| Stereochemistry | ACHIRAL |
| Molecular Formula | C15H11O6 |
| Molecular Weight | 287.2442 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 1 |
SHOW SMILES / InChI
SMILES
OC1=CC2=[O+]C(C3=CC=C(O)C(O)=C3)=C(O)C=C2C(O)=C1
InChI
InChIKey=VEVZSMAEJFVWIL-UHFFFAOYSA-O
InChI=1S/C15H10O6/c16-8-4-11(18)9-6-13(20)15(21-14(9)5-8)7-1-2-10(17)12(19)3-7/h1-6H,(H4-,16,17,18,19,20)/p+1
| Molecular Formula | C15H10O6 |
| Molecular Weight | 286.2363 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
Cyanidin is a natural anthocyanidin present in fruits and vegetables, attenuates the development of several diseases, including asthma, diabetes, atherosclerosis, and cancer, through its anti-inflammatory effects. Its mechanism of action is still undefined, but it was revealed that cyanidin specifically recognizes an IL-17A binding site in the IL-17A receptor subunit (IL-17RA) and inhibits the IL-17A/IL-17RA interaction and thus can be used as a drug for the treatment of IL-17A-dependent inflammatory diseases and cancer. In addition, cyanidin was capable of inhibiting osteoclast formation and thus might have therapeutic potential for osteolytic diseases.
Approval Year
PubMed
Patents
Sample Use Guides
in mice: To examine the effect of A18 (also called cyanidin) on IL-17A–induced epidermal cell proliferation, it was intradermally injected the ears of female WT C57BL/6 mice with PBS or with IL-17A alone or together with A18 for six consecutive days. After the injections, the mice treated with IL-17 alone exhibited IL-17A–dependent epidermal hyperplasia, whereas the mice treated with both IL-17 and A18 exhibited reduced hyperplasia.
Route of Administration:
Other
It was studied the mechanisms of cyanidin for stimulatory insulin secretion from pancreatic β-cells. Cyanidin (1–300 µM) stimulated insulin secretion and cyanidin (80 to 300 µM) increased intracellular Ca2+ signals in a concentration-dependent manner. The Ca2+ signals were abolished by nimodipine, an l-type voltage-dependent Ca2+ channel (VDCC) blocker or under extracellular Ca2+ free conditions. Stimulation of cells with cyanidin activated currents typical for VDCCs and up-regulated the expression of glucose transporter 2 (GLUT2), Kir6.2, and Cav1.2 genes.
