Tasigna vs Cabometyx
Both are tyrosine kinase inhibitors. Here is how Tasigna and Cabometyx compare on class, mechanism, dosing, approval and supply.
At a glance
Key differences
- Same class. Both Tasigna and Cabometyx are tyrosine kinase inhibitors, so they work through the same broad mechanism. Differences between them tend to be about dosing, route, how selective they are, and side effects rather than what they target.
- How they are taken. Both are given by the oral route.
- Time on the market. Tasigna was first approved by the FDA in 2007, Cabometyx in 2016. That gives Tasigna roughly 9 more years of real-world use and long-term safety data.
- Who markets them. Tasigna is marketed by Novartis; Cabometyx by Exelixis.
- Same drug, more than one brand. Cabozantinib is sold as Cabometyx / Cometriq — the same active ingredient marketed under different brand names, typically for different approved uses or doses.
What each one treats
Tasigna is a kinase inhibitor indicated for the treatment of: Adult and pediatric patients greater than or equal to 1 year of age with newly diagnosed Philadelphia chromosome positive chronic myeloid leukemia (Ph+ CML) in chronic phase. ( 1.1 ) Adult patients with chronic phase (CP) and accelerated phase (AP) Ph+ CML resistant to or intolerant to prior therapy that included imatinib. ( 1.2 ) Pediatric patients greater than or equal to 1 year of age with Ph+ CML-CP and CML-AP resistant or intolerant to prior tyrosine-kinase inhibitor (TKI) therapy. ( 1.3 ) 1.1 Adult and Pediatric Patients With Newly Diagnosed Ph+ CML-CP Tasigna is indicated for the treatment of adult and pediatric patients greater than or equal to 1 year of age with newly diagnosed Philadelphia chromosome positive chronic myeloid leukemia (Ph+ CML) in chronic phase. 1.2 Adult Patients With Resistant or Intolerant Ph+ CML…
CABOMETYX is a kinase inhibitor indicated for the treatment of patients with advanced renal cell carcinoma (RCC). ( 1.1 ) patients with advanced renal cell carcinoma, as a first-line treatment in combination with nivolumab ( 1.1 ) patients with hepatocellular carcinoma (HCC) who have been previously treated with sorafenib ( 1.2 ) adult and pediatric patients 12 years of age and older with locally advanced or metastatic differentiated thyroid cancer (DTC) that has progressed following prior VEGFR-targeted therapy and who are radioactive iodine-refractory or ineligible ( 1.3 ) adult and pediatric patients 12 years of age and older with previously treated, unresectable, locally advanced or metastatic, well-differentiated pancreatic neuroendocrine tumors (pNET). ( 1.4 ) adult and pediatric patients 12 years of age and older with previously treated, unresectable, locally advanced or metastat…
How each one works
12.1 Mechanism of Action Nilotinib is an inhibitor of the BCR-ABL kinase. Nilotinib binds to and stabilizes the inactive conformation of the kinase domain of ABL protein. In vitro, nilotinib inhibited BCR-ABL mediated proliferation of murine leukemic cell lines and human cell lines derived from patients with Ph+ CML. Under the conditions of the assays, nilotinib was able to overcome imatinib resistance resulting from BCR-ABL kinase mutations, in 32 out of 33 mutations tested. Nilotinib inhibited the autophosphorylation of the following kinases at IC50 values as indicated: BCR-ABL (20 to 60 nM), PDGFR (69 nM), c-KIT (210 nM), CSF-1R (125 to 250 nM), and DDR1 (3.7 nM).
12.1 Mechanism of Action In vitro biochemical and/or cellular assays have shown that cabozantinib inhibits the tyrosine kinase activity of MET, VEGFR-1, -2 and -3, AXL, RET, ROS1, TYRO3, MER, KIT, TRKB, FLT-3, and TIE-2. These receptor tyrosine kinases are involved in both normal cellular function and pathologic processes such as oncogenesis, metastasis, tumor angiogenesis, drug resistance, and maintenance of the tumor microenvironment.
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Which medicine is right for a given person depends on their diagnosis, other conditions, other medicines, kidney and liver function, pregnancy, and cost or reimbursement — none of which this page knows. Two drugs in the same class are not automatically interchangeable. Never start, stop or switch a prescription medicine on the basis of a web page; that decision belongs to you and your clinician or pharmacist.
How this page is built
The facts on this page are pulled directly from official U.S. FDA datasets — they are not written from memory. Each field below names the dataset it came from, so you can check it yourself.
- FDA Drug Label (openFDA) ↗ Indications, mechanism of action and pharmacologic class
- Drugs@FDA ↗ First FDA approval date and the company holding the application
- FDA Drug Shortage Database ↗ Current US supply / shortage status
Plain-English summaries and drug-class explainers are written and reviewed by Sreepriya Prasannan (MSc Digital Transformation of Life Sciences (Innopharma Education / Griffith College); MSc & BSc Botany). Data is retrieved automatically from the sources above and cross-checked with AI-assisted verification (Anthropic's Claude) — brand and generic names are matched against the exact FDA product record so that a combination product or a different formulation cannot be mistaken for the drug on this page. An editor reviews the result before publication. We describe this in full in our editorial standards and corrections policy. The FDA data on this page was last retrieved on 12 Oct 2026. How every register is built: methodology · fixes we have made: corrections log.