BPC-157 10mg + TB-500 10mg Bundle

Visao Geral

BPC-157 (Body Protection Compound-157, Bepecin, PL 14736) e um(a) sintetico(a) pentadecapeptide composto(a) por 15 aminoacidos (GEPPPGKPADDAGLV), derivado(a) de a partial sequence of a larger Body Protection Compound protein naturally encontrado(a) em human gastric juice.[1][2]

Originally isolado(a) by Dr. Predrag Sikiric's grupo de pesquisa no(a) University of Zagreb in 1993, BPC-157 is one do(a) a maioria extensively studied cytoprotective peptides in preclinical literature. It has been studied across gastrointestinal, musculoskeletal, neurological, and vascular models.[8]

A key distinguishing feature is its exceptional stability — BPC-157 resists enzymatic degradacao in human gastric juice for over 24 hours.[3][9]

The U.S. FDA placed BPC-157 no(a) Categoria 2 Substancia Farmaceutica a Granels list in September 2023, citing potential immunogenicity risks and insufficient safety data for human manipulacao.[4] WADA explicitly banned BPC-157 under S0 (Non-approved Substances) eficaz January 1, 2022.[5]

Mecanismo de Acao

VEGFR2 Activation (Primary Target)

BPC-157 liga-se a and ativa vascular endothelial fator de crescimento receptor 2 (VEGFR2) on celulas endoteliais. Diferentemente de standard ligands, BPC-157 promove VEGFR2 internalizacao — um(a) critico(a) step in activating downstream repair pathways.[7][10]

VEGFR2-Akt-eNOS Cascade

Upon VEGFR2 binding, BPC-157 desencadeia fosforilacao of Akt (Protein Kinase B), que ativa endothelial nitric oxide synthase (eNOS), producing nitric oxide (NO) — essencial para angiogenese and vascular repair.[7]

Src-Caveolin-1-eNOS Pathway

BPC-157 promove fosforilacao of Src and Caveolin-1 (Cav-1). Under normal conditions, Cav-1 inibe eNOS — BPC-157 disrupts this inhibitory complex, enhancing NO production.[10]

FAK-Paxillin Pathway

In tendon fibroblastos, BPC-157 ativa focal adhesion kinase (FAK) and paxillin, essencial para migracao celular, adhesion, and cytoskeletal organization during reparo tecidual.[11]

JAK-2 / Growth Hormone Receptor Upregulacao

BPC-157 ativa JAK-2, linked to upregulacao of hormonio do crescimento receptors (GHR) on tendon fibroblastos, enhancing tissue sensitivity to hormonio do crescimento.[11][12]

Egr-1/NAB2 Feedback Loop

ERK1/2 ativacao upregula Egr-1 and simultaneamente its corepressor NAB2, establishing a feedback loop que previne uncontrolled angiogenic signaling.[13]

Nitric Oxide System Modulation (Bidirectional)

BPC-157 exibe um(a) unico(a) modulatory interaction com o(a) NO system — it counteracts ambos(as) L-NAME (NOS inhibitor → hipertensao) and L-arginine (NOS substrate → hipotensao), acting como um(a) homeostatic buffer rather do que a strict agonist or antagonist.[14]

Dopamine/Serotonin System Regulation

BPC-157 antagonizes o efeitos of dopamine receptor blockers (haloperidol) and agonists (amphetamine), assim como serotonin syndrome precursors — suggesting a regulatory influence on these neurotransmitter systems rather do que direto(a) ligacao ao receptor.[15]

Aplicacoes de Pesquisa

BPC-157 has been studied in rodent gastric-lesion, tendon-transection and ischemia models, among others:

1. Gastrointestinal Models — Rodent gastric-lesion and fistula models.[8]
2. Musculoskeletal Models — Rodent tendon-transection, ligament and muscle-injury models; biomechanical endpoints reported.[16][17]
3. CNS Models — Rodent TBI, spinal-cord compression and carotid-occlusion models; edema and histology endpoints reported.[18][19]
4. Vascular Occlusion Models — Collateral-vessel endpoints in rodent occlusion models (Budd-Chiari, Pringle maneuver).[20]
5. Corneal Models — Corneal-transparency and neovascularizacao endpoints.[21]
6. Liver Models — Rodent bile-duct-ligation and toxin-induced liver-injury models; enzyme and bilirubin endpoints.[22]
7. Dopaminergic/Serotonergic Models — Rodent catalepsy, amphetamine and ketamine behavioral models.[15]

Resumo da Pesquisa Pre-clinica

Key Preclinical Studies

Parametros Farmacocineticos