BPC-157 + TB-500 Blend

Component Composition

This product is supplied as a single lyophilized vial containing two structurally distinct synthetic peptides.

BPC-157 is a 15-amino-acid linear pentadecapeptide with sequence Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val (single-letter: GEPPPGKPADDAGLV). Molecular formula C62H98N16O22, molecular weight 1419.54 g/mol, CAS 137525-51-0, PubChem CID 9941957. The peptide contains no aromatic residues; HPLC-UV detection is conducted at 214-220 nm.

TB-500 is the synthetic acetylated heptapeptide Ac-Leu-Lys-Lys-Thr-Glu-Thr-Gln (single-letter: Ac-LKKTETQ), corresponding to residues 17-23 of the parent protein thymosin beta-4 (Tβ4). Molecular formula C38H68N10O14, molecular weight 889.02 g/mol, CAS 885340-08-9, PubChem CID 62707662. The 7-mer also contains no aromatic residues and HPLC-UV detection is again at 214-220 nm; a vendor reporting 280 nm purity is systematically missing non-aromatic impurities. Each component meets ≥99% purity per batch, with lot-specific results in the Certificate of Analysis library.

BPC-157 Research Summary

BPC-157 was first described by the Sikirić research group at the University of Zagreb in 1991-1993 as a fragment of a putative ~40 kDa 'body protection compound' protein isolated from human gastric juice^[6]. The 1993 paper framed the work in terms of a stomach-stress-organoprotection hypothesis and reported observations across rat preparations of gastric mucosal injury under various stressors. The parent protein has never been formally sequenced or assigned a UniProt entry; the 15-residue synthetic sequence (GEPPPGKPADDAGLV) is the only material that has been the subject of subsequent research. Approximately 87% of the ~200 BPC-157 papers indexed on PubMed have Sikirić as first or senior author, and approximately 81% have co-author Seiwerth; the citation network is effectively a single laboratory.

Gastrointestinal research models account for the largest body of published BPC-157 literature. Rat preparations of gastric ulceration, NSAID-induced gastrointestinal lesions, intestinal anastomosis, and inflammatory bowel injury have been the most frequently used systems, with the 2018 Zagreb review framing the molecule as a cytoprotective mediator across these preparations. A development-stage preparation designated PL14736 was the subject of early-phase clinical investigation as a candidate for inflammatory bowel disease but did not advance to Phase 2 or Phase 3 efficacy trials in the peer-reviewed record.

Tendon-injury preparations have been a second sustained focus in the BPC-157 literature and the area where the only substantive non-Zagreb original mechanism work has been concentrated. The Chang research group at Chang Gung University, Taiwan, reported observations on cell survival, fibroblast migration markers, and Vinculin/F-actin distribution in cultured tendon explants and in vivo rat Achilles transection preparations^[2]. Rat skin wound and burn preparations have been used to investigate BPC-157 across the dermatology literature, with reported observations on re-epithelialization rate and angiogenesis markers in standardized excisional models. In rat muscle-injury research, the most-cited preclinical paper specifically addressed muscle recovery under conditions of systemic corticosteroid administration (Pevec 2010), reporting observations on gastrocnemius muscle structure and functional measurements following crush injury, in animals receiving and not receiving systemic dexamethasone^[16].

The only independent pharmacokinetic study (Xu 2022) reported plasma half-lives of approximately 15 minutes intravenous in rat and 5 minutes intravenous in beagle dog, with bioavailability of 14-19% in rats and 45-51% in dogs and no drug accumulation across 7 days of repeated dosing^[7]. This is the single peer-reviewed pharmacokinetic dataset originating outside the Zagreb research orbit. The full BPC-157 literature review is available on the BPC-157 component PDP.

TB-500 Research Summary

TB-500 (Ac-LKKTETQ) is the synthetic 7-mer corresponding to residues 17-23 of full thymosin beta-4 (Tβ4, UniProt P62328), a 43-amino-acid intrinsically disordered protein originally isolated from calf thymus in 1981^[8]. The two molecules differ by more than 5x in mass: the 7-mer at ~889 Da versus full Tβ4 at ~4921 Da. This disambiguation is load-bearing. Every RegeneRx-sponsored Phase 2 and Phase 3 trial of thymosin beta-4 used the full 43-mer; published human-efficacy claims for 'thymosin beta-4' describe the full parent, not the LKKTETQ fragment.

The strongest reproducible mechanism finding in the Tβ4 literature is 1:1 binding of monomeric ATP-G-actin via the LKKTET motif at residues 17-22, with affinity in the sub-micromolar range (Safer 1991)^[3]. X-ray crystallography (Irobi 2004) demonstrated that essentially the entire 43-residue chain wraps the actin monomer in solution, with LKKTET as the high-affinity contact region^[4]. The single most-cited direct comparison between the full 43-mer and the LKKTETQ 7-mer in any in vivo readout is Philp et al. (2003) in db/db diabetic and aged-mouse dermal wound models^[9]. This small-animal paper from the Goldstein/Kleinman collaboration is the foundation of the commercial premise that the 7-mer recapitulates full-Tβ4 activity; equivalence in corneal, cardiac, or other indications has not been independently established.

