CC-90003
/ BMS
- LARVOL DELTA
Home
Next
Prev
1 to 8
Of
8
Go to page
1
October 16, 2023
Unraveling TIMP1: a multifaceted biomarker in colorectal cancer.
(PubMed, Front Genet)
- "Drug sensitivity analysis, conducted using the DepMap database, revealed that colorectal cancer cell lines exhibiting elevated levels of TIMP1 expression were more responsive to certain drugs, such as CC-90003, Pitavastatin, Atuveciclib, and CT7001, compared to those with low levels of TIMP1. Furthermore, TIMP1 expression was positively correlated with that of ferroptosis-related genes, such as GPX4 and HSPA5. TIMP1 can be used as a biomarker for colorectal cancer and is associated with the immunological microenvironment, drug sensitivity, and ferroptosis inhibition in this disease."
Biomarker • IO biomarker • Journal • Colorectal Cancer • Gastrointestinal Cancer • Oncology • Solid Tumor • CXCL1 • CXCL10 • CXCL8 • GPX4 • HAVCR2 • HSPA5 • MMP1 • MMP3 • SPP1 • TIMP1
May 20, 2017
A phase Ia study of CC-90003, a selective extracellular signal-regulated kinase (ERK) inhibitor, in patients with relapsed or refractory BRAF or RAS-mutant tumors.
(ASCO 2017)
- P1a; "ERK inhibition may be an attractive target for the management of mutant RAS or BRAF-driven tumors, however proof-of-concept demonstration for CC-90003 was limited by a lack of objective responses, an unfavorable PK profile and unanticipated neurotoxicity."
P1 data • Biosimilar • Cardiovascular • Oncology
December 27, 2021
Inhibition of EZH2 ameliorates hyperoxaluria-induced kidney injury through the JNK/FoxO3a pathway.
(PubMed, Life Sci)
- "EZH2 inhibition protects against oxalate-induced TECs injury and reduces CaOx crystal deposition in the kidney may by modulating the JNK/FoxO3a pathway; EZH2 may be a promising therapeutic target in TECs injury."
Journal • Immunology • Inflammation • Nephrology • Renal Disease • CASP3 • EZH2 • IL6
December 07, 2021
Targeting ERK induced cell death and p53/ROS-dependent protective autophagy in colorectal cancer.
(PubMed, Cell Death Discov)
- "Furthermore, in the xenograft mouse model, the effect was obtained remarkably in the combinational treatment group of CC90003 plus CQ, comparing with that of the single treatment groups. In a word, our results demonstrated that targeting ERK leads to cell death and p53/ROS-dependent protective autophagy simultaneously in colorectal cancer, which offers new potential targets for clinical therapy."
Journal • Colorectal Cancer • Gastrointestinal Cancer • Oncology • Solid Tumor
September 08, 2021
Remote ischemic post‑conditioning alleviates ischemia/reperfusion‑induced intestinal injury via the ERK signaling pathway‑mediated RAGE/HMGB axis.
(PubMed, Mol Med Rep)
- "In addition, RIPOC was demonstrated to suppress the NF‑κB (p65)/NLR family pyrin domain containing 3 (NLRP3) inflammatory pathways in the intestinal I/R injury mouse models via the ERK pathway. The findings of the present study demonstrated that RIPOC helped to protect mice with an intestinal I/R injury by downregulating the ERK pathway."
Journal • Immunology • Infectious Disease • Inflammation • Reperfusion Injury • Respiratory Diseases • HMGB1 • PCR • RELA
March 23, 2021
Investigation into the Role of ERK in Tyrosine Kinase Inhibitor-Induced Neuropathy.
(PubMed, Toxicol Sci)
- "The MEA assay with hiPSC-PNs was sensitive to CIPN-associated drugs cisplatin, sunitinib, colchicine, and importantly, to CC-90003 in concordance with clinical neuropathy incidence. Biochemical data together with in vitro MEA data for CC-90003 and 12 of its structural analogs, all having similar ERK inhibitory activity, revealed that CC-90003 disrupted in vitro neuronal electrophysiology likely via on-target ERK inhibition combined with off-target kinase inhibition and translocator protein inhibition. This approach could prove useful for assessing CIPN risk and interrogating mechanisms of drug-induced neuropathy."
Journal • Oncology • Pain
February 23, 2019
Targeting ERK1/2 protein-serine/threonine kinases in human cancers.
(PubMed, Pharmacol Res)
- "The best treatments include the combination of B-Raf and MEK inhibitors (dabrafenib and trametinib, encorafenib and binimetinib, vemurafenib and cobimetanib)...Ulixertinib, MK-8353, and GDC-0994 are orally effective, potent, and specific inhibitors of ERK1/2 that are in early clinical trials for the treatment of various advanced/metastatic solid tumors...The decrease in RSK phosphorylation appears to be a result of ERK inhibition and the decrease in ERK1/2 phosphorylation is related to the inability of MEK to catalyze the phosphorylation of the ERK-MK-8353 complex; these decreases characterize the ERK dual mechanism inhibition paradigm. Additional work will be required to determine whether ERK inhibitors will be successful in the clinic and are able to forestall the development of drug resistance of the MAP kinase pathway."
Journal • Review
October 03, 2018
Efficacy of a Covalent ERK1/2 Inhibitor, CC-90003, in KRAS Mutant Cancer Models Reveals Novel Mechanisms of Response and Resistance.
(PubMed, Mol Cancer Res)
- "Here, a covalent ERK1/2 inhibitor (CC-90003) is demonstrated to have preclinical efficacy in models of KRAS mutant tumors, which present a therapeutic challenge for currently available therapies."
Clinical • Journal • Preclinical
1 to 8
Of
8
Go to page
1