sin 10

Molsidomine (Corvaton) 是一种长效的、口服活性的血管扩张药，在肝脏中代谢可被为活性代谢物Linsidomine。 其中Linsidomine 是一种不稳定的化合物，能够产生NO，可用作血管舒张剂。

Beta-defensin 103 isoform X1, pig 是一种抗菌肽、在多种生物体内被发现，参与了先天性免疫防线。

Beta-defensin 103 isoform X1, pig TFA 是一种抗菌肽、在多种生物体内被发现，参与了先天性免疫防线。

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

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.

Acetyl-Adhesin (1025-1044) amide，为变形链球菌细胞表面粘连蛋白20肽段，充当抗菌肽，特异性阻止粘连素同唾液受体结合，避免变形链球菌再定植。

Ferroptosis-IN-10 (compound D1) 作为一种铁死亡抑制剂,显示出22 nM的IC50.此外,它在氧-糖缺乏 复氧 (OGD R) 模型下展现出神经保护活性.

PROTAC IDO1 Degrader-1 is the first potent IDO1 (indoleamine 2,3-dioxygenase 1) degrader that hijacks IDO1 to CRBN E3 ligase to introduce IDO1 into UPS and eventually achieve ubiquitination and degradation (DC50=2.84 μM). PROTAC IDO1 Degrader-1 moderately improves the tumor-killing activity of H ER2 CAR-T cells[1]. PROTAC IDO1 Degrader-1 (compound 2c) (10 μM; 24 hours) notably decreases IDO1 level induced by IFN-γ[1].PROTAC IDO1 Degrader-1 and IFN-γ (5 ng mL) are incubated with HeLa cells for 24 h, and a significant dose-dependent degradation is observed. PROTAC IDO1 Degrader-1 combined with chimeric antigen receptor-modified T (CAR-T) cells can improve the tumor-killing activity of HER-2 CAR-T cells[1].PROTAC IDO1 Degrader-1 induces significant and persistent degradation of IDO1 with maximum degradation (dmax) of 93% in HeLa cells[1]. [1]. Hu M, et al. Discovery of the first potent proteolysis targeting chimera (PROTAC) degrader of indoleamine 2,3-dioxygenase 1. Acta Pharm Sin B. 2020;10(10):1943-1953.

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.)