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Lificiguat (YC-1) induces cell cycle arrest and inhibits tumor growth both in vitro and in vivo via the up-regulation of p21 (CIP1/WAP1) expression in HA22T cells. Lificiguat (YC-1) induces apoptosis and inhibits tumour growth of breast cancer cells via down-regulation of EZH2 by activating c-Cbl and ERK. Lificiguat (YC-1) inhibited the aggregation of and ATP release from washed rabbit platelets induced by arachidonic acid (AA), collagen, U46619, platelet-activating factor (PAF), and thrombin in a concentration-dependent manner. Lificiguat (YC-1) also disaggregated the clumped platelets caused by these inducers. Lificiguat (YC-1) increases the catalytic rate of the enzyme and sensitizes the enzyme toward its gaseous activators nitric oxide or carbon monoxide. Lificiguat (YC-1) activation of sGC can occur independently of heme, but that activation is substantially increased when the heme moiety is present in the enzyme.
Compared with tumors from vehicle-treated mice, tumors from YC-1-treated mice were statistically significantly smaller (P<.01 for all comparisons), expressed lower levels of HIF-1 alpha (P<.01 for all comparisons), were less vascularized (P<.01 for all comparisons), and expressed lower levels of HIF-1-inducible genes, regardless of tumor type.
| Molecular Weight | 304.34 |
| Formula | C19H16N2O2 |
| CAS Number | 170632-47-0 |
| Solubility (25°C) | DMSO ≥ 36 mg/mL |
| Storage |
Powder -20°C 3 years ; 4°C 2 years In solvent -80°C 6 months ; -20°C 1 month |
[5] Ko FN, et al. Blood. YC-1, a novel activator of platelet guanylate cyclase.
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