Carfilzomib (PR-171) 868540-17-4

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Molecular Weight: 719.91 Carfilzomib (PR-171) is an irreversible Proteasome Inhibitor with IC50 of


Carfilzomib inhibits proliferation in a variety of cell lines and
patient-derived neoplastic cells, including multiple myeloma, and
induced intrinsic and extrinsic apoptotic signaling pathways and
activation of c-Jun-N-terminal kinase (JNK). Carfilzomib reveals
enhanced anti-MM activity compared with bortezomib, overcome resistance
to bortezomib and other agents, and acts synergistically with
dexamethasone (Dex). Carfilzomib shoes preferential in vitro inhibitory
potency against the ChT-L activity in the β5 subunit, with over 80%
inhibition at doses of 10 nM. Short exposure to low-dose Carfilzomib
leads to preferential binding specificity for the β5 constitutive 20S
proteasome and the β5i immunoproteasome subunits.


Measurement of caspase
activity in ANBL-6 cells pulsed with Carfilzomib reveals substantial
increases in caspase-8, caspase-9, and caspase-3 activity after 8 hours,
giving a 3.2-, 3.9- and 6.9-fold increase, respectively, over control
cells after 8 hours. In carfilzomib pulse-treated cells, the
mitochondrial membrane integrity is decreased to 41% (Q1 + Q2), compared
with 75% in vehicle-treated control cells. In another study, Carfilzomib has also shown preclinical effectiveness against hematological and solid malignancies. Carfilzomib directly inhibits osteoclasts formation and bone resorption.


Carfilzomib moderately reduces tumor growth in an in vivo xenograft
model. Carfilzomib effectively decreases multiple myeloma cell viability
following continual or transient treatment mimicking. Carfilzomib
increases trabecular bone volume, decreases bone resorption and enhances
bone formation in non-tumor bearing mice.

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