proteasome inhibitor


Also found in: Wikipedia.

pro·te·a·some in·hi·bi·tor

(prō'tē-ă-sōm in-hib'i-tŏr)
Medication to treat multiple myeloma by blocking proteasomes to disrupt growth.
References in periodicals archive ?
The source and identity of this endogenous inhibition is not known; however, the presence of such a proteinaceous proteasome inhibitor in RBCs has been reported (14-18).
"You detect a lot more proteins when you add a proteasome inhibitor," says Yewdell.
Earlier, Bristol-Myers (BMY) announced that the Committee for Medicinal Products for Human Use, or CHMP, of the European Medicines Agency, has adopted a positive opinion on a Type-II variation application for Empliciti - elotuzumab - plus pomalidomide and low-dose dexamethasone for the treatment of adult patients with relapsed and refractory multiple myeloma who have received at least two prior therapies, including lenalidomide and a proteasome inhibitor, and have demonstrated disease progression on the last therapy.
Food and Drug Administration (FDA) approved Empliciti (elotuzumab) injection for intravenous use in combination with pomalidomide and dexamethasone (EPd) for the treatment of adult patients with multiple myeloma who have received at least two prior therapies, including lenalidomide and a proteasome inhibitor. In ELOQUENT-3, a randomized, open-label, Phase 2 trial, EPd demonstrated benefit in patients with relapsed or refractory multiple myeloma, doubling both median progression-free survival (PFS) and overall response rate (ORR) versus pomalidomide and dexamethasone (Pd).
Data from the primary analysis of ELOQUENT-3 were published in the New England Journal of Medicine in November 2018 and supported the approval of EPd by the US Food and Drug Administration for the treatment of adult patients with RRMM who have received at least two prior therapies, including lenalidomide and a proteasome inhibitor.
The cancer often becomes resistant to treatment, and indeed patients in Dreamm-2 were refractory to anti-CD38 antibody treatment, an immunomodulatory drug, and a proteasome inhibitor.
Bristol-Myers Squibb Company announced that the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency has adopted a positive opinion on a Type-II variation application for Empliciti (elotuzumab) plus pomalidomide and low-dose dexamethasone (EPd) for the treatment of adult patients with relapsed and refractory multiple myeloma who have received at least two prior therapies, including lenalidomide and a proteasome inhibitor (PI), and have demonstrated disease progression on the last therapy.
-- (BUSINESS WIRE)--Bristol-Myers Squibb Company (NYSE:BMY) today announced that the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency has adopted a positive opinion on a Type-II variation application for Empliciti (elotuzumab) plus pomalidomide and low-dose dexamethasone (EPd) for the treatment of adult patients with relapsed and refractory multiple myeloma who have received at least two prior therapies, including lenalidomide and a proteasome inhibitor (PI), and have demonstrated disease progression on the last therapy.
In Europe, daratumumab is indicated in combination with bortezomib, melphalan and prednisone for the treatment of adult patients with newly diagnosed multiple myeloma who are ineligible for autologous stem cell transplant; as monotherapy for the treatment of adult patients with relapsed and refractory multiple myeloma, whose prior therapy included a proteasome inhibitor and an immunomodulatory agent and who have demonstrated disease progression on the last therapy; and in combination with lenalidomide and dexamethasone, or bortezomib and dexamethasone, for the treatment of adult patients with multiple myeloma who have received at least one prior therapy.
refractory to at least one IMiD, one proteasome inhibitor and one anti-CD38 monoclonal antibody).
In cells treated with a proteasome inhibitor, Nrf1 escapes degradation by the proteasome and is accumulated as two main forms, both of which do not correspond to glycosylated Nrf1.
Herein, we identify the combination of a proteasome inhibitor with an epigenetic modulator (histone deacetylase inhibitor (HDACi)) as a potent therapeutic strategy to overcome the deleterious effects of TP53 GOF mutations.

Full browser ?