{ "id": "ephpbpx8ee", "slug": "dabrafenib-trametinib-regimen", "title": "Dabrafenib/trametinib regimen", "updated": "2026-09-30", "topic_path": [ { "id": "life", "label": "Life and health", "api_url": "https://www.edgepedia.org/api/v1/topics/life" }, { "id": "life.health", "label": "Human health and medicine", "api_url": "https://www.edgepedia.org/api/v1/topics/life.health" }, { "id": "life.health.medicines", "label": "Medicines and therapeutics", "api_url": "https://www.edgepedia.org/api/v1/topics/life.health.medicines" }, { "id": "life.health.medicines.cancer-chemotherapy", "label": "Cancer chemotherapy and regimens", "api_url": "https://www.edgepedia.org/api/v1/topics/life.health.medicines.cancer-chemotherapy" }, { "id": "life.health.medicines.cancer-chemotherapy.targeted-agent-regimens", "label": "Targeted agent regimens", "api_url": "https://www.edgepedia.org/api/v1/topics/life.health.medicines.cancer-chemotherapy.targeted-agent-regimens" } ], "geo": [ { "id": "geo.nongeo.t2001.life.health.medicines.cancer-chemotherapy", "label": "Non-geographic · 2001 to 2020: Cancer chemotherapy and regimens", "api_url": "https://www.edgepedia.org/api/v1/geo/geo.nongeo.t2001.life.health.medicines.cancer-chemotherapy", "path": [ { "id": "geo.nongeo", "label": "Non-geographic", "api_url": "https://www.edgepedia.org/api/v1/geo/geo.nongeo" }, { "id": "geo.nongeo.t2001", "label": "Non-geographic · 2001 to 2020", "api_url": "https://www.edgepedia.org/api/v1/geo/geo.nongeo.t2001" }, { "id": "geo.nongeo.t2001.life", "label": "Life and health", "api_url": "https://www.edgepedia.org/api/v1/geo/geo.nongeo.t2001.life" }, { "id": "geo.nongeo.t2001.life.health", "label": "Human health and medicine", "api_url": "https://www.edgepedia.org/api/v1/geo/geo.nongeo.t2001.life.health" }, { "id": "geo.nongeo.t2001.life.health.medicines", "label": "Medicines and therapeutics", "api_url": "https://www.edgepedia.org/api/v1/geo/geo.nongeo.t2001.life.health.medicines" }, { "id": "geo.nongeo.t2001.life.health.medicines.cancer-chemotherapy", "label": "Cancer chemotherapy and regimens", "api_url": "https://www.edgepedia.org/api/v1/geo/geo.nongeo.t2001.life.health.medicines.cancer-chemotherapy" } ] } ], "excerpt": "The dabrafenib/trametinib regimen, also called dabrafenib and trametinib, is an oral targeted-therapy combination that blocks the MAPK pathway in BRAF V600-mutated cancers, first FDA-approved for melanoma in 2014.", "snippet": "The dabrafenib/trametinib regimen, also called dabrafenib and trametinib, is an oral targeted-therapy combination that blocks the MAPK pathway in BRAF V600-mutated cancers, first FDA-approved for melanoma in 2014.", "node": "life.health.medicines.cancer-chemotherapy.targeted-agent-regimens", "markdown": "# Dabrafenib/trametinib regimen\n\nThe dabrafenib/trametinib regimen is an oral targeted-therapy combination that pairs dabrafenib, a selective inhibitor of mutated BRAF V600 kinase, with trametinib, a selective MEK1/MEK2 inhibitor, to block the MAPK pathway at two points in BRAF V600-mutated cancers. It is approved for unresectable or metastatic melanoma with a BRAF V600E or V600K mutation, adjuvant treatment of resected stage III melanoma, BRAF V600E-mutated non-small-cell lung cancer, anaplastic thyroid cancer, pediatric BRAF V600E-mutated low-grade glioma, and, since June 2022, any previously treated unresectable or metastatic solid tumor with a BRAF V600E mutation in patients 6 years of age and older.