Bortezomib Raw Materials Powder Bortezomib

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Bortezomib Powder Usage and Synthesis.

Bortezomib was the first proteasome inhibitor to be used clinically. The proteasome is present in all eukaryotic cells and degrades more than 80% of the proteins in the cell. It can reversibly inhibit the function of proteasome, thus inhibiting protein degradation, leading to protein accumulation and apoptosis. Because multiple myeloma (MM) constantly replicates and secretes myeloma proteins, it is more sensitive to proteasomes than normal cells and can be used as a second-line treatment for MM and mantle cell lymphomas.

Uses and functions of Bortezomib.

Bortezomib is the first proteasome inhibitor approved by the U.S. FDA for multiple myeloma, a blood cancer. Reversible inhibitor of 26S proteasome, a bark-shaped polyprotein particle, found in the nucleus and cytoplasm of all eukaryotic cells. Targeting the ubiquitin-proteasome pathway.

In vitro study of Bortezomib.

Bortezomib, a boric acid dipeptide, is a highly selective reversible inhibitor of the 26S proteasome, which acts on the degradation of misfolded proteins and is necessary for cell cycle regulation. Exposure to Bortezomib stabilized p21, p27, and p53, as well as the pro-apoptotic Bid and Bax proteins, microcapsulin-1, and inhibitor κb-α, which prevented the activation of the cell survival pathway induced by nuclear factor κB. Bortezomib also promotes the activation of pro-apoptotic c-Jun-NH2 terminal kinase and endoplasmic reticulum stress response. Alterations in these cellular protein levels lead to inhibition of proliferation, migration, and promotion of apoptosis in cancer cells. Bortezomib can penetrate into cells and inhibit proteasoma-mediated intracellular longevity proteolysis, inhibiting 50% proteolysis at a concentration of ~ 0.1 μM. Bortezomib had an IC50 value of 7 nM for a group of 60 cancer cell lines derived from National Cancer Institute (NCI) multiple human tumors.PC-3 cells treated with Bortezomib (100 nM) for 8 h resulted in cell accumulation in the G2-M phase and a corresponding decrease in the number of G1 phase cells. Bortezomib killed PC-3 cells at 24 and 48 hours with IC50 of 100 and 20 nM, respectively. Treatment with Bortezomib induces nuclear condensation after 16-24 hours. Bortezomib causes PARP cleavage in a time-dependent manner at concentrations as low as 100 nM, producing effects after 24 hours of treatment.

Product method of Bulk Bortezomib Powder.

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