The Tβ4 clinical record spans approximately 25 years and is dominated by RegeneRx Biopharmaceuticals using the full 43-mer. The Phase 3 ophthalmic program (RGN-259) comprises three completed dry-eye trials (ARISE-1 n=317, ARISE-2 n=601, ARISE-3 n=700) and one completed European neurotrophic keratopathy trial (SEER-3), all of which missed their pre-specified primary endpoints. The cardiac intravenous program (RGN-352) was placed on FDA clinical hold in March 2011 and never enrolled patients. Two independent replications contradicted the cardiac headline findings: Zhou et al. (2012) reported that full-length Tβ4 after myocardial infarction did not reprogram epicardial cells into cardiomyocytes^[17], and Banerjee et al. (2012) reported that global and cardiac-specific Tβ4 knockout mice are born at Mendelian ratios with normal heart and coronary vessel development^[18].

RegeneRx filed SEC Form 15 in August 2023, terminating its public-company reporting obligations. A separate Phase 1/2 study sponsored by Hudson Biotech (NCT07487363) is the first publicly registered US trial using the LKKTETQ 7-mer by name, in stable atherosclerotic cardiovascular disease with cardiovascular-biomarker endpoints (recruiting as of May 2026); it is the first 7-mer-specific human trial in approximately 25 years of Tβ4 clinical development^[14]. The full TB-500 literature review is available on the TB-500 component PDP.

Pathway Independence

The published mechanism literature for BPC-157 and TB-500 maps onto two distinct molecular target sets. BPC-157 has been characterized within the nitric oxide (NO) signaling axis and the VEGFR2-Akt-eNOS angiogenesis pathway across rat models of gastric mucosal injury and tendon injury; the receptor-binding profile in human tissue has not been characterized in the peer-reviewed literature^[1][2]. TB-500 (and the full Tβ4 parent protein) has been characterized within the actin-sequestration mechanism, forming a 1:1 complex with monomeric ATP-G-actin via the LKKTET contact residues 17-22 of the parent protein^[3][4].

No published peer-reviewed study has identified a shared molecular target, a converging signaling pathway, or a documented pharmacokinetic interaction between the two molecules in any cellular or animal system. The body of mechanism work on each compound has been conducted by separate research groups (Sikirić at Zagreb and Chang at Chang Gung for BPC-157; Goldstein at GWU and the Sosne/Kleinman collaboration for TB-500 and full Tβ4) within separate preclinical model systems.

The two compounds are frequently mentioned together in non-clinical commerce contexts as a single-vial preparation. The pathway-independence framing here is a description of the literal mechanism literature on each compound, not an assertion about combined biological activity.

Combined Administration Literature

No peer-reviewed combined-administration studies of BPC-157 and TB-500 exist in the published clinical or preclinical literature as of May 2026. A PubMed search for the two compound names in combination returns no primary research articles characterizing co-administration in any model system. The two compounds have been studied separately, by separate research groups, in separate preclinical preparations, across roughly 30 years. Readers seeking the component literature should consult the BPC-157 and TB-500 individual PDP entries on this site, which contain the full per-compound reference list.

The combined-vial commercial format predates any peer-reviewed combined-administration data. The format originated in the equine veterinary and Australian compounding channel in the late 2000s and migrated into the broader research-peptide commerce sector without a corresponding research literature.

The one regulatory enforcement data point involving this specific compound pair is the Emma Brooks case: a Canadian university volleyball athlete sanctioned by U Sports / CCES with a 4-year suspension (ending 3 December 2028) for BPC-157 + TB-500 use during the August-September 2024 competition window^[10]. The case is administrative, not a peer-reviewed pharmacology study, but it is the only documented enforcement data point tying the two compounds together.

Replication and Clinical Status

Both BPC-157 and TB-500 were removed from FDA 503A Category 2 (Do-Not-Compound) effective April 22, 2026, though removal does not confer Category 1 status or compoundability. The Pharmacy Compounding Advisory Committee (PCAC) has scheduled both compounds for review on the July 23, 2026 Day 1 docket: BPC-157 for an ulcerative colitis indication and TB-500 for a wound-healing indication^[11][12]. The World Anti-Doping Agency bans both compounds at all times: BPC-157 under S0 (Non-Approved Substances) and TB-500 under S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics). Australia's Therapeutic Goods Administration has scheduled BPC-157 as Schedule 9 (Prohibited Substance) effective July 1, 2026.

Two independently registered active human trials are currently recruiting, neither of which studies the combined preparation. Hudson Biotech sponsors NCT07437547 (BPC-157 Phase 2 for acute hamstring muscle strain repair, n=120 estimated, recruiting since February 2026)^[13] and NCT07487363 (TB-500 LKKTETQ 7-mer Phase 1/2 in stable atherosclerotic cardiovascular disease with cardiovascular-biomarker endpoints, n=80, recruiting as of May 2026)^[14]. Both trials examine each compound in isolation. No registered human trial of the BPC-157 + TB-500 combination exists on ClinicalTrials.gov as of May 2026.