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MedChemExpress - Model Azadirachtin - ...

MedChemExpress - Model Azadirachtin - 11141-17-6

Azadirachtin is an oral active triterpenoid compound with anticancer, antimalarial, anti-inflammatory, and insecticidal activities. Azadirachtin induces cell apoptosis through the mitochondrial pathway (by inhibiting Bcl-2/Bax ratio or activating Apaf-1 and caspase-3) or through death receptors (by inhibiting TNFR activation). Additionally, Azadirachtin exerts its anti-inflammatory effects by inhibiting NF-кB signaling pathway activation, and it exhibits insecticidal activity by inducing apoptosis in insect cells[1][2][3][4][5][6].

Azadirachtin

MCE China：Azadirachtin

Brand：MedChemExpress (MCE)

Cat. No.HY-126741

CAS：11141-17-6

Purity：99.06%

Storage：-20°C, protect from light *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Shipping：Room temperature in continental US; may vary elsewhere.

Description：Azadirachtin is an oral active triterpenoid compound with anticancer, antimalarial, anti-inflammatory, and insecticidal activities. Azadirachtin induces cell apoptosis through the mitochondrial pathway (by inhibiting Bcl-2/Bax ratio or activating Apaf-1 and caspase-3) or through death receptors (by inhibiting TNFR activation). Additionally, Azadirachtin exerts its anti-inflammatory effects by inhibiting NF-кB signaling pathway activation, and it exhibits insecticidal activity by inducing apoptosis in insect cells.

In Vitro：Azadirachtin (3-24 μM, 6 h) exerts its anti-inflammatory effects in Retinoic acid (HY-14649)-induced A549 (lung carcinoma) cells by inhibiting the NF-κB signaling pathway[3]. Azadirachtin (135 μM, 24 h) induces cell cycle arrest and mitochondria-mediated apoptosis in human cervical cancer (HeLa) cells[5]. Azadirachtin (50 μg/mL, 22-24 h) inhibits the early sporogonic development of Plasmodium berghei and blocks its transmission effect[6].

In Vivo：Azadirachtin (10 μg/kg, i.g., once daily, 3 days a week for 14 weeks) carcinogenesis in the DMBA (HY-W011845)-induced hamster buccal pouch (HBP) carcinoma model by modulating xenobiotic metabolism enzymes, DNA damage, antioxidants, invasion, and angiogenesis.[4].

IC50 & Target：Caspase 3

References：

[1]. Shu B, Jia J, Zhang J, Sethuraman V, Yi X, Zhong G. DnaJ homolog subfamily A member1 (DnaJ1) is a newly discovered anti-apoptotic protein regulated by azadirachtin in Sf9 cells. BMC Genomics. 2018;19(1):413. Published 2018 May 29. [Content Brief]

[2]. Fernandes SR, et al. Chemistry, bioactivities, extraction and analysis of azadirachtin: State-of-the-art. Fitoterapia. 2019 Apr;134:141-150. [Content Brief]

[3]. Thoh M, et al. Azadirachtin interacts with retinoic acid receptors and inhibits retinoic acid-mediated biological responses. J Biol Chem. 2011 Feb 11;286(6):4690-702. doi: 10.1074/jbc.M110.169334. Epub 2010 Dec 2. Retraction in: J Biol Chem. 2013 Mar 22;288(12):8563. [Content Brief]

[4]. Priyadarsini RV, et al. The neem limonoids azadirachtin and nimbolide inhibit hamster cheek pouch carcinogenesis by modulating xenobiotic-metabolizing enzymes, DNA damage, antioxidants, invasion and angiogenesis. Free Radic Res. 2009 May;43(5):492-504. [Content Brief]

[5]. Priyadarsini RV, et al. The neem limonoids azadirachtin and nimbolide induce cell cycle arrest and mitochondria-mediated apoptosis in human cervical cancer (HeLa) cells. [Content Brief]

[6]. Tapanelli S, et al. Transmission blocking effects of neem (Azadirachta indica) seed kernel limonoids on Plasmodium berghei early sporogonic development. Fitoterapia. 2016 Oct;114:122-126. [Content Brief]

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