Wolverine Stack BPC/157-TB-500

What the Wolverine Stack is

Two peptides — BPC-157 and TB-500 — co-lyophilised into one vial at a 1:1 mass ratio. It is a physical mixture. Nothing in the vial is a new molecule, no chemistry has occurred between the two components, and the stack is not a compound in its own right.

The name is a comic-book reference. It is not a description of anything that has been measured.

No study has ever tested this combination

One partial exception is worth naming precisely, because it is sometimes cited as though it were combination evidence and it is not. A 2021 retrospective chart review of intraarticular injections at a single Orlando clinic included some patients who received BPC-157 together with thymosin beta-4. That was an unblinded, uncontrolled review of seventeen charts with outcomes recalled by telephone months later, and the authors used no validated instruments^[10]. It is not a study of this combination in any meaningful sense, and it was not a study of Ac-LKKTETQ.

Component specifications

A blend is a mixture, not a compound. The blend itself has no CAS number, no molecular formula, no molecular weight and no PubChem CID — those identifiers describe single chemical substances, and inventing one for a two-component mixture would be a fabrication. We print N/A above and give the real identifiers for each component below, from PubChem.

The WADA lines above are data, reproduced from the 2026 Prohibited List^[11]. See the anti-doping section for what they mean.

Where the evidence stands

Component 1 — BPC-157 rodent

A synthetic pentadecapeptide corresponding to a partial sequence of a protein isolated from human gastric juice^[1]. The preclinical literature is large: transected rat Achilles tendon models showing improvement against saline controls on biomechanical, functional, microscopic and macroscopic measures^[1]; and cell-culture work showing increased fibroblast migration and survival under oxidative stress, with F-actin formation and dose-dependent FAK and paxillin phosphorylation — but explicitly no direct effect on fibroblast proliferation^[2]. A 2019 review found consistently positive soft-tissue findings while noting the work is overwhelmingly in small rodent models and that efficacy in humans is yet to be confirmed^[3].

The key negative finding

A 2025 narrative review in Current Reviews in Musculoskeletal Medicine found that human data are extremely limited — three pilot studies in total (intraarticular knee pain, interstitial cystitis, and an intravenous safety and pharmacokinetics assessment), and concluded that until well-designed clinical trials are conducted, BPC-157 should be considered investigational^[4]. There is no large randomised controlled trial, and no regulatory approval anywhere. A structural caveat: a large fraction of the positive findings originate from a single research group, so the evidence base has had far less independent replication than its volume suggests^[3].

Component 2 — TB-500 in vitro rodent

The vial contains Ac-LKKTETQ, a seven-residue fragment — not the 43-amino-acid thymosin β4 that the literature studied. Analytical chemists who characterised commercial TB-500 preparations by high-resolution mass spectrometry identified the active ingredient as the N-acetylated 17–23 fragment of Tβ4 — the actin-binding domain, with an acetyl group on the N-terminus^[5]. Almost everything cited in support of “TB-500” was done with the 43-residue protein: a different molecule, a different mass, a different pharmacokinetic profile.

There are zero human studies of TB-500. Not a randomised trial, not a pilot, not a case series. The only human-relevant analytical work is a doping-control method-development paper^[5].

The key negative finding — the oncology signal

Thymosin β4 overexpression in SW480 human colon carcinoma cells markedly increased invasiveness, with increased levels and enzymatic activity of matrix metalloproteinase-7 (MMP-7) — an enzyme that degrades basement membrane; in matched patient samples, Tβ4 mRNA, β-catenin, c-Myc and MMP-7 were all higher in metastatic liver lesions than in the primary colorectal tumours they came from^[6]. Overexpression also triggered epithelial-mesenchymal transition — scattering morphology, E-cadherin loss, cytosolic β-catenin accumulation — through upregulation of integrin-linked kinase^[7]. And the loss-of-function experiment agrees: disrupting Tβ4 expression by TALEN gene editing in B16F10 murine melanoma cells significantly decreased lung metastasis in a murine model^[8].

These are studies of endogenous Tβ4 inside tumour cells, not of exogenously administered TB-500 in a healthy organism — a real distinction, and we are not going to erase it. But the mechanism implicated (actin remodelling driving cell migration, ILK/β-catenin signalling, E-cadherin loss, MMP-7 induction) is precisely the mechanism by which this peptide family is claimed to promote repair. Nobody has administered TB-500 to a healthy animal over an extended period and looked at tumour incidence. Until someone does, the question is open.

TB-500 is prohibited by WADA by name under S2.3, at all times, and it is detectable: a validated LC-MS method confirmed N-acetylated LKKTETQ down to 0.01 ng/mL in equine urine^[9].

The fixed-ratio problem

This is a genuine research limitation, not a legal disclaimer.

• You cannot attribute an effect to a component. Anything observed in a two-peptide preparation could be the BPC-157, the TB-500, an interaction, or the vehicle. A blend destroys attribution by construction — and the whole marketing premise of this stack is an interaction claim that the format itself makes untestable.
• You cannot vary the doses independently. The ratio is locked at 1:1 by mass. Note that this is not 1:1 molar: BPC-157 is 1419.5 g/mol and TB-500 is 889.0 g/mol, so an equal-mass blend delivers roughly 1.6 times as many TB-500 molecules as BPC-157 molecules. Nobody chose that; it is an artefact of pricing peptides by the milligram.
• You cannot run a component-controlled comparison. Without single-component arms, there is nothing to compare against.

A researcher who wants interpretable data buys the singles and mixes to a ratio they control. A blend is a convenience format. That is what it is for.

Regulatory and anti-doping status

Reproduced from the WADA 2026 Prohibited List^[11], effective 1 January 2026:

• BPC-157 — named explicitly in S0, Non-Approved Substances. Prohibited at all times, in and out of competition. Specified Substance.
• TB-500 — named explicitly in S2.3, Growth Factors and Growth Factor Modulators (“Thymosin-β4 and its derivatives e.g. TB-500”). Prohibited at all times. non-Specified Substance, which carries the more severe sanctioning framework under the World Anti-Doping Code.

Both components of this stack are named on the current List. WADA’s List changes annually, and individual federations may differ from it. The only authoritative source is the athlete’s own federation’s current prohibited list — not this page, and not any vendor’s.

Neither component has been approved for human therapeutic use by the FDA or by any other governmental regulatory health authority.

What we don’t know

• Whether BPC-157 and TB-500 interact at all. Nobody has looked.
• Whether co-administration alters the pharmacokinetics of either. Uncharacterised.
• Whether 1:1 by mass is a sensible ratio, or any better than 3:1 or 1:5. No experiment has compared it to anything.
• Whether the oncology signal associated with full-length Tβ4 transfers to the Ac-LKKTETQ fragment — with or without BPC-157 present.
• Long-term safety of the combination in any species — entirely uncharacterised.
• Per-kilogram dosing in animal models does not scale to humans, and nothing on this page should be read as implying that it does.

We supply this stack for laboratory research. The per-component preclinical science is interesting. The combination has never been studied, the synergy claim has no support, and the oncology literature on the Tβ4 family is the most important thing on this page — which is why it is above this line rather than below it.