| Stereochemistry | ACHIRAL |
| Molecular Formula | C25H26O3 |
| Molecular Weight | 374.4721 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 1 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
OC(=O)\C=C\C1=CC=C(C=C1)C2=CC=C(O)C(=C2)C34CC5CC(CC(C5)C3)C4
InChI
InChIKey=QAWBIEIZDDIEMW-FPYGCLRLSA-N
InChI=1S/C25H26O3/c26-23-7-6-21(20-4-1-16(2-5-20)3-8-24(27)28)12-22(23)25-13-17-9-18(14-25)11-19(10-17)15-25/h1-8,12,17-19,26H,9-11,13-15H2,(H,27,28)/b8-3+
| Molecular Formula | C25H26O3 |
| Molecular Weight | 374.4721 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 1 |
| Optical Activity | NONE |
Adarotene (ST1926) is a new pro-apoptotic and cytodifferentiating antitumour drug, belongs to the so-called class of atypical retinoids. Adarotene is active on its own or in combination with other chemotherapeutics for the treatment of a vast number of experimental tumors. It was found in preclinical investigations the potential therapeutic use it in chronic myeloid leukemia (CML), against Rhabdomyosarcoma and for treatment of Adult T-cell leukemia/lymphoma (ATL). ST1926 induced an early DNA damage response, which led to increase in apoptosis, in addition to S-phase cell cycle arrest and a reduction in protein levels of the cell cycle kinase CDK1. The presence of the phenolic hydroxyl group on adarotene structure allows a rapid O-glucuronidation as a major mechanism of elimination of the drug, favoring a fast excretion of its glucuronide metabolite in the urines.
Originator
Approval Year
PubMed
Patents
Sample Use Guides
for mice: Stock ST1926 (ADAROTENE) solution was diluted in 1:1 cremophor/ethanol solution (10 µL stock ST1926 containing 0.6 mg in 40 µL cremophor/ethanol). Each animal received by gavage 50 µL of ST1926 solutions, equivalent to 30 mg/kg body weight (average mouse weight, 20 g) as this dosage was reported to cause survival advantage in AML mice with no signs of toxicity
Route of Administration:
Oral
Were used 3 HTLV-1–transformed cell lines (HuT-102, MT-2, and C8166) and 3 HTLV-1–negative cell lines (CEM, Jurkat, and MOLT-4) to test for the effects of ST1926 (ADAROTENE) on cell growth and viability. ST1926 concentrations ranging from 0 05 to 5 µM as these are pharmacologically achievable were used. ST1926 treatment resulted in a time-dependent growth inhibition of all tested cell lines. In general, both HTLV-1–negative and –positive cell lines were equally sensitive to ST1926. A threshold level at 0.5 µM concentration was noted, with similar growth suppressive effects as 10-fold higher concentrations, except for CEM cells. 1 µM ST1926 caused a growth inhibition that was almost complete in primary ATL cells from the newly diagnosed acute ATL patients and >60% in the relapsed one. In contrast, resting and phytohemagglutinin-stimulated normal T cells from 3 healthy donors were resistant to ST1926 up to 10 μM.
