Why Choose Us?

3

Research-Grade
Purity

All peptides have a guaranteed purity of at least 99%.

2

Manufactured in
the USA

Our top-quality products are manufactured right here in the United States.

1

Fast
Shipping

Your products arrive at your door quickly. Plus, shipping is free for orders over $100.

4

Guaranteed
Freshness

Products are stored at -20° and shipped in cool shield bubble mailers.

5

Independently
Tested

Each batch is independently tested to ensure product purity and dosage.

Why Choose Us?

3

Research-Grade
Purity

All peptides have a guaranteed purity of at least 99%.

2

Manufactured in
the USA

Our top-quality products are manufactured right here in the United States.

1

Fast
Shipping

Your products arrive at your door quickly. Plus, shipping is free for orders over $100.

4

Guaranteed
Freshness

Products are stored at -20° and shipped in cool shield bubble mailers.

5

Independently
Tested

Each batch is independently tested to ensure product purity and dosage.

GMP TB500 Vial Transparent Vial Only

What is TB-500?

TB-500 is a synthetic acetylated peptide (Ac-LKKTETQ) modeled after the active site of thymosin β4 (Tβ4), a protein known for its actin-binding and tissue repair functions. Although TB-500 is structurally related to Tβ4, its biological activity has not been conclusively demonstrated. Recent studies have focused on its metabolic fate and analytical detection, rather than direct functional outcomes (Rahaman et al. 2024).

Researchers quantified TB-500 and six metabolites in vitro and in rat urine. Four primary metabolites—Ac-LKKTE, Ac-LKK, Ac-LK, and Ac-L—were confirmed with authentic standards. Ac-LK was the most abundant early metabolite (0–6 h), while Ac-LKK persisted up to 72 h. Among these, only Ac-LKKTE showed significant in-vitro wound healing activity, suggesting that prior reports of TB-500’s biological effects may actually be attributable to this metabolite (Rahaman et al. 2024).

Separately, studies on the parent compound Tβ4 demonstrated enhanced axonal remodeling, oligodendrogenesis, and vessel density in a rat stroke model, despite no change in infarct volume. This suggests a mechanism of structural recovery rather than neuroprotection (Morris et al. 2010).

References

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