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TB-500 Fragment 17-23

LKKTETQ · TB-500 Fragment 17-23

C
Animal replicated
RouteInjectableGray-market only
C
Evidence grade: Animal replicated

Effect demonstrated in multiple animal studies; human data sparse or extrapolated. Grades summarize evidence quality, not whether a compound is appropriate, legal, or risk-free.

At a glance
What it is
LKKTETQ — Leu-Lys-Lys-Thr-Glu-Thr-Gln — Actin-Binding Domain — What the Community Calls 'TB-500' — TB-4 Fragment, Actin-Binding Peptide, Heptapeptide.
Why people use it
Used primarily for tissue repair and healing and muscle and performance.
What the evidence supports
Smart N, Risebro CA, Melville AAD, et al. (2007). Thymosin beta4 induces adult epicardial progenitor mobilization and neovascularization. Nature. 445:177-182. [Landmark Nature paper; full Tβ4; epicardial progenitor cell mobilization; cardiac repair; the foundational paper for Tβ4 healing mechanism.]
If you only read one thing

TB-500 (LKKTETQ) is the community's most widely used healing peptide stack component. It appears in the Wolverine Stack, the GLOW Stack, and is sold by virtually every major peptide vendor. The pharmacological rationale (actin-binding domain drives cell migration; cell migration enables healing) is coherent. The full Thymosin Beta-4 protein has clinical trial evidence including a Phase 2b cardiac trial (NCT05984134). LKKTETQ itself has zero human clinical trials. The community is using a 7-AA fragment assuming it recapitulates the pharmacology of a 43-AA protein, when: (1) no comparative pharmacokinetic study of fragment vs full protein has been published; (2) full Tβ4 has additional receptor interactions and signaling pathways beyond actin sequestration that LKKTETQ does not cover; (3) every human safety and efficacy data point is from the full protein. LKKTETQ may work exactly as community users expect — the actin-binding domain is the primary mechanism, and the fragment approach is pharmacologically reasonable. Whether it works as well as the full protein is unknown.

Published literature
0human trials0human studies4animal0in vitro
Evidence reality check
Human evidence
No human studies
0 observational; RCT evidence not present in corpus.
Preclinical base
4 lab signals
4 animal; 0 in-vitro/mechanistic.
Evidence snapshot
Smart N, Risebro CA, Melville AAD, et al. (2007). Thymosin beta4 induces adult epicardial progenitor mobilization and neovascularization. Nature. 445:177-182. [Landmark Nature paper; full Tβ4; epicardial progenitor cell mobilization; cardiac repair; the foundational paper for Tβ4 healing mechanism.]
From the chapter quick-reference block.
Properties
Not injectable
Evidence
CAnimal replicated
The Community Naming Situation
'TB-500' is used in the peptide community to refer to the LKKTETQ fragment, not to the full 43-AA Thymosin Beta-4 protein. This naming has created persistent confusion because: (1) most published research uses full Tβ4, not the fragment; (2) clinical trials use full Tβ4; (3) the full protein is sold separately by some vendors as 'Thymosin Beta-4' or 'Tβ4'; (4) the community assumes the fragment recapitulates the parent's pharmacology because the actin-binding domain is considered the primary active sequence. Whether LKKTETQ fully recapitulates full Tβ4 pharmacology has NOT been established in controlled comparative trials.
The Actin-Binding Mechanism
Thymosin Beta-4's primary characterized function is G-actin sequestration: it binds G-actin (globular actin monomers) and prevents their polymerization into F-actin (filamentous actin). This regulates the cellular pool of free actin available for polymerization, controlling cell shape changes, cell migration, and cytoskeletal remodeling. The LKKTETQ sequence (positions 17-23) was identified as the minimum actin-binding domain via structure-activity studies. When cells need to migrate — as endothelial cells, smooth muscle cells, and progenitor cells do during tissue repair — the dynamic regulation of actin polymerization by Tβ4 (and by extension LKKTETQ) is essential. This is why TB-500 promotes systemic cell migration for healing.
Evidence for Fragment vs Full Protein
The Phase 2b cardiac trial (NCT05984134; n=90; acute MI; recombinant Tβ4) uses FULL 43-AA Thymosin Beta-4. Phase 2 wound healing trials use FULL Tβ4. Phase 1 safety in healthy volunteers used FULL Tβ4 IV. ZERO human clinical trials use LKKTETQ specifically. Fragment pharmacology: the community assumes LKKTETQ recapitulates the full Tβ4 actin-binding pharmacology because the domain is conserved. Full Tβ4 also signals through thymosin receptors, regulates gene expression, and activates additional pathways that the LKKTETQ fragment alone may not address.
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