Sentences with word «vemurafenib»

The FDA has approved the MEK inhibitor cobimetinib in combination with the BRAF inhibitor vemurafenib for the treatment of advanced metastatic or unresectable BRAF - mutated melanoma.

They found that combining that drug with the cediranib, an investigational drug that targets a group of proteins known to be involved in blood vessel formation, had synergistic effects against cell lines that were resistant to treatment with vemurafenib alone but not those sensitive to single - agent therapy.

Around 40 to 50 per cent of melanoma patients have a faulty BRAF gene and they can be treated with the targeted drugs vemurafenib or dabrafenib.

In the latest example, researchers from Penn Medicine and other institutions found that treating metastatic thyroid cancer patients harboring a BRAF mutation with the targeted therapy vemurafenib — originally approved for melanoma patients with the mutation — showed promising anti-tumor activity in a third of patients.

It included a total of 577 patients randomized to receive either encorafenib plus binimetinib (192 patients), encorafenib alone (194 patients), or vemurafenib alone (191 patients).

«We need to confirm this synergistic activity of vemurafenib and cediranib across a broader range of melanoma models, investigate why the particular combination is effective, and find biomarkers that predict which patients with BRAF - mutant melanoma should receive this combination,» says Friedman, who is a research fellow in Dermatology at Harvard Medical School.

One targeted treatment is a gene - silencing drug called vemurafenib.

By analyzing tumor biopsies from patients who relapsed on vemurafenib, researchers are learning how tumors become resistant: Often they restore the growth pathway that the drug blocks by activating a protein further downstream called MEK.

The US Food and Drug Administration (FDA) has approved the MEK inhibitor cobimetinib (Cotellic) in combination with the BRAF inhibitor vemurafenib for the treatment of advanced metastatic or unresectable BRAF - mutated melanoma.

To find out, they treated advanced melanomas with JNJ, Nutlin - 3 and a chemotherapeutic drug used in the clinic today named vemurafenib.

Importantly, mutations in the BRAF gene that are seen in more than half of advanced melanomas were absent in mucosal melanoma, explaining the ineffectiveness of BRAF - targeted treatments like vemurafenib.

Koya R.C., Mok S., Otte N., Blacketor K.J., Comin - Anduix B., Tumeh P.C., Minasyan A., Graham N., Graeber T.G., Chodon T., Ribas A. BRAF inhibitor vemurafenib improves the antitumor activity of adoptive cell immunotherapy.

The combination of the BRAF inhibitor encorafenib with the MEK inhibitor binimetinib yielded improved progression - free survival over vemurafenib in a phase III trial of patients with advanced BRAF V600 — mutant melanoma.

A validation cohort of 240 patients treated with vemurafenib (BRAF inhibitor) and cobimetinib (MEK inhibitor) yielded similar results.

In the Cancer Cell article, the researchers describe how various anticancer drugs, including cisplatin and the targeted therapy vemurafenib, which targets melanomas with the BRAF mutation, become more effective when co-delivered with phenformin.

In related news The FDA approved a new chemotherapy drug for melanoma, called vemurafenib, last August.

Researchers at Moffitt Cancer Center in Tampa, Fla., and colleagues in California have found that the XL888 inhibitor can prevent resistance to the chemotherapy drug vemurafenib, commonly used for treating patients with melanoma.

Based on these promising preclinical results, Dr. Amaravadi and his team have already launched a clinical trial for patients with advanced BRAF mutant melanoma to see how well - tolerated HCQ is with the BRAF inhibitor vemurafenib.

Studies have shown that melanoma patients who have both BRAF and PTEN mutations may have a poorer response to dabrafenib and vemurafenib therapy.

Several agents that directly target BRAF have been approved by the Food and Drug Administration for the treatment of melanoma patients who have the mutation, including dabrafenib and vemurafenib.

While patients often improve on the drug and live longer than they would on standard treatment (results will be presented Sunday at ASCO), the drug, vemurafenib, usually stops working within a year.

In cohort one, 10 patients had a partial response to vemurafenib, and an additional nine achieved stable disease for at least six months, for a combined disease control rate of 73 percent.

Since around half the cases of malignant melanoma are driven by mutation in the BRAF gene, the team focused on combinations that might address intrinsic resistance to the BRAF inhibitor vemurafenib.

Another drug, vemurafenib — PLX - 4032 — works well initially, but the tumors develop resistance within 6 to 7 months.

For example, vemurafenib is more effective in melanoma containing BRAFV600E mutation, than melanoma cells with wild type BRAF protein.

In the first in human trial of PLX4032 / vemurafenib our team has provided critical PK / PD data that led to the first in class / first in human FDA - approved BRAF inhibitor.

Our work was instrumental in several FDA approvals of breakthrough anti-cancer drugs (vemurafenib, dabrafenib + trametinib, vemurafenib + cobimetinib, pembrolizumab, talimogene laherparepvec) and resulted in almost 100 manuscripts, including New England Journal of Medicine, Lancet, Journal of Clinical Oncology, JAMA, Nature.

Previously published retrospective clinical studies and in vitro data regarding the association of radiotherapy with inhibitors of mutant BRAF kinase (vemurafenib) suggest a radiosen - sitization (cell cycle arrest in G1, DNA repair decrease, restore dradiation - induced apoptosis) and an increased radiation - induced toxicity [56, 58].

One such targeted drug is vemurafenib (Zelboraf ®), which was approved by the Food and Drug Administration (FDA) in 2011 for the treatment of some patients with melanoma who have a specific mutation in the BRAF gene as detected by an FDA - approved test.

In the encorafenib monotherapy group, these included palmoplantar erythrodysesthesia syndrome (14 %), myalgia (10 %), and arthralgia (9 %); in the vemurafenib group, the only such adverse event was arthralgia (6 %).

Fewer patients in the combination group reported grade 3/4 adverse events than in either of the other groups, at 58 % compared with 66 % in the encorafenib group and 63 % of the vemurafenib patients.

The combination group had a lower risk of progression or death compared with the vemurafenib group, with a hazard ratio of 0.54 (95 % CI, 0.41 — 0.71; P <.0001).

The median progression - free survival was 14.9 months in the combination therapy group, compared with 9.6 months with encorafenib monotherapy and 7.3 months with vemurafenib.

A confirmed response was reported in 63 % of the encorafenib - plus - binimetinib group, compared with 51 % of the encorafenib group and 40 % of the vemurafenib group.

This is an early version of the drug vemurafenib, which has extended the lives of hundreds of people with skin cancer.

The most common adverse events seen with cobimetinib / vemurafenib were diarrhea, photosensitivity reaction, nausea, pyrexia, and vomiting.

The targeted therapies are vemurafenib (Zelboraf ®), dabrafenib (Tafinlar ®), trametinib (Mekinist ®), and cobimetinib (Cotellic ®).

All patients were treated with the BRAF inhibitor vemurafenib and were then randomly assigned to cobimetinib or placebo.

With a median follow - up of 14 months, patients assigned to combination treatment with cobimetinib and vemurafenib had a progression - free survival of 12.3 months compared with 7.2 months for those on vemurafenib alone.