a Complete Response Letter in December 2024, and a European marketing application was filed in 2025. This page is an educational dosing reference, not medical advice.
Open Protocolarrow_forwardRecombinant Growth FactorBecaplermin
Becaplermin (Regranex, rhPDGF-BB) is a topical recombinant platelet-derived growth factor-BB wound-healing gel and the first growth-factor drug ever approved for a chronic wound. It is a homodimeric protein expressed in Saccharomyces cerevisiae yeast from an inserted PDGF B-chain gene, supplied as a 0.01% aqueous sodium-carboxymethylcellulose gel containing 100 micrograms of becaplermin per gram [1][7]. Mechanistically it binds PDGF beta-receptors on fibroblasts and other mesenchymal cells, driving chemotactic recruitment, proliferation, extracellular-matrix and collagen deposition, angiogenesis and granulation-tissue formation in the wound bed [1][6]. The headline Becaplermin dosage is a thin once-daily layer of the 0.01% gel applied to a debrided lower-extremity diabetic neuropathic ulcer; the amount is calculated from ulcer length x width, recalculated as the wound shrinks, and continued for up to 20 weeks [1][4]. In the pivotal phase III trial the 100 mcg/g gel achieved complete wound closure in 50% of patients versus 35% with placebo [2]. Systemic absorption is negligible. Becaplermin received FDA approval in December 1997; a 2008 boxed warning about increased cancer mortality in patients using three or more tubes was removed by the FDA in December 2018 after long-term cohort data showed no elevated risk [3][5]. The subcutaneous reconstitution figures on this page are an educational reference only, because the drug is topical and is never injected.
Open Protocolarrow_forwardRegenerative PeptidePentadeca Arginate
Pentadeca Arginate (PDA, also marketed as BPC-157 arginate) is a stabilized arginate-salt form of the 15-amino-acid pentadecapeptide BPC-157 (sequence Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val), a synthetic fragment derived from a body-protection compound found in human gastric juice [1]. Suppliers replace the conventional acetate counter-ion with arginine, a change promoted as improving stability and shelf life, although no peer-reviewed study has yet evaluated PDA as a distinct molecule, so every mechanism, pharmacokinetic, and efficacy claim below is extrapolated from BPC-157 research [7]. Mechanistically, BPC-157 is a cytoprotective, pro-angiogenic peptide that up-regulates and activates the VEGFR2-Akt-eNOS pathway, modulates nitric-oxide signaling, and accelerates tendon, ligament, muscle, and gut healing in rodent models [1][3][4][5]. The typical Pentadeca Arginate dosage extrapolated from BPC-157 protocols is roughly 250-500 mcg injected subcutaneously once or twice daily, with some users reaching about 1,000 mcg/day during an acute repair phase, run for around 4-8 weeks [7]. BPC-157 has a very short plasma half-life (under 30 minutes in animals) yet produces durable tissue effects, a recognized pharmacokinetic-pharmacodynamic disconnect [2]. Neither BPC-157 nor Pentadeca Arginate is approved by the FDA or EMA for any indication; BPC-157 was placed on the FDA's Category 2 bulk-drug-substances list over safety concerns, and PDA is sold strictly for research and educational use. This page is an educational dosing reference, not medical advice.
Open Protocolarrow_forwardTissue Repair & HealingTB-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.
Open Protocolarrow_forwardResearch PeptideAra-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.
Open Protocolarrow_forwardTissue Repair & HealingBPC-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.
Open Protocolarrow_forwardTissue Repair & HealingKPV
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.
Open Protocolarrow_forwardTherapeutic BlendBPC-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.
Open Protocolarrow_forwardTherapeutic BlendTri-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.
Open Protocolarrow_forwardSynergistic StackTB-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.
Open Protocolarrow_forward