[23](https://www.accessdata.fda.gov/drugsatfda_docs/nda/2023/217514Orig1s000OtherR.pdf) • [1](https://www.ncbi.nlm.nih.gov/books/NBK447415/) • [2](https://pmc.ncbi.nlm.nih.gov/articles/PMC10841289/) [Colorectal cancer](https://www.edgepedia.org/colorectal-cancer) is excluded from the label because of intrinsic resistance to BRAF inhibition.[1](https://www.ncbi.nlm.nih.gov/books/NBK447415/)\n\n| Key fact | Detail |\n|---|---|\n| Standard dose | Dabrafenib 150 mg orally twice daily plus trametinib 2 mg orally once daily, continuously[3](https://www.eviq.org.au/getmedia/d3073999-3536-4eb8-b5ad-a7efd5514d74/ID-1619-Melanoma-metastatic-daBRAFEnib-and-tRAMEtinib-protocol-and-PI.pdf.aspx) |\n| First US approval | Accelerated approval of the combination for BRAF V600E/K melanoma on 9 January 2014; regular approval on 20 November 2015[4](https://www.gsk.com/en-gb/media/press-releases/gsk-gains-accelerated-fda-approval-for-combination-use-of-mekinist-trametinib-and-tafinlar-dabrafenib/) • [5](https://www.prnewswire.com/news-releases/novartis-receives-fda-regular-approval-for-tafinlar--mekinist-to-treat-aggressive-form-of-melanoma-based-on-long-term-survival-data-300182818.html) |\n| First-line melanoma efficacy | 12-month overall survival 72% vs 65% with vemurafenib; median PFS 11.4 vs 7.3 months; ORR 64% vs 51%[6](https://pubmed.ncbi.nlm.nih.gov/25399551/) |\n| Pooled long-term outcomes | Median PFS 11.1 months, median OS 25.9 months, ORR 68%, 5-year PFS 19%, 5-year OS 34%[3](https://www.eviq.org.au/getmedia/d3073999-3536-4eb8-b5ad-a7efd5514d74/ID-1619-Melanoma-metastatic-daBRAFEnib-and-tRAMEtinib-protocol-and-PI.pdf.aspx) |\n| Adjuvant benefit | 5-year relapse-free survival 52% vs 36% with placebo in resected stage III melanoma (COMBI-AD)[7](https://www.pro.novartis.com/uk-en/medicines/oncology/tafinlar-mekinist/melanoma/efficacy) |\n| Signature toxicity | Pyrexia in roughly 50-71% of patients, managed by temporary dose interruption[1](https://www.ncbi.nlm.nih.gov/books/NBK447415/) |\n| Colorectal cancer | Doublet median PFS only 3.5 months; triplet regimens add an EGFR antibody[8](https://ascopubs.org/doi/10.1200/JCO.2015.63.2471) |\n\n## How it works\n\nBRAF V600 mutations are found in up to 50% of melanomas.[9](https://www.pro.novartis.com/uk-en/medicines/oncology/tafinlar-mekinist/melanoma/moa) [Dabrafenib](https://www.edgepedia.org/dabrafenib) inhibits the mutated BRAF V600 kinase, while trametinib is a reversible, highly selective inhibitor of MEK1 and MEK2, which sit downstream of BRAF.[9](https://www.pro.novartis.com/uk-en/medicines/oncology/tafinlar-mekinist/melanoma/moa)\n\nThe rationale for vertical dual blockade is that resistance to single-agent BRAF inhibitors is associated with reactivation of the MAPK pathway, so inhibiting the pathway at two nodes suppresses signaling more completely and delays resistance.[10](https://doi.org/10.1056/nejmoa1210093) The combination is synergistic or additive in BRAF V600-mutant melanoma, NSCLC, and anaplastic thyroid cancer cell lines, delays the emergence of resistance in melanoma xenografts, and reduces ERK-driven gene expression that promotes tumor growth.[11](https://www.novartis.com/sg-en/sites/novartis_sg/files/Mekinist-Jul2023.SIN-app101023-pdf.pdf) • [9](https://www.pro.novartis.com/uk-en/medicines/oncology/tafinlar-mekinist/melanoma/moa) A practical corollary is reduced paradoxic cutaneous toxicity: cutaneous squamous-cell carcinoma occurred in 2% of combination patients versus 9% with dabrafenib monotherapy, and 1% versus 18% with vemurafenib in COMBI-v.