TASIGNA 200MG
Nilotinib hydrochloride monohydrate 200mg
What it does
Nilotinib is a medication used to treat certain types of blood cancer, particularly chronic myeloid leukemia (CML).
Commonly used for: chronic myeloid leukemia (CML), blood cancer
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Sourcing - Kenya onlyRegistration & product details
Source: Rwanda Food and Drugs Authority · fetched 2026-03-11 22:07:36 · updated 2026-09-21 02:30:20
Drug Interactions
139Pharmacodynamic Warnings
Nilotinib appears in TABLE 9: Drugs that prolong the QT interval
Nilotinib appears in TABLE 15: Drugs that cause myelosuppression
Severe (5)
Antipsychotics, Second Generation - increases exposure
Nilotinib is predicted to increase the exposure to antipsychotics, second generation (cariprazine). Avoid.
Nilotinib - increases exposure
Grapefruitjuiceispredictedtoincreasetheexposureto nilotinib.Avoid.rTheoretical
Nilotinib - increases exposure
Clarithromycin is predicted to increase the exposure to nilotinib. Avoid. Also see TABLE 9 p. 1519.
Nilotinib - decreases exposure
Mitotane is predicted to moderately decrease the exposure to nilotinib. Avoid. Also see TABLE 15 p. 1520
Nilotinib - decreases exposure
StJohn’swortispredictedtodecreasetheexposureto nilotinib.Avoid.rTheoretical
Moderate (35)
Alfentanil - increases exposure
Nilotinib is predicted to increase the exposure to opioids (alfentanil, buprenorphine, fentanyl, oxycodone). Monitor and adjust dose.
Amlodipine - increases exposure
Nilotinib is predicted to increase the exposure to calcium channel blockers (amlodipine, felodipine, lacidipine, lercanidipine, nicardipine, nifedipine, nimodipine). Monitor and adjust dose.
Antiarrhythmics - increases exposure
Nilotinib is predicted to increase the exposure to antiarrhythmics (propafenone). Monitor and adjust dose.
Atorvastatin - increases exposure
Nilotinib is predicted to increase the exposure to statins (atorvastatin). Monitor and adjust dose.
Bosutinib - increases exposure
Nilotinib is predicted to increase the exposure to bosutinib. Avoid or adjust dose. Also see TABLE 15 p. 1520 → Also see TABLE 9 p. 1519
Unknown (99)
Abemaciclib - increases exposure
Nilotinib is predicted to increase the exposure to abemaciclib.
Acalabrutinib - increases exposure
Nilotinib is predicted to increase the exposure to acalabrutinib. Avoid or monitor.
Alphablockers - increases exposure
Nilotinibispredictedtoincreasetheexposuretoalphablockers (tamsulosin).oTheoretical
Alprazolam - increases exposure
Nilotinib is predicted to increase the exposure to alprazolam.
Antihistamines,non-Sedating - increases exposure
Nilotinib is predicted to increase the exposure to antihistamines, non-sedating (mizolastine).
Data from BNF 85 (British National Formulary). This is not a substitute for professional medical advice. Matched via: exact
About this medicine
Nilotinib is a medication used to treat certain types of blood cancer, particularly chronic myeloid leukemia (CML).
What it treats
- chronic myeloid leukemia (CML)
- blood cancer
How it works
Nilotinib works by blocking signals that tell cancer cells to grow and divide, helping to stop the cancer from spreading.
Who it's for
Nilotinib is for adults diagnosed with specific types of blood cancer, especially CML.
Cautions
- • Be cautious if taking medications that can affect heart rhythm (QT interval).
- • Use with care if taking drugs that can lower blood cell counts (myelosuppression).
AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.
Clinical monograph: Nilotinib
BNF-referencedNilotinib is a targeted therapy and a potent tyrosine kinase inhibitor specifically designed to treat chronic myeloid leukaemia (CML) that is positive for the Philadelphia chromosome. It works by inhibiting the BCR-ABL fusion protein, which is responsible for the uncontrolled proliferation of leukemic cells. Nilotinib is known for its ability to overcome resistance mechanisms that may arise with other therapies, such as imatinib, making it a suitable option for patients who are intolerant or resistant to previous treatments.
Indications
- Chronic phase Philadelphia chromosome-positive chronic myeloid leukaemia
- Accelerated phase Philadelphia chromosome-positive chronic myeloid leukaemia
Mechanism of action
Nilotinib specifically inhibits the tyrosine kinase activity of the BCR-ABL protein, which is constitutively active in chronic myelogenous leukaemia. By binding to the ATP-binding site of BCR-ABL with higher affinity than imatinib, it effectively blocks the signaling pathways that lead to cell proliferation and survival, thereby reducing the number of leukemic cells. Additionally, Nilotinib has inhibitory effects on other kinases such as c-Kit and PDGF, which may provide broader therapeutic potential in certain hematological malignancies.
Pharmacodynamics
Nilotinib is classified as an antineoplastic agent and a transduction inhibitor. Its primary target is the BCR-ABL fusion protein, which plays a crucial role in the pathogenesis of CML. By inhibiting this protein, Nilotinib disrupts several signaling pathways involved in cell growth and division, leading to reduced leukemic cell proliferation. The drug also has effects on other related pathways, indicating potential therapeutic use in various myeloproliferative diseases.
Pharmacokinetics
Nilotinib is well-absorbed from the gastrointestinal tract, with peak plasma concentrations occurring within 3 hours after oral administration. It has a bioavailability of approximately 30-50%. The drug is highly protein-bound (approximately 97%) and is metabolized primarily by the liver via CYP3A4. The elimination half-life of Nilotinib is around 15-20 hours, allowing for twice-daily dosing. It is excreted mainly in feces, with minimal renal excretion of unchanged drug.
