| Stereochemistry | ACHIRAL |
| Molecular Formula | C17H12Cl3N5O2 |
| Molecular Weight | 424.668 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
NC(=O)C1=C(N)N(CC2=CC(Cl)=C(C(=O)C3=CC=C(Cl)C=C3)C(Cl)=C2)N=N1
InChI
InChIKey=WNRZHQBJSXRYJK-UHFFFAOYSA-N
InChI=1S/C17H12Cl3N5O2/c18-10-3-1-9(2-4-10)15(26)13-11(19)5-8(6-12(13)20)7-25-16(21)14(17(22)27)23-24-25/h1-6H,7,21H2,(H2,22,27)
| Molecular Formula | C17H12Cl3N5O2 |
| Molecular Weight | 424.668 |
| 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 |
Carboxyamidotriazole (L651582) is a carboxyamide-amino-imidazole compound originally developed as a coccidiostat, an antiprotozoal agent that acts upon Coccidia parasites. Carboxyamidotriazole (L651582) is an orally-active agent with potential antineoplastic activity. Carboxyamidotriazole binds to and inhibits non-voltage-operated Ca2 channels, blocking both Ca2 influx into cells and Ca2 release from intracellular stores and resulting in the disruption of calcium channel-mediated signal transduction and inhibition of vascular endothelial growth factor (VEGF) signaling, endothelial proliferation, and angiogenesis. This agent may also inhibit tumor cell growth, invasion, and metastasis.
CNS Activity
Originator
Approval Year
Cmax
AUC
T1/2
Sourcing
PubMed
Sample Use Guides
Carboxyamidotriazole at a dose of 250 mg was administered daily.
Route of Administration:
Oral
The inhibitory effects of carboxyamidotriazole (L651582) on cancer proliferation, adhesion, and motility in vitro and in vivo in a model of ovarian cancer progression were studied. L651582 reversibly inhibited up to 60% of the autocrine motility factor-stimulated tumor cell motility and tumor cell adhesion to tissue culture plastic. Autocrine motility factor-stimulated phosphoinositide metabolism was reduced significantly by treatment of the cells with 3 microM L651582 (P = 0.022). Thymidine incorporation and clonogenic growth of A2058 human melanoma, MDA-MB-231 human breast cancer, OVCAR-3 human ovarian cancer, and 5R-transformed rat embryo fibroblast cell lines were inhibited 60%-80% by 1-10 microM L651582. Intraperitoneal injection of OVCAR-3 cells causes malignant ascites, peritoneal carcinomatosis, and serosal and visceral seeding that, if left untreated, are lethal to nude mice. Intraperitoneal L651582 markedly prolonged survival of nude mice heavily laden with ovarian cancer [mean survival time of treated group divided by mean survival time of control group = 220% (P less than 0.03)].