[12](https://air.unimi.it/bitstream/2434/425634/2/NewEnglandJournMedicine_CombinedGraf_2014.pdf) • [6](https://pubmed.ncbi.nlm.nih.gov/25399551/)\n\n## How it is done\n\nThe standard regimen is dabrafenib 150 mg orally twice daily plus trametinib 2 mg orally once daily, taken continuously until progression or unacceptable toxicity; trametinib must be taken on an empty stomach, one hour before or two hours after food.[3](https://www.eviq.org.au/getmedia/d3073999-3536-4eb8-b5ad-a7efd5514d74/ID-1619-Melanoma-metastatic-daBRAFEnib-and-tRAMEtinib-protocol-and-PI.pdf.aspx) In the adjuvant setting after complete resection of stage III BRAF V600-mutant melanoma, the same doses are given for 12 months.[13](https://www.eviq.org.au/getmedia/6cb6b367-670a-41fc-8e2b-befa1a7c5abe/ID-3678-Melanoma-adjuvant-daBRAFEnib-and-tRAMEtinib-protocol-and-PI.pdf.aspx) Dabrafenib is metabolized by CYP3A4 and CYP2C8 to hydroxy-dabrafenib, an active metabolite with twofold higher potency against mutant BRAF, and reaches steady state after about 14 days; pediatric dosing is weight-based and formulation-dependent.[1](https://www.ncbi.nlm.nih.gov/books/NBK447415/)\n\nIntermittent dosing does not help: the SWOG S1320 phase 2 trial found continuous dosing yields superior progression-free survival compared with 5-weeks-on/3-weeks-off scheduling.[14](https://link.springer.com/article/10.1007/s11864-022-01006-7)\n\nPyrexia is the signature toxicity, reported in approximately 50% of patients across studies and up to 71% in the early-phase trial; temporary dose interruption is an effective management strategy, and therapy may be restarted at the same or a reduced dose level, with resumption or dose reduction guided by the severity and recurrence of pyrexia and the prescribing instructions.[1](https://www.ncbi.nlm.nih.gov/books/NBK447415/) • [10](https://doi.org/10.1056/nejmoa1210093) • [13](https://www.eviq.org.au/getmedia/6cb6b367-670a-41fc-8e2b-befa1a7c5abe/ID-3678-Melanoma-adjuvant-daBRAFEnib-and-tRAMEtinib-protocol-and-PI.pdf.aspx) Other common adverse reactions (incidence ≥20%) are fatigue, nausea, chills, headache, diarrhea, vomiting, arthralgia, and rash; decreased ejection fraction occurred in 8% of combination patients in COMBI-v.[7](https://www.pro.novartis.com/uk-en/medicines/oncology/tafinlar-mekinist/melanoma/efficacy) • [6](https://pubmed.ncbi.nlm.nih.gov/25399551/)\n\n## Origin\n\nThe combination's benefit was first demonstrated in the phase 1/2 trial NCT01072175 in 247 patients with BRAF V600-mutant metastatic melanoma, reported by [Keith T. Flaherty](https://www.edgepedia.org/keith-t-flaherty) and colleagues in the New England Journal of Medicine in 2012; in its randomized part, median PFS was 9.4 months with dabrafenib 150 mg plus trametinib 2 mg versus 5.8 months with dabrafenib alone (HR 0.39; P<0.001), and the response rate was 76% versus 54%.[10](https://doi.org/10.1056/nejmoa1210093) Earlier work the combination built on was the METRIC trial of single-agent trametinib in BRAF-mutated melanoma, reported by Keith T. Flaherty and colleagues in 2012.