Betulinic acid Medical Intermediate

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  • Betulinic acid Medical Intermediate

PRODUCTS DETAILS

Basic Information
Product name Betulinic acid
Grade Pharma grade
Appearance White or off-white
Assay 98%
Shelf life 2 years
Packing 25kg/drum
Condition Stable, but store cool. Incompatible with strong oxidizing agents, calcium gluconate, barbiturates, magnesium sulfate, phenytoin, B group sodium vitamins.
Betulinic acid (472-15-1) is a natural Lupane triterpenoid from white birch tree (Betula pubescens). Induces apoptosis in a variety of cell lines.1 Induces mitochondrial permeability transition pore opening.2 ?Acts as a chemosensitizer for anticancer drug treatment in chemoresistant colon cancer cell lines.3 Cell permeable.Betulinic Acid is a natural pentacyclic triterpenoid. Betulinic Acid displays anti-inflammatory and anti-HIV activity. Betulinic Acid selectively induces apoptosis in tumor cells by directly activating the mitochondrial pathway of apoptosis through a p53- and CD95-independent mechanism. Betulinic Acid also exhibits TGR5 agonist activity. Betulinic acid (BetA) has been used: 1.to test its effects as an antiviral agent against Dengue virus (DENV). 2.as a sterol regulatory element-binding protein (SREBP) inhibitor to repress the lipid metabolism and proliferation of clear cell renal cell carcinoma (ccRCC) cells. 3.as a treatment to test its anti-tumor properties for cell viability and apoptotic cell death assays in multiple myeloma models.Betulinic acid, a pentacyclic triterpene, selectively induces apoptosis in tumor cells by directly activating the mitochondrial pathway of apoptosis through a p53- and CD95-independent mechanism.Natural triterpenoid that displays anti-HIV and antitumor activity. Induces the production of reactive oxygen species (ROS) and activates NF- κ B. Exhibits TRG5 agonist activity (EC 50 = 1.04 μ M).This compound is a pentacyclic triterpene obtained from Betula and Zizyphus species,which shows selective cytotoxicity against human melanoma cells (Shoeb2006). It generates reactive oxygen species, activates MAPK cascade, inhibitstopoisomerase I, inhibits angiogenesis, modulates pro-growth transcriptionalactivators, modulates the activity of aminopeptidase-N, and thereby inducesapoptosis in cancer cells (Desai et al. 2008; Fulda 2008).

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