sin 10

Molsidomine (Corvaton) is an orally active, long-acting vasodilating drug. It metabolizes in the liver to the active metabolite linsidomine, that releases nitric oxide (NO) upon decay as the actual vasodilating compound.

Beta-defensin 103 isoform X1, pig, is an antimicrobial peptide found in various organisms, essential for the initial defense mechanisms of the innate immune system against pathogens [1].

Beta-defensin 103 isoform X1, pig TFA, is an antimicrobial peptide found in various living organisms, crucial for the initial defense of the innate immune system against pathogens [1].

c-Fms-IN-10, a derivative of thieno [3,2-d] pyrimidine, is a kinase inhibitor of FMS (Colony-stimulating factor-1 receptor, CSF-1R; IC50: 2 nM) with anti-tumor activity.

Pan-KRAS-IN-10 (Compound 58) acts as an inhibitor of the human tumor mutant gene KRAS. It suppresses the proliferation of KRAS mutant cells, specifically AsPC-1 (G12D mutant) and SW480 (G12V mutant), with IC50 values of 0.7 and 0.24 nM, respectively.

Orazipone inhibits cytokine production and histamine release; an NSAID.

FOBISIN101 is a novel inhibitor of all 14-3-3 isoforms in 14-3-3 PPIs.

Ferroptosis-IN-10 (compound D1) is an inhibitor of ferroptosis, demonstrating a potent IC50 value of 22 nM. It exhibits neuroprotective activity in the oxygen-glucose deprivation/reoxygenation (OGD/R) model.

PROTAC IDO1 Degrader-1, a pioneering compound, efficiently targets indoleamine 2,3-dioxygenase 1 (IDO1) for ubiquitination and degradation by recruiting IDO1 to the CRBN E3 ligase, thereby facilitating its entry into the ubiquitin-proteasome system (UPS) with a DC50 of 2.84 μM. This compound also moderately enhances the tumor-killing efficacy of HER2 CAR-T cells[1].

DW532 is one of simplified analogues of hematoxylin that has shown broad-spectrum inhibition on tyrosine kinases and in vitro anti-cancer activities. DW532 inhibited EGFR and VEGFR2 in vitro kinase activity (the IC50 values were 4.9 and 5.5 μmol/L, respectively), and suppressed their downstream signaling. DW532 dose-dependently inhibited tubulin polymerization via direct binding to tubulin, thus disrupting the mitotic spindle assembly and leading to abnormal cell division. In a panel of human cancer cells, DW532 (1 and 10 μmol/L) induced G2/M phase arrest and cell apoptosis, which subsequently resulted in cytotoxicity. Knockdown of BubR1 or Mps1, the two core proteins of the spindle assembly checkpoint dramatically decreased DW532-induced cell cycle arrest in MDA-MB-468 cells. Moreover, treatment with DW532 potently and dose-dependently suppressed angiogenesis in vitro and in vivo. ( Acta Pharmacol Sin. 2014 Jul;35(7):916-28.)