[15](https://doi.org/10.1056/nejmoa1203421)\n\nTwo phase 3 trials followed: COMBI-d (NCT01584648), a quadruple-masked trial started in May 2012 in 423 previously untreated patients comparing the combination with dabrafenib plus placebo, reported by [Georgina V. Long](https://www.edgepedia.org/georgina-v-long) and colleagues in 2014;[12](https://air.unimi.it/bitstream/2434/425634/2/NewEnglandJournMedicine_CombinedGraf_2014.pdf) • [16](https://clinicaltrials.gov/study/NCT01584648) and COMBI-v (NCT01597908), reported by [Caroline Robert](https://www.edgepedia.org/caroline-robert) and colleagues in 2015, in which 704 patients were randomized to the combination versus vemurafenib 960 mg twice daily and the study was stopped early for efficacy in July 2014.[6](https://pubmed.ncbi.nlm.nih.gov/25399551/) The FDA granted accelerated approval of the combination for BRAF V600E/K unresectable or metastatic melanoma on 9 January 2014, contingent on COMBI-d, and converted it to regular approval on 20 November 2015 based on survival data.[4](https://www.gsk.com/en-gb/media/press-releases/gsk-gains-accelerated-fda-approval-for-combination-use-of-mekinist-trametinib-and-tafinlar-dabrafenib/) • [5](https://www.prnewswire.com/news-releases/novartis-receives-fda-regular-approval-for-tafinlar--mekinist-to-treat-aggressive-form-of-melanoma-based-on-long-term-survival-data-300182818.html) The two drugs had first been approved individually, as monotherapies for BRAF V600E melanoma, on May 29, 2013.[2](https://pmc.ncbi.nlm.nih.gov/articles/PMC10841289/)\n\n## Variants\n\n**Colorectal cancer triplets.** In BRAF V600-mutant metastatic colorectal cancer, the doublet achieved a median PFS of only 3.5 months, better than standard chemotherapy (2.5 months) but far below the 9.4 months seen in melanoma; feedback reactivation of MAPK signaling, likely driven by EGFR, was proposed as the limiting mechanism.[8](https://ascopubs.org/doi/10.1200/JCO.2015.63.2471) This supports triplet regimens adding an EGFR antibody.\n\n**Basket and tissue-agnostic use.** The ROAR basket trial (one trial testing a drug across many different tumor types) of dabrafenib plus trametinib in BRAF V600E-mutated rare cancers, reported by [Vivek Subbiah](https://www.edgepedia.org/vivek-subbiah) and colleagues in [Nature Medicine](https://www.edgepedia.org/nature-medicine) in 2023, enrolled eight cohorts with investigator-assessed response rates of 56% in anaplastic thyroid cancer, 53% in biliary tract cancer, 54% in low-grade glioma, 89% in hairy cell leukemia, 33% in high-grade glioma, and 50% in multiple myeloma.[17](https://doi.org/10.1038/s41591-023-02321-8) Together with NCI-MATCH and a pediatric study, ROAR supported the June 22, 2022 tissue-agnostic accelerated approval for previously treated BRAF V600E solid tumors, the first tumor-agnostic BRAF/MEK combination approval.[2](https://pmc.ncbi.nlm.nih.gov/articles/PMC10841289/) • [17](https://doi.org/10.1038/s41591-023-02321-8) For pediatric BRAF V600E-mutated low-grade glioma requiring systemic therapy, approved March 16, 2023, the combination achieved an ORR of 47% versus 11% with carboplatin plus vincristine, and median PFS 20.1 versus 7.4 months.[2](https://pmc.ncbi.nlm.nih.gov/articles/PMC10841289/)\n\n**Brain metastases.** A 2025 systematic review and meta-analysis of eleven studies in melanoma brain metastases found pooled 6-month overall survival of 76%, 1-year OS 45%, and pooled ORR 45%; dabrafenib is thought to penetrate the blood-brain barrier better than vemurafenib.[18](https://link.springer.com/article/10.1007/s12672-025-02778-8)\n\n## Applications\n\nIn first-line metastatic melanoma, COMBI-v showed 12-month overall survival of 72% versus 65% with vemurafenib (HR for death 0.69; P=0.005), median PFS 11.4 versus 7.3 months (HR 0.56), and ORR 64% versus 51%.