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Product Details
Bortezomib (PS-341),179324-69-7,IC-0232466
Bortezomib (PS-341), as a dipeptide boronic acid proteasome inhibitor with antitumor activity, can potently inhibiit 20S proteasome with Ki of 0.6 nM by targeting a threonine residue[1]. In vitro, Bortezomib can retain NF-kappaB in the cytoplasm and inhibit cell growth with IC50 of 22.5 nM, in a dose/time-dependent way[2]. Bortezomib inhibited growth and induced apoptosis of PEL (primary effusion lymphomas) cell lines with IC50 values of 3.4-5.0 nM[3]. In vitro, 1 µmol/L-10 nmol/L bortezomib can activate the Akt pathway via increased SRC-3 (Steroid receptor coactivator-3)[4]. In vitro, 20 nM bortezomib induces apoptotic cell death and promotes G0/G1 phase arrest[5]. In vivo, BALB/c mice were treated with 1 mg/kg bortezomib intraperitoneally once weekly for 2 weeks increased phosphorylation of JNK (c-Jun N-terminal kinase) and extracellular signal-regulated protein kinase (ERK) in the spinal cord[6]. In vivo, mice were treated with bortezomib (2 mg/kg, i.v.) on Day1 and Day4 each week for continuous 4 weeks. bortezomib-treated mice showed enhanced mechanical hyperalgesia, decreased tail nerve conduction and sciatic nerve demyelination[7].
Bortezomib (PS-341), as a dipeptide boronic acid proteasome inhibitor with antitumor activity, can potently inhibiit 20S proteasome with Ki of 0.6 nM by targeting a threonine residue[1]. In vitro, Bortezomib can retain NF-kappaB in the cytoplasm and inhibit cell growth with IC50 of 22.5 nM, in a dose/time-dependent way[2]. Bortezomib inhibited growth and induced apoptosis of PEL (primary effusion lymphomas) cell lines with IC50 values of 3.4-5.0 nM[3]. In vitro, 1 µmol/L-10 nmol/L bortezomib can activate the Akt pathway via increased SRC-3 (Steroid receptor coactivator-3)[4]. In vitro, 20 nM bortezomib induces apoptotic cell death and promotes G0/G1 phase arrest[5]. In vivo, BALB/c mice were treated with 1 mg/kg bortezomib intraperitoneally once weekly for 2 weeks increased phosphorylation of JNK (c-Jun N-terminal kinase) and extracellular signal-regulated protein kinase (ERK) in the spinal cord[6]. In vivo, mice were treated with bortezomib (2 mg/kg, i.v.) on Day1 and Day4 each week for continuous 4 weeks. bortezomib-treated mice showed enhanced mechanical hyperalgesia, decreased tail nerve conduction and sciatic nerve demyelination[7].
