| Stereochemistry | ABSOLUTE |
| Molecular Formula | C35H44O16 |
| Molecular Weight | 720.7143 |
| Optical Activity | UNSPECIFIED |
| Defined Stereocenters | 16 / 16 |
| E/Z Centers | 1 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
[H][C@@]12OC=C[C@]1(O)[C@@H]3C[C@H](O2)[C@]4(O[C@@]34C)[C@]5(C)[C@H](O)[C@]6([H])OC[C@@]7([C@@H](C[C@H](OC(=O)C(\C)=C\C)[C@@]8(CO[C@](O)(C(=O)OC)[C@@]58[H])[C@@]67[H])OC(C)=O)C(=O)OC
InChI
InChIKey=FTNJWQUOZFUQQJ-NDAWSKJSSA-N
InChI=1S/C35H44O16/c1-8-15(2)24(38)49-18-12-19(48-16(3)36)32(26(39)43-6)13-46-21-22(32)31(18)14-47-34(42,27(40)44-7)25(31)29(4,23(21)37)35-20-11-17(30(35,5)51-35)33(41)9-10-45-28(33)50-20/h8-10,17-23,25,28,37,41-42H,11-14H2,1-7H3/b15-8+/t17-,18+,19-,20+,21-,22-,23-,25+,28+,29-,30+,31+,32+,33+,34+,35+/m1/s1
| Molecular Formula | C35H44O16 |
| Molecular Weight | 720.7143 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ABSOLUTE |
| Additional Stereochemistry | No |
| Defined Stereocenters | 16 / 16 |
| E/Z Centers | 1 |
| Optical Activity | UNSPECIFIED |
Azadirachtin, a complex tetranortriterpenoid limonoid from the neem seeds, is one of the most effective botanical insecticides and has been widely used in pest control, having very low mammalian toxicity. Recent toxicological reports showed that azadirachtin could induce apoptosis in various insect cell lines by dysregulating InR- and PI3K/AKT/TOR pathways, then stimulated apoptosis by activating tAtg5.
Approval Year
Conditions
| Condition | Modality | Targets | Highest Phase | Product |
|---|---|---|---|---|
PubMed
Patents
Sample Use Guides
The acute oral toxicity in rats fed technical grade azadirachtin ranged from greater than 3,540 mg/kg to greater than 5,000 mg/kg, the highest dose tested when administered undiluted to albino rats.
The single-dose oral toxicity LD50 of the formulated product Azatin-EC fed to rats was 4,241 mg/kg; considered practically nontoxic
Route of Administration:
Oral
Azadirachtin (AZA) primarily induced autophagy in Spodoptera litura cultured cell line (SL-1 cell) by dysregulating InR- and PI3K/AKT/TOR pathways, then stimulated apoptosis by activating tAtg5. The PI3K/AKT/TOR signaling pathway was investigated in SL-1 cells to explore the molecular mechanism underlying the autophagy induced by AZA. The PI3K signaling pathway negatively controls autophagy. The results demonstrated decreased PI3K (85KD) in SL-1 cells following treatment with 2.5 μg/mL AZA for 24 h. It was also evaluated the AZA cytotoxicity using the WST-8 test to verify whether AZA was capable of inducing autophagy in SL-1 cells. The results showed that SL-1 cell proliferation was inhibited in a dose-dependent manner after 24 h exposure. The inhibition activity can be significantly observed at a low concentration of 0.625 μg/mL. The cell viability rates were 80.19%, 74.72%, 69.41%, 67.43%, 66.22%, 63.83% and 49.84% at the concentrations of 1.25, 2.5, 5, 10, 20, 40 and 80 μg/mL, respectively.
