SC 560 is reported to be a Cox-1 and Cox-2 inhibitor, and is highly selective for Cox-1 (IC₅₀ of 0.009 μM) over Cox-2 (IC₅₀ of 6.3 μM). SC 560 also inhibits UTP-stimulated and basal cAMP levels. Cox-1 is shown to catalyze the conversion of Arachidonic Acid (20:4, n-6) into PGH2 (Prostaglandin H2, ), which is the precursor of thromboxanes and other prostaglandins, therefore SC 560 also suppresses TXB2 (Thromboxane B2, ) and PGE2 (Prostaglandin E2, ) production. SC 560 also displays the ability to induce cell growth inhibition by causing cell cycle arrest at the G₁ phase. Mechanistic studies show that SC 560 causes apoptosis of cells by eliciting reactive oxygen species and simultaneously decreasing the levels of anti-apoptotic proteins XIAP and survivin. Additional experiments suggest that SC 560 also activates caspase-3 and caspase-7 which results in apoptosis of cells.

>98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

Solid

SC-560

Off-white solid

1.33 g/cm³ (Predicted)

440.58° C at 760 mmHg (Predicted)

n²⁰_D 1.56 (Predicted)

DMSO : 35.3 mg/mL (100 mM)

MFCD02179214

COX-1,COX-2

Preincubation of COX-1 with SC-560 inhibits the conversion of arachidonic acid to PGE2 in a concentration-dependent manner. The IC50 of SC-560 for COX-2 is 6.3 μM, nearly 1,000-fold higher than with COX-1. SC-560 shows a dose and time dependent inhibitory effect on HCC cell growth. SC-560 also inhibits colony formation in soft agar and induces apoptosis in HCC cells in a dose-dependent manner. Moreover, SC-560 decreases the levels of the anti-apoptotic proteins survivin and XIAP and activates caspase 3 and 7 in a dose and time dependent fashion.

Oral dosing with either 10 or 30 mg/kg SC-560 1 hour before assay completely inhibits ionophore-stimulated TxB2production, indicating that SC-560 is orally bioavailable and inhibits COX-1 in vivo. SC-560 extensively distributes into rat tissues, and has a CL approaching hepatic plasma flow. The drug displays low less than 15% and formulation dependent bioavailability after oral administration and demonstrates kidney toxicity.