[6](https://pubmed.ncbi.nlm.nih.gov/25399551/) COMBI-d reported median OS of 25.1 versus 18.7 months with dabrafenib monotherapy (HR 0.71).[5](https://www.prnewswire.com/news-releases/novartis-receives-fda-regular-approval-for-tafinlar--mekinist-to-treat-aggressive-form-of-melanoma-based-on-long-term-survival-data-300182818.html) In the pooled COMBI-d/COMBI-v analysis (563 patients), median PFS was 11.1 months, median OS 25.9 months, ORR 68% with 19% complete responses, and 5-year PFS and OS were 19% and 34%; 5-year OS reached 71% among complete responders.[3](https://www.eviq.org.au/getmedia/d3073999-3536-4eb8-b5ad-a7efd5514d74/ID-1619-Melanoma-metastatic-daBRAFEnib-and-tRAMEtinib-protocol-and-PI.pdf.aspx) In adjuvant COMBI-AD (870 patients), median relapse-free survival was not reached versus 16.6 months with placebo, with 5-year relapse-free survival of 52% versus 36%.[13](https://www.eviq.org.au/getmedia/6cb6b367-670a-41fc-8e2b-befa1a7c5abe/ID-3678-Melanoma-adjuvant-daBRAFEnib-and-tRAMEtinib-protocol-and-PI.pdf.aspx) • [7](https://www.pro.novartis.com/uk-en/medicines/oncology/tafinlar-mekinist/melanoma/efficacy)\n\n**Sequencing against immunotherapy.** The DREAMseq trial (ECOG-ACRIN EA6134), reported by [Michael B. Atkins](https://www.edgepedia.org/michael-b-atkins) and colleagues in 2022, randomized 265 treatment-naive patients with BRAF V600-mutant metastatic melanoma to nivolumab/ipilimumab first followed by dabrafenib/trametinib at progression, or the reverse. Two-year overall survival favored immunotherapy first (71.8% vs 51.5%; log-rank P=.010).[19](https://doi.org/10.1200/jco.22.01763) Frontline nivolumab/ipilimumab responses were more durable (88% ongoing versus <50% with dabrafenib/trametinib), and crossover at progression was feasible in only 52% of patients, which partly explains the survival difference.[19](https://doi.org/10.1200/jco.22.01763)\n\n## Limitations and alternatives\n\n**Resistance.** About 15-20% of patients show primary resistance, and roughly 50% of patients on dabrafenib/trametinib acquire secondary resistance, with MAPK pathway reactivation the dominant mechanism, via RAS mutations, BRAF amplification or alternative splicing, CRAF/ARAF overexpression, or mutations in NRAS, MEK1/2, or AKT1/3.[20](https://pmc.ncbi.nlm.nih.gov/articles/PMC9564158/) • [14](https://link.springer.com/article/10.1007/s11864-022-01006-7) In colorectal cancer, EGFR signaling maintains BRAF-MEK-ERK signaling in the face of BRAF inhibition.[17](https://doi.org/10.1038/s41591-023-02321-8) Resistance to BRAF/MEK inhibition may also create an immunosuppressive tumor microenvironment lacking functional CD103+ dendritic cells, which impairs subsequent immunotherapy.[19](https://doi.org/10.1200/jco.22.01763)\n\n**Comparison with other BRAF/MEK doublets.** Cross-trial reviews place the BRAF/MEK doublets together at response rates of approximately 65-70%, median PFS around 12 months, and median OS around 24 months.[14](https://link.springer.com/article/10.1007/s11864-022-01006-7) A decade-wide review of dabrafenib/trametinib trials found a median PFS of 4.5 months and median OS of 11.5 months across all indications, with cumulative grade 3-5 adverse event incidence rising from 25% to 50% as off-label indications were studied, a caution about the breadth of the evidence base outside the pivotal melanoma setting.[21](https://aacrjournals.org/mct/article-lookup/doi/10.1158/1535-7163.MCT-23-0805)\n\n**Neoadjuvant combination with immunotherapy.