LSKL, Inhibitor of Thrombospondin (TSP-1)

LSKL, Inhibitor of Thrombospondin (TSP-1) is a latency-associated protein (LAP)-TGFβ derived tetrapeptide and a competitive TGF-β1 antagonist. LSKL, Inhibitor of Thrombospondin (TSP-1) inhibits the binding of TSP-1 to LAP and alleviates renal interstitial fibrosis and hepatic fibrosis. LSKL, Inhibitor of Thrombospondin (TSP-1) suppresses subarachnoid fibrosis via inhibition of TSP-1-mediated TGF-β1 activity, prevents the development of chronic hydrocephalus and improves long-term neurocognitive defects following subarachnoid hemorrhage (SAH). LSKL, Inhibitor of Thrombospondin (TSP-1) can readily crosse the blood-brain barrier^[1][2]. IC50 & Target:TGF-β1^[1] In Vitro: The KTFR sequence from ADAMTS1 is responsible for the interaction with the LSKL, Inhibitor of Thrombospondin (TSP-1) (LSKL peptide) from the latent form of TGF-β, leading to its activation. There is a stable binding mode between LSKL, Inhibitor of Thrombospondin (TSP-1) and ADAMTS1 KTFR sequence, characterized by 3 salt bridges and 2 hydrogen bonds^[2]. In Vivo: LSKL, Inhibitor of Thrombospondin (TSP-1) (1 mg/kg; intraperitoneal injection; male Sprague-Dawley rats) is protective against subarachnoid fibrosis, attenuates ventriculomegaly and effectively suppresses hydrocephalus. LSKL, Inhibitor of Thrombospondin (TSP-1) treatment inhibits TGF-β1 activity and subsequent Smad2/3 signaling^[1].
LSKL, Inhibitor of Thrombospondin (TSP-1) (30 mg/kg, i.p.) successfully inhibits transforming growth factor (TGF) β-Smad signal activation induced by partial hepatectomy. LSKL, Inhibitor of Thrombospondin (TSP-1) successfully attenuates TGF-β-Smad signal activation by antagonizing TSP-1, but not by reducing TSP-1 protein expression. LSKL, Inhibitor of Thrombospondin (TSP-1) accelerates hepatocyte proliferation after hepatectomy^[3].