TB-500 5mg Recovery
Synthetic 17-aa fragment of thymosin beta-4. The other major name in regeneration research, studied for cell migration and angiogenesis.
The essential partner to BPC-157. Thymosin Beta-4 fragment — systemic cell migration, angiogenesis, deep muscle recovery. Complementary to BPC-157, which acts locally. The standard combo of advanced recovery protocols.
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One sealed vial of TB-500 5mg, lyophilised, without individual labelling.
Bacteriostatic water for reconstitution and 1 ml precision syringes graduated in 100 units, sold separately. The vial alone cannot be used as is.
Don't forget the essentials
Our TB-500 5 mg vial is the ideal pilot format to initiate a first regenerative research protocol without committing to extended stock. With 5 mg of lyophilized peptide at HPLC purity >=99 percent, this format covers 2 full loading dose injections (2.5 mg) or a 2-week pilot phase — perfect for validating a first cycle before moving to the 10 mg flagship format.
Each Atlas Lab vial ships with a complete Certificate of Analysis (COA). TB-500 5 mg is intended for independent researchers, experimental sports medicine clinics, and laboratories prioritizing supply flexibility. Dispatched Tuesday and Friday, France delivery within 2 to 3 days in isothermal packaging.
Why choose 5 mg? Reduced initial investment, concentration flexibility (2 ml = 2.5 mg/ml, 1 ml = 5 mg/ml), coverage of 2 loading injections. The perfect pilot format to document a first response before committing to more extended research.
01Mechanism of action
TB-500 (Thymosin Beta-4 peptide, or active fragment of Tbeta-4) is a synthetic peptide derived from Thymosin Beta-4, a 44-amino-acid protein initially identified in the thymus and widely distributed across mammalian tissues. Most research suppliers offer either the full 1-44 sequence (Tbeta-4) or the active 17-23 fragment (LKKTETQ), the latter considered the key functional site responsible for several documented biological effects.
The established primary mechanism of TB-500 is G-actin (monomeric actin) sequestration via a specific binding site, which regulates actin-filamentary dynamics and cellular motility. This fundamental action influences the migration of fibroblasts, corneal keratocytes, endothelial progenitors, and epicardial cardiac progenitors in studied models.
Published work has documented several convergent secondary pathways. First, mobilization of endothelial progenitor cells (EPCs) from bone marrow to injury sites, observed in cardiac and vascular repair models. Second, upregulation of VEGF (Vascular Endothelial Growth Factor) and stimulation of local angiogenesis, critical for post-ischemic tissue revascularization. Finally, anti-inflammatory modulation via the NF-kappaB axis and documented reduction of pro-inflammatory markers (TNF-alpha, IL-1beta) in various murine models.
At the tissue level, the preclinical literature has reported accelerated healing in multiple systems: cornea, skin, Achilles tendon, ligament, post-infarction cardiac muscle, colic mucosa. TB-500 displays plasma stability superior to classical regenerative peptides, with documented systemic diffusion making it a subject of particular interest for repair models distant from the injection site.
As with any research peptide, these data come exclusively from preclinical models (rodent, porcine, in vitro) and limited studies. No marketing authorization exists for human therapeutic use: TB-500 remains strictly a peptide intended for exploratory research.
TB-500 is a synthetic 7-amino-acid fragment (Leu-Lys-Lys-Thr-Glu-Thr-Gln, LKKTETQ, 889.0 Da) corresponding to the active sequence of thymosin β-4 (Tβ4, 43 aa, 4960 Da), a ubiquitously expressed endogenous protein involved in the cytoskeleton. The canonical molecular mechanism of Tβ4 is monomeric G-actin sequestration via its β-thymosin domain (17-35), preventing premature polymerisation into F-actin filaments and freeing actin for rapid cytoskeletal rearrangements during cell migration. The LKKTETQ fragment (TB-500) partially retains this G-actin binding activity. Tβ4 also exerts anti-fibrotic effects via its N-terminal acetylated metabolite Ac-SDKP (N-acetyl-seryl-aspartyl-lysyl-proline, cleaved by prolyl-endopeptidase), which inhibits activated fibroblast proliferation and type I collagen accumulation. Documented signalling pathways include Integrin-Linked Kinase (ILK) activation, NF-κB downregulation, and modulation of several pro-regenerative microRNAs (miR-146a, miR-124).
Similar peptides
TB-500 occupies a central position in the regenerative research peptide class, with a distinctive profile that differentiates it from other candidates in the same category. Compared to BPC-157 (protective pentadecapeptide), TB-500 acts via G-actin sequestration and systemic mobilization of endothelial progenitors, whereas BPC-157 favors an NO-dependent pathway and more local VEGFR2 modulation. Both peptides are often associated in research protocols to explore the synergy of their complementary mechanisms, particularly in tendon and cardiac repair models.
Compared to classical growth factors such as GH (Growth Hormone) or IGF-1, TB-500 presents a significantly more targeted action profile on cell migration and matrix remodeling, without the systemic endocrine anabolic effects characteristic of GH/IGF-1. This specificity makes it a preferred candidate for protocols seeking to stimulate tissue regeneration without disrupting the somatotropic axis.
Compared to full-sequence Tbeta-4 (44 amino acids), the TB-500 fragment (LKKTETQ, residues 17-23) offers more economical synthesis, superior stability, and similar pharmacokinetics in most studied models. Some publications have however suggested that the full sequence might present a slightly different immunomodulatory profile, which remains an open subject of investigation.
Compared to GHK-Cu (copper peptide) or IGF-1 LR3, TB-500 stands out for its systemic mobilization of EPC progenitors from bone marrow, a characteristic relatively unique in this class. On the research peptide market, TB-500 ranks in the top 3 most requested regenerative peptides alongside BPC-157 and CJC-1295. Commercialization for human therapeutic use remains prohibited in France, Europe, and the United States.
TB-500 occupies a complementary position to BPC-157 in research healing/regeneration protocols. Where BPC-157 acts primarily via NO/VEGF/Egr-1 on digestive, tendinous and vascular tissues, TB-500 targets actin-cytoskeleton dynamics and the Ac-SDKP anti-fibrotic axis, with documented predominance on cardiac muscle, cornea and diabetic skin. Compared to full-length Tβ4 (4960 Da), TB-500 offers the pharmacological advantage of lower molecular mass (889 Da, better tissue diffusion) but loses the complete anti-apoptotic and angiogenic properties of the native protein. Compared to IGF-1 LR3 (long R3 IGF-1, 9111 Da), TB-500 does not directly stimulate cell proliferation but favours migration and tissue reorganisation. Compared to collagen precursors (bioactive hydrolysed collagen peptides, massive doses required), TB-500 acts at preclinical micromolar doses with a targeted molecular mechanism. The TB-500 + BPC-157 synergy is proposed as a "regenerative stack" in grey literature, validated by several rodent preclinical studies showing additive effects on multi-compartmental tendon injury models.