Home NF-κB NF-κB inhibitor - HIV inhibitor - Autophagy modulator - Apoptosis related activator - Akt activator - Nrf2 activator Neferine For research use only.

Neferine

Synonyms: (R)-1,2-Dimethoxyaporphine

Neferine ((R)-1,2-Dimethoxyaporphine), a natural component of Nelumbo nucifera, has antitumor efficiency. Neferine induces apoptosis in renal cancer cells. Neferine prevents autophagy through activation of Akt/mTOR pathway and Nrf2 in muscle cells. Neferine strongly inhibits NF-κB activation. Neferine possesses a number of therapeutic effects such as anti-diabetic, anti-aging, anti-microbial, anti-thrombotic, anti-arrhythmic, anti-inflammatory and even anti-HIV.

Neferine Chemical Structure

Neferine Chemical Structure

CAS No. 2292-16-2

Purity & Quality Control

Neferine Related Products

Signaling Pathway

NF-κB Signaling Pathways

NF-κB Signaling Pathway

Biological Activity

Description Neferine ((R)-1,2-Dimethoxyaporphine), a natural component of Nelumbo nucifera, has antitumor efficiency. Neferine induces apoptosis in renal cancer cells. Neferine prevents autophagy through activation of Akt/mTOR pathway and Nrf2 in muscle cells. Neferine strongly inhibits NF-κB activation. Neferine possesses a number of therapeutic effects such as anti-diabetic, anti-aging, anti-microbial, anti-thrombotic, anti-arrhythmic, anti-inflammatory and even anti-HIV.
Targets
NF-κB [4]
In vitro
In vitro

Neferine induces reactive oxygen species mediated caspase-dependent apoptosis in liver and lung cancer cells, reverses the multidrug resistance in human breast cancer cells (MCF-7/ADM), human hepatocarcinoma (HepG2/ADR) and human gastric carcinoma cells (SGC7901/VCR). Neferine enhances the cytotoxic potential of cisplatin in A549 cells and augments cisplatin inducecd Sub-G1 accumulation. It inhibits the migration and invasion of human lung cancer cells and lowers the antioxidant enzyme activities. Neferine sensitizes the lung cancer cells to cisplatin and induces apoptosis through G1 cell cycle arrest, upstream ROS production, depletion of cellular antioxidant pool, reduction of mitochondrial membrane potential (ΔΨm) with increased expression of Bax, Bad, Bak, down regulates the expression of Bcl2, release of cytochrome c, cleaved caspase-9, cleaved caspase-3 and PARP[1].
Cell Research Cell lines A549 cells
Concentrations 1-30μM
Incubation Time 12h, 24h, 48h and 72h
Method

The cells are seeded at a density of 1x104 cells/well, and were allowed to attach for overnight in a CO2 incubator. Cells are then treated with different concentrations of cisplatin/neferine and incubated for different time periods (12h, 24h, 48h and 72h). After the treatment period, 20 μl of MTT reagent (5mg/ml) in 100 μl medium is added and incubated at 37°C for 4 h after aspirating the medium with neferine and cisplatin. Then the media with MTT is flicked off, the purple formazan crystals are dissolved in 200 μl of DMSO and the absorbance is recorded with a microquant plate reader at 570 nm.
In Vivo
In vivo

Neferine has an antifibrosis effect on CCl4-induced hepatic fibrosis in mice, possibly partly due to the decreased expression of TGF-β1 in the liver[2]. The plasma concentration-time curves of neferine (10, 20 and 50 mg/kg, i.g.) shows double absorption peaks with the first peak at 10 min and the second peak at 1 h. The tβ1/2 are 15.6 h, 22.9 h and 35.5 h, for each of these doses, respectively. Neferine distributes rapidly into different organ systems, with the highest concentrations found in the liver, followed by the lung, kidney and heart at doses of 10 or 20 mg/kg. At 50 mg/kg dose, concentrations of the kidney and lung are higher than those of others. Moreover, this compound is mainly metabolized in the liver and converted partially by CYP2D6 to liensinine, isoliensinine, desmethyl-liensinine and desmethyl-isoliensinine[3].
Animal Research Animal Models Adult male Kunming mice
Dosages 5, 10, 20 mg/kg
Administration i.p.

Chemical Information & Solubility

Molecular Weight 624.77 Formula

C38H44N2O6
CAS No. 2292-16-2 SDF Download Neferine SDF
Smiles CN1CCC2=CC(=C(C=C2C1CC3=CC=C(C=C3)OC)OC4=C(C=CC(=C4)CC5C6=CC(=C(C=C6CCN5C)OC)OC)O)OC
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