| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| 25mg |
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| 50mg |
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| 100mg |
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| 250mg |
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| Other Sizes |
Purity: ≥98%
| Targets |
ALK (IC50 = 0.7 nM)
ALK (anaplastic lymphoma kinase); TRKA, TRKB, TRKC (tropomyosin receptor kinases A, B, and C). Belizatinib is a multi-target receptor tyrosine kinase inhibitor that primarily inhibits ALK and TRK family kinases. It exhibits high affinity for wild-type recombinant ALK kinase, which is overexpressed in certain tumors, and also potently inhibits TRK A, B, and C. |
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| ln Vitro |
TSR-011 inhibits tropomyosin receptor kinase (TRK) A, B, and C (IC50 < 3nM) and exhibits a high affinity for wild-type recombinant ALK kinase activity (IC50 value = 0.7 nM)[1].
In vitro, belizatinib inhibits ALK with an IC50 of 0.7 nM and TRK A, B, and C with IC50 values <3 nM. It exhibits high affinity for wild-type recombinant ALK kinase activity. TSR-011 has demonstrated antitumor activity in preclinical studies. The compound effectively inhibits the growth of tumor cells that overexpress ALK or TRK and disrupts signaling transduction mediated by these kinases. |
| ln Vivo |
TSR-011 TSR-011 exhibits a persistent and strong suppression of ALK-dependent tumor growth in mouse models. It is well-tolerated[1].
In vivo, belizatinib (TSR-011) exerts sustained and potent inhibition of ALK-dependent tumor growth in mouse models. It is well-tolerated in these models. The compound demonstrates persistent suppression of ALK-dependent tumor growth. These in vivo efficacy data supported the advancement of belizatinib into clinical trials for patients with ALK-positive solid tumors and lymphomas. |
| Enzyme Assay |
Belizatinib has an IC50 of less than 3 nM for TRK A, B, and C and an IC50 of 0.7 nM for ALK, making it a strong inhibitor of tropomyosin receptor kinase (TRK).
The enzyme inhibition assay for belizatinib typically involves recombinant ALK or TRK kinases incubated with ATP and a peptide substrate in the presence of varying concentrations of the compound. Kinase activity is measured by quantifying phosphorylated substrate using methods such as radioactive ATP incorporation, time-resolved fluorescence resonance energy transfer (TR-FRET), or luminescent kinase assays. IC50 values are calculated from dose-response curves. For ALK, the IC50 is 0.7 nM, and for TRK A, B, and C, IC50 values are less than 3 nM. |
| Cell Assay |
Cells overexpressing ALK or TRK (e.g., ALK-positive lymphoma or NSCLC cell lines) are cultured in appropriate medium and treated with increasing concentrations of belizatinib (typically ranging from 0.1 nM to 10 μM). Cell viability is assessed using MTT, CCK-8, or CellTiter-Glo assays after 48-72 hours of treatment. Apoptosis is evaluated by Annexin V/PI staining and flow cytometry. Signaling pathway inhibition is confirmed by Western blotting for phosphorylated ALK, STAT3, ERK, and other downstream effectors.
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| Animal Protocol |
Mouse xenograft models are established by subcutaneous implantation of ALK-dependent tumor cells (e.g., ALK-positive lymphoma or NSCLC cells) into immunodeficient mice. When tumors reach a certain size (e.g., 100-200 mm³), belizatinib is administered orally at various doses (typically 10-50 mg/kg) daily or twice daily. Tumor volumes are measured with calipers every 2-3 days, and body weights are monitored for tolerability. At study termination, tumors are excised, weighed, and analyzed for ALK phosphorylation and downstream signaling by immunohistochemistry and Western blotting.
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| ADME/Pharmacokinetics |
Belizatinib is orally bioavailable with favorable pharmacokinetic properties. It has a molecular weight of 577.7 g/mol and a logP of 3.99. The compound is well-absorbed after oral administration and achieves sufficient systemic exposure to inhibit ALK and TRK kinases in vivo. Detailed human pharmacokinetic parameters from clinical trials (NCT02048488) have been evaluated, including absorption, distribution, metabolism, and excretion profiles. Belizatinib is metabolized primarily by hepatic cytochrome P450 enzymes.
