
CJC-1295 vs Modified GRF (1-29): The DAC vs No-DAC Distinction, Explained
CJC-1295 with DAC has a 6-8 DAY half-life; Modified GRF (1-29) clears in ~30 minutes. Same modified GHRH(1-29) backbone, one bolt-on linker, ~1,000x PK difference.

No. TB-500 is a synthetic 7-amino-acid fragment of thymosin beta-4, not the full protein. It corresponds to residues 17-23 (LKKTETQ), the actin-binding region of the 43-residue parent peptide. Confusing the two is universal in the research-peptide market, the labels get used interchangeably even though they're different molecules at the bench.
The Bottom Line
- —Full thymosin beta-4 (Tβ4) is a 43-aa peptide, ~4,963 Da, N-terminally acetylated, originally isolated from calf thymus (Goldstein AL, 1972, PNAS).
- —TB-500 is a synthetic 7-aa fragment (LKKTETQ, ~889 Da) covering residues 17-23 of Tβ4, designed around the minimal actin-binding motif characterized by Van Troys et al., 1996, EMBO J.
- —Both fall under WADA S2.5 (banned in and out of competition, WADA 2026 Prohibited List).
- —Vendor labels are not standardized. Cross-COA reviews show roughly 60-70% of "TB-500" vials are actually full Tβ4, not the 7-aa fragment.
- —HPLC plus mass spec on a third-party COA is the only way to know which molecule you've actually got.
If you came here from the Wikipedia page on thymosin beta-4 and noticed the article never clarifies what "TB-500" actually is relative to the full Tβ4 protein, you're not alone. That gap is the entire reason this post exists. Below is the molecular breakdown, the citation trail, and the reason the names get used interchangeably in the research-peptide market even though they shouldn't.
TB-500 is a 7-amino-acid synthetic fragment (LKKTETQ, ~889 Da) corresponding to residues 17-23 of thymosin beta-4. The full Tβ4 protein is 43 residues (~4,963 Da), N-terminally acetylated, and was first isolated from calf thymus by Allan Goldstein's group in 1972 (Goldstein AL, 1972, PNAS, PMID 5028892). They are not the same molecule.
Full thymosin beta-4 is a small, highly conserved, intrinsically disordered protein. Sequence (single-letter):
Ac-SDKPDMAEIEKFDKSKLKKTETQEKNPLPSKETIEQEKQAGES
Key specs:
This is the molecule that drove the wound-healing literature: corneal epithelial repair (Sosne et al., 2007, Exp Eye Res, PMID 17409495), cardiac progenitor mobilization after MI (Smart et al., 2011, Nature, PMID 21654747), and dermal regeneration (Hsiao HY et al., 2014, Wound Repair Regen, PMID 25140030). When a paper says "Tβ4" or "thymosin beta-4", this is what they mean.
TB-500 is the synthetic 7-mer LKKTETQ, residues 17-23 of Tβ4. Specs:
The 17-23 region wasn't chosen randomly. Van Troys and colleagues mapped the actin-binding interface of Tβ4 by alanine scanning and truncation, and the LKKT motif (residues 17-20) plus the immediately downstream ETQ turned out to be the minimal contiguous sequence that retained measurable actin contact (Van Troys et al., 1996, EMBO J, PMID 8670856). RegeneRx Biopharmaceuticals, which held the Tβ4 IP for clinical development, also explored short fragments. The 7-aa LKKTETQ became the working synthetic surrogate because it was cheap to make, stable in solution, and reproduced at least some of the in vitro pro-migratory activity of full-length Tβ4.
The TB-500 designation itself traces to the equine-veterinary application. The horse-racing literature in the mid-2000s used "TB-500" as the product code for the synthetic 7-mer fragment marketed for tendon and ligament repair in racehorses. The grey-market peptide industry adopted the name wholesale, then stopped distinguishing it from full Tβ4 over the next decade.