** The randomized phase 2 NeoTrio trial (2024) in resectable stage III BRAF V600-mutant melanoma found that 6 weeks of concurrent pembrolizumab plus dabrafenib/trametinib before surgery gave the highest pathological response rate (80%, with ten complete responses, versus 55% with pembrolizumab alone and 50% with sequential therapy) but was the most toxic arm, with 55% grade 3/4 adverse events and 40% discontinuation; the investigators suggest that, pending longer follow-up, immunotherapy and targeted therapy should not be combined in the neoadjuvant setting.[22](https://www.nature.com/articles/s41591-024-03077-5)\n\n## References\n\n1. [Dabrafenib Therapy and BRAF Genotype, NCBI Medical Genetics Summaries](https://www.ncbi.nlm.nih.gov/books/NBK447415/)\n2. [FDA Approval Summary: Dabrafenib in combination with trametinib for BRAF V600E mutation-positive low-grade glioma](https://pmc.ncbi.nlm.nih.gov/articles/PMC10841289/)\n3. [eviQ protocol 1619: Melanoma metastatic daBRAFEnib and tRAMEtinib](https://www.eviq.org.au/getmedia/d3073999-3536-4eb8-b5ad-a7efd5514d74/ID-1619-Melanoma-metastatic-daBRAFEnib-and-tRAMEtinib-protocol-and-PI.pdf.aspx)\n4. [GSK gains accelerated FDA approval for combination use of Mekinist (trametinib) and Tafinlar (dabrafenib)](https://www.gsk.com/en-gb/media/press-releases/gsk-gains-accelerated-fda-approval-for-combination-use-of-mekinist-trametinib-and-tafinlar-dabrafenib/)\n5. [Novartis receives FDA regular approval for Tafinlar + Mekinist to treat aggressive form of melanoma based on long-term survival data](https://www.prnewswire.com/news-releases/novartis-receives-fda-regular-approval-for-tafinlar--mekinist-to-treat-aggressive-form-of-melanoma-based-on-long-term-survival-data-300182818.html)\n6. [Improved overall survival in melanoma with combined dabrafenib and trametinib (COMBI-v, NEJM 2015)](https://pubmed.ncbi.nlm.nih.gov/25399551/)\n7. [TAFINLAR + MEKINIST Efficacy in Melanoma (Novartis Pro Portal)](https://www.pro.novartis.com/uk-en/medicines/oncology/tafinlar-mekinist/melanoma/efficacy)\n8. [Combined BRAF and MEK Inhibition With Dabrafenib and Trametinib in BRAF V600–Mutant Colorectal Cancer](https://ascopubs.org/doi/10.1200/JCO.2015.63.2471)\n9. [TAFINLAR (dabrafenib) + MEKINIST (trametinib) mechanisms of action (Novartis Pro Portal)](https://www.pro.novartis.com/uk-en/medicines/oncology/tafinlar-mekinist/melanoma/moa)\n10. [Keith T. Flaherty and colleagues (2012). Combined BRAF and MEK Inhibition in Melanoma with BRAF V600 Mutations. New England Journal of Medicine.](https://doi.org/10.1056/nejmoa1210093)\n11. [Mekinist (trametinib) Summary of Product Characteristics / prescribing information](https://www.novartis.com/sg-en/sites/novartis_sg/files/Mekinist-Jul2023.SIN-app101023-pdf.pdf)\n12. [Combined BRAF and MEK Inhibition versus BRAF Inhibition Alone in Melanoma (COMBI-d, NEJM 2014)](https://air.unimi.it/bitstream/2434/425634/2/NewEnglandJournMedicine_CombinedGraf_2014.pdf)\n13. [Melanoma adjuvant daBRAFEnib and tRAMEtinib (eviQ protocol ID 3678)](https://www.eviq.org.au/getmedia/6cb6b367-670a-41fc-8e2b-befa1a7c5abe/ID-3678-Melanoma-adjuvant-daBRAFEnib-and-tRAMEtinib-protocol-and-PI.pdf.aspx)\n14. [BRAF Inhibitor Resistance in Melanoma: Mechanisms and Alternative Therapeutic Strategies (Current Treatment Options in Oncology)](https://link.springer.com/article/10.1007/s11864-022-01006-7)\n15. [Keith T. Flaherty and colleagues (2012). Improved Survival with MEK Inhibition in BRAF-Mutated Melanoma. New England Journal of Medicine.](https://doi.org/10.1056/nejmoa1203421)\n16. [COMBI-d trial record (NCT01584648)](https://clinicaltrials.gov/study/NCT01584648)\n17. [Vivek Subbiah and colleagues (2023). Dabrafenib plus trametinib in BRAFV600E-mutated rare cancers: the phase 2 ROAR trial. Nature Medicine.](https://doi.org/10.1038/s41591-023-02321-8)\n18. [The safety and efficacy of dabrafenib plus trametinib for patients with brain metastatic melanoma: a systematic review and meta-analysis](https://link.springer.com/article/10.1007/s12672-025-02778-8)\n19. [Michael B. Atkins and colleagues (2022). Combination Dabrafenib and Trametinib Versus Combination Nivolumab and Ipilimumab for Patients With Advanced BRAF-Mutant Melanoma: The DREAMseq Trial, ECOG-ACRIN EA6134. Journal of Clinical Oncology.](https://doi.org/10.1200/jco.22.01763)\n20. [Head-to-Head Comparison of BRAF/MEK Inhibitor Combinations Proposes Superiority of Encorafenib Plus Trametinib in Melanoma](https://pmc.ncbi.nlm.nih.gov/articles/PMC9564158/)\n21. [Assessing Patient Risk, Benefit, and Outcomes in Drug Development: A Decade of Dabrafenib and Trametinib Clinical Trials (Molecular Cancer Therapeutics)](https://aacrjournals.org/mct/article-lookup/doi/10.1158/1535-7163.MCT-23-0805)\n22. [Neoadjuvant pembrolizumab, dabrafenib and trametinib in BRAFV600-mutant resectable melanoma: the randomized phase 2 NeoTrio trial](https://www.nature.com/articles/s41591-024-03077-5)\n23. [217514Orig1s000OtherR (accessdata.fda.gov)](https://www.accessdata.fda.gov/drugsatfda_docs/nda/2023/217514Orig1s000OtherR.pdf)\n\n---\n*Topic: Encyclopedia › Life and health › Human health and medicine › Medicines and therapeutics › Cancer chemotherapy and regimens › Targeted agent regimens*\n\n*Initially written Sep 29, 2026 · Reviewed: Sep 30, 2026 · Edited: Sep 30, 2026 · Last review: Sep 30, 2026*\n\n*Copyright 2026 EdgeChat AI, a subsidiary of Biostate AI.*\n\nLicense: Edgepedia Community License 1.0, https://www.edgepedia.org/edgepedia/license\n", "same_as": [], "url": "https://www.edgepedia.org/dabrafenib-trametinib-regimen", "markdown_url": "https://www.edgepedia.org/dabrafenib-trametinib-regimen.md", "license": { "name": "Edgepedia Community License 1.0", "url": "https://www.edgepedia.org/edgepedia/license", "summary": "Free with credit, commercial use included. AI training is open to everyone. For other uses, organizations over USD 100M in revenue or 100M monthly users license separately.", "spdx": "LicenseRef-Edgepedia-Community-1.0" }, "credit": "\"Dabrafenib/trametinib regimen\", Edgepedia (EdgeChat), https://www.edgepedia.org/dabrafenib-trametinib-regimen. Edgepedia Community License 1.0.", "credit_md": "\"[Dabrafenib/trametinib regimen](https://www.edgepedia.org/dabrafenib-trametinib-regimen)\", Edgepedia (EdgeChat), [https://www.edgepedia.org/dabrafenib-trametinib-regimen](https://www.edgepedia.org/dabrafenib-trametinib-regimen). [Edgepedia Community License 1.0](https://www.edgepedia.org/edgepedia/license).", "credit_html": "\"Dabrafenib/trametinib regimen\", Edgepedia (EdgeChat), https://www.edgepedia.org/dabrafenib-trametinib-regimen. Edgepedia Community License 1.0.", "speakable": "The dabrafenib/trametinib regimen, also called dabrafenib and trametinib, is an oral targeted-therapy combination that blocks the MAPK pathway in BRAF V600-mutated cancers, first FDA-approved for melanoma in 2014." }