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| Toxicity/Toxicokinetics |
Belizatinib is well-tolerated in preclinical mouse models at efficacious doses. In clinical trials (NCT02048488), adverse events were monitored in patients with solid tumors and lymphomas. The safety profile includes commonly observed toxicities associated with kinase inhibitors, such as gastrointestinal disturbances, fatigue, and hematological abnormalities. Dose-limiting toxicities and maximum tolerated dose were determined in Phase 1 studies. The compound was generally well-tolerated at therapeutic doses.
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| References | |
| Additional Infomation |
Belizatinib (TSR-011) was developed by Tesaro and evaluated in a Phase 1/2 clinical trial (NCT02048488) for the treatment of solid tumors and lymphomas. The trial investigated the safety, pharmacokinetics, and preliminary antitumor activity of belizatinib in patients with advanced malignancies, including those with ALK gene alterations. Belizatinib has a molecular formula of C₃₃H₄₄FN₅O₃ and a molecular weight of 577.7 g/mol. It is supplied as a white to off-white solid powder. The compound is a multi-target receptor tyrosine kinase inhibitor that suppresses tumor cell proliferation by blocking cancer-related signaling pathways.
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| Molecular Formula |
C33H44FN5O3
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| Molecular Weight |
577.73
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| Exact Mass |
577.342
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| Elemental Analysis |
C, 68.61; H, 7.68; F, 3.29; N, 12.12; O, 8.31
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| CAS # |
1357920-84-3
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| Related CAS # |
1357920-84-3;1388225-79-3 (TSR-011 isomer);
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| PubChem CID |
57345941
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| Appearance |
White to off-white solid powder
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| Density |
1.3±0.1 g/cm3
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| Index of Refraction |
1.631
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| LogP |
3.99
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| Hydrogen Bond Donor Count |
3
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| Hydrogen Bond Acceptor Count |
6
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| Rotatable Bond Count |
8
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| Heavy Atom Count |
42
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| Complexity |
909
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| Defined Atom Stereocenter Count |
0
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| SMILES |
FC1C([H])=C([H])C(=C([H])C=1[H])C(N([H])C1=NC2C([H])=C([H])C(=C([H])C=2N1C1([H])C([H])([H])C([H])([H])C([H])(C(N([H])C([H])(C([H])([H])[H])C([H])([H])[H])=O)C([H])([H])C1([H])[H])C([H])([H])N1C([H])([H])C([H])([H])C([H])(C(C([H])([H])[H])(C([H])([H])[H])O[H])C([H])([H])C1([H])[H])=O
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| InChi Key |
WSTUJEXAPHIEIM-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C33H44FN5O3/c1-21(2)35-30(40)24-8-12-27(13-9-24)39-29-19-22(20-38-17-15-25(16-18-38)33(3,4)42)5-14-28(29)36-32(39)37-31(41)23-6-10-26(34)11-7-23/h5-7,10-11,14,19,21,24-25,27,42H,8-9,12-13,15-18,20H2,1-4H3,(H,35,40)(H,36,37,41)
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| Chemical Name |
4-fluoro-N-[6-[[4-(2-hydroxypropan-2-yl)piperidin-1-yl]methyl]-1-[4-(propan-2-ylcarbamoyl)cyclohexyl]benzimidazol-2-yl]benzamide
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| Synonyms |
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
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| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.7309 mL | 8.6546 mL | 17.3091 mL | |
| 5 mM | 0.3462 mL | 1.7309 mL | 3.4618 mL | |
| 10 mM | 0.1731 mL | 0.8655 mL | 1.7309 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
 TRK signaling pathways. Binding of neurotrophins to TRK proteins induces receptor dimerization, phosphorylation, and activation of the downstream signaling cascades via PI3K, RAS/MAPK/ERK, and PLC-gamma.Pharmacol Ther.2017 May;173:58-66. |
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 TheEML4-ALKfusion is formed via an abnormal rearrangement on chromosome 2 which juxtaposes part of the N-terminus ofEML4to a portion of the C-terminus ofALK.Cancer J.2015 Sep-Oct;21(5):378-82. |
 Specific ALK tyrosine kinase point mutations have been identified as imparting only resistance to crizotinib (L1196M) or enabling resistance to both crizotinib and second generation ALK inhibitors (G1202R).Cancer J.2015 Sep-Oct;21(5):378-8 |
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