| Property | Thymosin Beta-4 (Tβ4) | TB-500 (as originally specified) |
|---|---|---|
| Length | 43 aa | 7 aa |
| Sequence | SDKPDMAEIEKFDKSKLKKTETQEKNPLPSKETIEQEKQAGES | LKKTETQ |
| Residues of parent | 1-43 | 17-23 |
| Avg mass | ~4,963 Da | ~889 Da |
| N-terminal acetylation | Yes (native) | No (typical synthesis) |
| Binds G-actin 1:1 | Yes, full Kd ~0.7 µM | Weaker, retains contact but not full sequestration |
| Half-life (plasma, est.) | Hours | Minutes (rapid renal clearance) |
| WADA status | Banned, S2.5 | Banned, S2.5 |
| Original source | Goldstein, 1972, PNAS | Van Troys, 1996, EMBO J; RegeneRx product literature |
The labels are a mess because the research-peptide supply chain treats "TB-500" as a marketing SKU, not a defined molecule. Of the cross-vendor COAs reviewed across the Janoshik and Finnrick public testing datasets, the majority of vials sold as "TB-500" are actually full 43-aa Tβ4, not the 7-aa fragment the name was coined for.
In a pull of 12 publicly posted COAs labelled "TB-500" from grey-market vendors (sampled across the Janoshik Analytical and Finnrick's independent testing dumps, 2023-2025):
So when someone on r/Peptides says "I'm running TB-500", the molecule they've actually pinned is full Tβ4 about two-thirds of the time. The dosing math that gets quoted in community protocols (2-2.5 mg twice weekly for loading) is calibrated against this de facto reality, not against the 7-mer the name technically refers to.
Reason 1: the original RegeneRx framing. RegeneRx ran clinical trials on full Tβ4 (their development code was RGN-259 for ophthalmic and RGN-352 for systemic). "TB-500" was a veterinary-product name for the 7-mer. The grey market pulled both into the same product line and stopped distinguishing.
Reason 2: cost of synthesis. Making a 43-aa peptide at ≥98% HPLC purity by solid-phase synthesis costs roughly 5-8x what the 7-mer costs per milligram. But the per-vial price difference between "TB-500" vendors is usually <20%. That price compression doesn't make economic sense unless most vendors are not actually shipping the 7-mer.
Reason 3: the community can't tell from the vial. Lyo TB-500 and lyo full Tβ4 look identical, dissolve in BAC water identically, and pin the same. The only way to know what you've actually got is HPLC retention time plus mass spec, which means you need a COA, and ideally a third-party one rather than the vendor's in-house run.
If you genuinely want the 7-mer LKKTETQ specifically, you need a COA that reports:
If the COA shows a mass of ~4,963 Da, what you have is full Tβ4. That's not bunk, that's just a different molecule than the label claims. For most healing applications, people argue this is actually preferable, full Tβ4 has the actual research evidence behind it. But you should know which one is in the vial.
For the buyer checklist + vendor screening flow, see our where to buy TB-500 guide.
The Tβ4 evidence base does not transfer 1:1 to the 7-mer. Pre-clinical and early clinical data, corneal wound healing (Sosne et al., 2007, PMID 17409495), cardiac progenitor mobilization (Smart et al., 2011, Nature, PMID 21654747), dermal repair (Hsiao et al., 2014, PMID 25140030) was generated using full 43-aa Tβ4, not the 7-mer.
In vitro studies of LKKTETQ show retained but reduced actin-binding activity, and some retained pro-migratory signaling in cultured cells. What you don't have is the systemic in vivo evidence that exists for full Tβ4. The 7-mer is a tool compound that captures part of the parent's activity, not a drop-in clinical substitute.
In community use, this distinction gets papered over because both molecules produce comparable subjective reports for soft-tissue recovery on the standard 2-2.5 mg twice-weekly protocol. From what people report, the felt effect of full Tβ4 and the felt effect of LKKTETQ are not clearly distinguishable in self-reports, partly because expectancy is huge and partly because both compounds have a real mechanism, the 7-mer just has less of it. YMMV.
The WADA Prohibited List has flagged this since at least 2014. Under section S2.5 "Growth factors and growth factor modulators", both full Tβ4 and TB-500 are banned in and out of competition for athletes subject to the WADA code (WADA 2026 Prohibited List). Equine racing authorities (BHA in the UK, ARCI in the US) banned TB-500 specifically around 2011-2013 after the Australian thoroughbred industry caught riders dosing horses pre-race.
The takeaway for the WADA-tested athlete: it doesn't matter which molecule is in the vial, both will fail a screen.
The BPC-157 plus TB-500 combination ("Wolverine stack") has been one of the most-discussed peptide pairings on r/Peptides since at least 2018. The reasoning is that the two compounds hit non-overlapping arms of the tissue-repair cascade: BPC-157 drives local angiogenesis through VEGFR2 and the Src-caveolin-1 pathway plus GH receptor upregulation, while TB-500 (or full Tβ4) drives cell migration through actin sequestration and turnover.
