A C-glycosyl compound that is isovitexin in which the hydrogen at position 8 is replaced by a β-D-glucosyl residue.

InChI=1S/C27H30O15/c28-6-12-17(32)21(36)23(38)26(41-12)15-19(34)14-10(31)5-11(8-1-3-9(30)4-2-8)40-25(14)16(20(15)35)27-24(39)22(37)18(33)13(7-29)42-27/h1-5,12-13,17-18,21-24,26-30,32-39H,6-7H2/t12-,13-,17-,18-,21+,22+,23-,24-,26+,27+/m1/s1

Vicenin-2 (VCN-2), an active constituent of the medicinal herb Ocimum Sanctum Linn or Tulsi, it can effectively induce anti-proliferative, anti-angiogenic and pro-apoptotic effect in CaP cells (PC-3, DU-145 and LNCaP) irrespective of their androgen responsiveness or p53 status;VCN-2 in combination with docetaxel (DTL) synergistically inhibited the growth of prostate tumors in vivo with a greater decrease in the levels of AR, pIGF1R, pAkt, PCNA, cyclin D1, Ki67, CD31, and increase in E-cadherin; it could as a single agent and in combination with DTL in carcinoma of prostate (CaP). [1]
Vicenin-2 has potential anti-inflammatory activity, can modify LPS-induced total nitrite and TNF-α production, in addition to the LPS-induced translocation of the nuclear factor NF-κB.[2]
vicenin-2 and scolymoside, can suppress high-glucose (HG)-induced vascular inflammatory processes in human umbilical vein endothelial cells (HUVECs) and mice, HG-induced vascular inflammatory responses are critical events underlying the development of various diabetic complications; therefore, suggests that vicenin-2 and scolymoside have significant therapeutic benefits against diabetic complications and atherosclerosis.[3]
Vicenin-2 or scolymoside can reduce cecal ligation and puncture (CLP)-induced septic mortality and pulmonary injury, indicate that vicenin-2 and scolymoside could be a potential therapeutic agent for treatment of various severe vascular inflammatory diseases via inhibition of the TGFBIp signaling pathway.[4]
Vicenin-2 has antithrombotic and antiplatelet activities.[5]

English website: Vicenin -2
Japanese website: Vicenin -2
Chinese website: Vicenin -2

[1] Nagaprashantha L D, Vatsyayan R, Singhal J, et al. Biochem Pharmacol, 2011, 82(9):1100-9.
[2] Marrassini C, Davicino R, Acevedo C, et al. J Nat Prod, 2011, 74(6):1503-7.
[3] Ku S K, Bae J S. Can J Physiol Pharm, 2016, 3(1): 287-95.
[4] Lee W, Ku S K, Bae J S. Inflammation, 2015, 38(6):2166-77.
[5] Lee W, Bae J S. Blood Coagul Fibrin, 2015, 26(6):628-34. 
[6] Qin L U. China Pharmacy, 2015(30):4271-3.