Contra-indications
- Hypersensitivity to nilotinib or any of its components
- Severe hepatic impairment
- Concomitant use with strong CYP3A4 inhibitors
Adverse effects
- Nausea
- Vomiting
- Fatigue
- Headache
- Rash
- Diarrhea
- Elevated liver enzymes
- QT interval prolongation
- Peripheral edema
- Thrombocytopenia
Interactions
- Grapefruit juice: Severe (increases exposure)
- Clarithromycin: Severe (increases exposure)
- Mitotane: Severe (decreases exposure)
- Second-generation antipsychotics: Severe (increases exposure)
- St. John's Wort: Severe (decreases exposure)
- Propafenone: Moderate (increases exposure)
- Midazolam: Moderate (increases exposure)
- Bosutinib: Moderate (increases exposure)
- Buspirone: Moderate (increases exposure)
- Calcium channel blockers: Moderate (increases exposure)
Precautions
- Monitor for signs of QT interval prolongation
- Regular monitoring of blood counts
- Assess liver function prior to and during treatment
- Consider cardiac monitoring in patients with cardiac risk factors
Pregnancy
Nilotinib should not be used during pregnancy unless the potential benefit justifies the potential risk to the fetus. Effective contraception is recommended during treatment and for 1 month after.
Breast-feeding
It is not known if nilotinib is excreted in human milk. Breastfeeding is not recommended during treatment.
Storage
Store at room temperature, away from light and moisture. Keep out of reach of children.
Formulations
- Nilotinib 150 mg capsules
- Nilotinib 200 mg capsules
- Nilotinib 300 mg capsules
AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.
Molecular reference: Nilotinib
PubChem CID 644241Molecular formula: C28H22F3N7O
Mechanism of action
Chronic myelogenous leukaemia (CML) is caused by the BCR-ABL oncogene. Nilotinib inhibits the tyrosine kinase activity of the BCR-ABL protein. Nilotinib fits into the ATP-binding site of the BCR-ABL protein with higher affinity than imatinib, over-riding resistance caused by mutations. The ability of AMN107 to inhibit TEL-platelet-derived growth factor receptor-beta (TEL-PDGFRbeta), which causes chronic myelomonocytic leukaemia, and FIP1-like-1-PDGFRalpha, which causes hypereosinophilic syndrome, suggests potential use of AMN107 for myeloproliferative diseases characterised by these kinase fusions (Stover et al, 2005; Weisberg et al, 2005). AMN107 also inhibits the c-Kit receptor kinase, including the D816V-mutated variant of KIT, at pharmacologically achievable concentrations, supporting potential utility in the treatment of mastocytosis, and gastrointestinal stromal tumours (Weisberg et al, 2005; von Bubnoff et al, 2005; Gleixner et al, 2006). Nilotinib, an inhibitor of Bcr-Abl tyrosine kinase, is an antineoplastic agent. Chronic myelogenous leukemia (CML) is a clonal myeloproliferative disorder characterized by the expansion of hematopoietic cells carrying the Philadelphia chromosome (Ph), resulting from a reciprocal translocation of the long arms of chromosomes 9 and 22. A novel fusion gene is formed, Bcr-Abl, which encodes a constitutively active, cytoplasmic form of protein tyrosine kinase. The unregulated activity of the Abl tyrosine kinase in Bcr-Abl is the cause of CML. Nilotinib is an orally active aminopyrimidine-derivative tyrosine kinase inhibitor that functions through competitive inhibition at the ATP-binding site of Bcr-Abl, leading to the inhibition of tyrosine phosphorylation of proteins that are involved in the intracellular signal transduction that Bcr-Abl mediates. Clinical resistance to imatinib in CML has been attributed to several mechanisms, but point mutations in the Bcr-Abl kinase domain appear to the most common, occurring in 30-90% of patients who develop resistance. The ability of nilotinib to overcome imatinib resistance resulting from Bcr-Abl kinase domain mutations has been demonstrated in vitro. In preclinical studies in cell-line models, nilotinib inhibited most (32 of 33) imatinib-resistant Bcr-Abl kinase domain mutant forms. 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. In vivo, nilotinib reduced the tumor size in a murine Bcr-Abl xenograft model. Nilotinib inhibited the autophosphorylation of the following kinases at IC50 values as indicated: Bcr-Abl (20-60 nM), PDGFR (69 nM), c-Kit (210 nM), CSF-1R (125-250 nM) and DDR (3.7 nM). It is an important challenge to better understand the mechanisms of tyrosine kinase inhibitors-induced apoptosis in CML cells. Thus, /the authors/ have investigated how this apoptosis can be modulated by extracellular factors. Apoptosis induced by imatinib and nilotinib was determined in BCR-ABL expressing cell lines and primary CML CD34+ cells. Both molecules induced apoptosis of BCR-ABL expressing cells. This apoptosis was inhibited by protein synthesis inhibition in both K562 and CML CD34+ cells. In K562, 80% inhibition of the BCR-ABL auto-phosphorylation by either imatinib or nilotinib induced a two fold increase in Bim-EL expression and induction of apoptosis in 48 hr. Bim accumulation preceded apoptosis induction which was completely abolished by depletion in Bim using shRNA. However, the anti-proliferative effect of imatinib was preserved in Bim-depleted cells. When K562 cells were cultured in a cytokine containing medium, the pro-apoptotic effect of nilotinib was decreased by 68% and this was related t
Pharmacodynamics
Nilotinib is a transduction inhibitor that targets BCR-ABL, c-kit and PDGF, for the potential treatment of various leukemias, including chronic myeloid leukemia (CML).
Biological pathways
Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.
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The same active ingredient registered across other registries we cover - including different brands.