| Stereochemistry | ACHIRAL |
| Molecular Formula | C22H44N2 |
| Molecular Weight | 336.5982 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
CCCC1(CCC)CCC2(CCN(CCCN(CC)CC)C2)CC1
InChI
InChIKey=SERHTTSLBVGRBY-UHFFFAOYSA-N
InChI=1S/C22H44N2/c1-5-10-21(11-6-2)12-14-22(15-13-21)16-19-24(20-22)18-9-17-23(7-3)8-4/h5-20H2,1-4H3
| Molecular Formula | C22H44N2 |
| Molecular Weight | 336.5982 |
| 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 |
Atiprimod is an oral azaspirane which was initially developed by Smith Kline and French Laboratories for treating rheumatoid arthritis (discontinued in phase I). Due to its anti-inflammatory, antineoplastic, and antiangiogenic properties, the drug was tested in patients with Neuroendocrine Carcinoma and Multiple Myeloma and reached phase II (discontinued). In vitro studies revealed that atiprimod exerts its action by inhibiting the phosphorylation of signal transducer and activator of transcription 3 (STAT3), blocking the signalling pathways of interleukin-6 and vascular endothelial growth factor (VEGF) and downregulating the anti-apoptotic proteins Bcl-2, Bcl-XL, and Mcl-1, thereby inhibiting cell proliferation, inducing cell cycle arrest, and inducing apoptosis.
Originator
Approval Year
Sourcing
PubMed
Sample Use Guides
Neuroendocrine Carcinoma: Atiprimod is administered orally as a single daily dose of 120 mg/day for 14 days, followed by a 14-day treatment-free period. Multiple Myeloma: atiprimod was given at ten dose levels - 30, 60, 90, 120, 180, 240, 300, 360, 420, and 480 mg/day or 180, 240, 300, 360, 420, and 480 mg/day (in combination with ursodiol).
Route of Administration:
Oral
U266-B1 cells were incubated with 8 uM atiprimod to measure how the drug suppresses IL-6 production. Atiprimod attenuated IL6 supernatant levels to 23, 42, 53, and 130 pg/ml at 1, 6, 8, and 16 hours, respectively. NF-kB activity in the same cell line was blocked after 4 h of incubation with 50 uM atiprimod and after 24 h when using 8 uM of the drug. The percentage of cells undergoing apoptotic cell death also increased from 10.89 to 46.27% after exposure to 8 uM atiprimod.