There's no published trial of the combination. There's no known direct contraindication either. People run them together at standard mono doses, 250 mcg BPC-157 subq 1-2x/day plus 2-2.5 mg TB-500 twice weekly during a 4-6 week loading phase, then either continue both at maintenance or drop one. The molecule-confusion problem applies here too: most "Wolverine stacks" are actually BPC-157 plus full Tβ4, not BPC-157 plus the 7-mer.
For the full TB-500 mechanism + dosing breakdown beyond the fragment-vs-protein distinction, see our TB-500 (Thymosin Beta-4) research guide.
TB-500, as originally specified, is a 7-amino-acid peptide (LKKTETQ, ~889 Da). Full thymosin beta-4 is a 43-aa peptide (~4,963 Da), small enough that most biochemists call it a peptide rather than a protein, though the line is fuzzy. The IUPAC convention is that anything under ~50 aa is a peptide.
Because in the grey-market peptide supply, "TB-500" labeled vials frequently contain full Tβ4, not the 7-mer. The names get used interchangeably in vendor catalogues and on Reddit even though the underlying molecules differ in length, mass, and (to a degree) activity. The interchange isn't technically correct, but it reflects what's actually shipped. Cross-COA review suggests roughly two-thirds of "TB-500" vials are full Tβ4.
Community protocols don't distinguish, both run at 2-2.5 mg twice weekly during loading (4-6 weeks), then 2 mg weekly for maintenance. Clinical Tβ4 trials used different routes (topical ophthalmic, IV) at different doses, so the subq research-use protocol is a community-derived convention rather than a published one. If your vial is the 7-mer specifically, the same mcg dose contains roughly 5.6x more moles than the equivalent dose of full Tβ4, the practical implications aren't well characterized.
Yes. Both TB-500 (the 7-mer) and full thymosin beta-4 are banned in and out of competition under section S2.5 of the WADA 2026 Prohibited List. The ban applies to all athletes subject to the WADA code. Equine racing bodies (BHA, ARCI) banned TB-500 specifically around 2011-2013 after misuse in thoroughbred racing surfaced.
You need a COA with both HPLC purity (≥98%) and mass spec confirmation. The 7-mer shows a parent ion around 888-890 Da; full Tβ4 shows ~4,963 Da. If the COA only reports HPLC purity without the mass, you don't know what molecule you have, you only know it's pure. Third-party tested COAs (Janoshik, Finnrick, Auxilium) are the standard, in-house vendor COAs are weaker evidence.
TB-500 and thymosin beta-4 are related but distinct molecules. Full Tβ4 is the 43-aa, ~4,963 Da N-acetylated peptide originally isolated from thymus and characterized through three decades of wound-healing and cardiac-regeneration research. TB-500 is the synthetic 7-aa fragment LKKTETQ (residues 17-23, ~889 Da) designed around the minimal actin-binding motif of Tβ4 and adopted as a veterinary-grade product code by RegeneRx in the mid-2000s.
In the research-peptide market the labels get used interchangeably, but the molecules aren't the same and the evidence bases don't fully transfer. If you're a researcher, a Wikipedia editor, or someone writing about either compound, the distinction is: Tβ4 = full 43-mer protein; TB-500 = 7-aa synthetic fragment; vendor "TB-500" = often actually full Tβ4 in practice. Both fall under WADA S2.5.
For the complete TB-500 research profile, including the full dosing protocols, vendor checklist, and primary-source citation index, see the TB-500 research profile on Next Pep.
Author: Karl Vorwerg, NextPep Research. Cross-referenced primary sources: Goldstein 1972 PMID 5028892, Van Troys 1996 PMID 8670856, Sosne 2007 PMID 17409495, Smart 2011 PMID 21654747, Hsiao 2014 PMID 25140030, WADA 2026 Prohibited List.
Last reviewed: 2026-05-08.
Research Disclaimer. All content on Next Pep is for informational and educational purposes only. It does not constitute medical advice, diagnosis, or treatment. Consult a licensed healthcare professional before considering any peptide protocol.

CJC-1295 with DAC has a 6-8 DAY half-life; Modified GRF (1-29) clears in ~30 minutes. Same modified GHRH(1-29) backbone, one bolt-on linker, ~1,000x PK difference.

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