533902-29-3
533902-29-3
Chemical Structure
LCKLSL
- CAS No.: 533902-29-3
- Formula:C30H57N7O8S
- Molecular Weight:675.88
InChIKey: HTBYABHLBWELKC-BTNSXGMBSA-N
SMILES: CC(C)C[C@@H](C(O)=O)NC([C@H](CO)NC([C@H](CC(C)C)NC([C@H](CCCCN)NC([C@H](CS)NC([C@H](CC(C)C)N)=O)=O)=O)=O)=O
Biological Activity: LCKLSL is a N-terminal hexapeptide and a competitive annexin A2 (AnxA2) inhibitor. LCKLSL potently inhibits the binding of tissue plasminogen activator (tPA) to AnxA2. LCKLSL also inhibits the generation of plasmin and has anti-angiogenic roles[1].
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LCKLSL | 99.72% | LCKLSL is a N-terminal hexapeptide and a competitive annexin A2 (AnxA2) inhibitor. LCKLSL potently inhibits the binding of tissue plasminogen activator (tPA) to AnxA2. LCKLSL also inhibits the generation of plasmin and has anti-angiogenic roles. | ||||||||||||||||||||
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Kemptide | 99.56% | Kemptide is a synthetic heptapeptide that acts as a specific substrate for cAMP-dependent protein kinase (PKA). | ||||||||||||||||||||
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LSKL, Inhibitor of Thrombospondin (TSP-1) | 99.34% | 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. | ||||||||||||||||||||
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LLVK | LLVK is a selective IκB phosphorylation inhibitor. LLVK reduces LPS-induced pro-inflammatory cytokines (IL-1β, IL-6, TNF-α). LLVK is promising for research of inflammatory bowel disease and rheumatoid arthritis. | |||||||||||||||||||||
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IKVAVC | IKVAVC is a derivative peptide of IKVAV with an artificially added cysteine (Cys) at its C-terminus. IKVAVC retains all the biological activities of the original IKVAV, mainly acting as a neural adhesion/differentiation signaling peptide, and is equipped with an engineered linker arm that enables covalent conjugation to molecular materials. IKVAV inhibits the migration and activation of fibroblasts, downregulates the TGF-β1 signaling pathway and endoplasmic reticulum stress, and promotes nerve repair. IKVAV regulates the phenotype of macrophages, shifting them from the pro-inflammatory M1 type to the pro-reparative M2 type. | |||||||||||||||||||||
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VKGILS-NH2 | 99.00% | VKGILS-NH2 is a reversed amino acid sequence control peptide for SLIGKV-NH2 (protease-activated receptor 2 (PAR2) agonist). VKGILS-NH2 has no effect on DNA synthesis in cells. | ||||||||||||||||||||
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Cys-Kemptide | Cys-Kemptide is a cysteine-terminated substrate peptide that can used to measure protein kinase A (PKA) activity. | |||||||||||||||||||||
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H-Leu-Ser-Lys-Leu-OH | H-Leu-Ser-Lys-Leu-OH (LSYL) is a latency-associated peptide at the amino terminus of LAP, with inhibitory effect on TGF-β1 activation. H-Leu-Ser-Lys-Leu-OH, binding with KRFK (HY-P3970), can block the signal transduction of TGF-β1, and prevent the progression of hepatic damage and fibrosis. | |||||||||||||||||||||
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SIGSLAK | SIGSLAK has the active site of E. coli penicillin-binding protein 1b. | |||||||||||||||||||||
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PAR-2 (1-6) (human) | 99.97% | PAR-2 (1-6) (human) (SLIGKV), a peptide ligand, is a PAR-2 agonist. | ||||||||||||||||||||
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L-Seryl-L-leucyl-L-leucyl-L-lysine | L-Seryl-L-leucyl-L-leucyl-L-lysine (SLLK) is the control peptide for LSKL (HY-P0299). | |||||||||||||||||||||
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