Nilotinib

Catalog No.S1033 Batch:S103311

Print

Technical Data

Formula

C28H22F3N7O
Molecular Weight 529.52 CAS No. 641571-10-0
Solubility (25°C)* In vitro DMSO 13 mg/mL (24.55 mM)
Water Insoluble
Ethanol Insoluble
In vivo (Add solvents to the product individually and in order)
Homogeneous suspension
CMC-NA
≥5mg/ml Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
Clear solution
4%DMSO 30%PEG300 5%Tween80 61%ddH2O

Validated by Selleck labs. Should you need adjustments to this formulation, contact our sales team for custom testing.

 3.000mg/ml (5.67mM) Taking the 1 mL working solution as an example, add 40 μL of 75 mg/ml clarified DMSO stock solution to 300 μL of PEG300, mix evenly to clarify it; add 50 μL of Tween80 to the above system, mix evenly to clarify; then continue to add 610 μL of ddH2O to adjust the volume to 1 mL. The mixed solution should be used immediately for optimal results. 
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Biological Activity

Description Nilotinib is a selective Bcr-Abl inhibitor with IC50 less than 30 nM in Murine myeloid progenitor cells. Nilotinib induces autophagy through AMPK activition.
Targets
Bcr-Abl [1]
(Murine myeloid progenitor cells)
<30 nM
In vitro Nilotinib inhibits proliferation, migration, and actin filament formation, as well as the expression of α-SMA and collagen in activated HSCs. Nilotinib induces apoptosis of HSCs, which is correlated with reduced bcl-2 expression, increases p53 expression, cleavage of PARP, as well as increases expression of PPARγ and TRAIL-R. Nilotinib also induces cell cycle arrest, accompanied by increased expression of p27 and downregulation of cyclin D1. Interestingly, Nilotinib not only inhibits activation of PDGFR, but also TGFRII through Src. Nilotinib significantly inhibits PDGF and TGFβ-simulated phosphorylation of ERK and Akt. Furthermore, PDGF- and TGFβ-activated phosphorylated form(s) of Abl in human HSCs are inhibited by Nilotinib. [2] Nilotinib inhibits most imatinib-resistant Bcr-Abl mutations, except for T315I. [3] Nilotinib inhibits PDGF-DD-mediated ERK1/2 activation, basal and PDGF-DD-mediated activation of PDGFRβ and Akt, and schwannoma proliferation. Nilotinib is more potent than imatinib, exerting its maximal inhibitory effect at concentrations lower than steady-state trough plasma levels. [4] Nilotinib also significantly reduces the expression levels of the genes for TGF-β1 and platelet-derived growth factor (PDGF). Nilotinib treatment also significantly inhibits the PDGF-induced proliferation of lung fibroblasts. [5] Nilotinib inhibits the proliferation of Ba/F3 cells expressing p210- and p190-Bcr-Abl, or K562 and Ku-812F cells with IC50 values ≤12 nM. [6]
In vivo Nilotinib reduces collagen deposition and α-SMA expression in CCl4 and BDL-induced fibrosis. Nilotinib could induce HSC undergoing apoptosis, which is correlated with downregulation of bcl-2. [2] Nilotinib attenuates the extent of lung injury and fibrosis. Nilotinib therapy significantly reduces the levels of hydroxyproline on days 14 and 21, which is accompanied by decreased expression levels of transforming growth factor (TGF)-β1 and PDGFRβ. [5] AMN107 prolongs survival of mice injected with Bcr-Abl-transformed hematopoietic cell lines or primary marrow cells, and prolongs survival in imatinib-resistant CML mouse models. [6]
Features A selective inhibitor of native and mutant Bcr-Abl.

Protocol (from reference)

Cell Assay:[4]
  • Cell lines

    Human primary Schwann and schwannoma cells

  • Concentrations

    1-10 μM

  • Incubation Time

    72 hours

  • Method

    Human primary Schwann and schwannoma cells are seeded on precoated 96-well plates. Nilotinib is added 40 minutes before stimulation with 100 ng/mL PDGF-DD, and cells are cultured for 72 hours (3 days). Because the half-life of Nilotinib is 18 hours, one-half of the originally added concentrations are added freshly every day. In addition to DAPI staining and determination of the total cell number, the more sensitive and accurate BrdU incorporation method is used to detect proliferating cells. Total cell amount (DAPI) and number of dividing cells (BrdU-positive) are blindly counted using an inverted fluorescent microscope and 200 × magnification. All cells in every well are counted. The total cell number per well differed between various cell batches and is 100–300 cells/well.
Animal Study:[6]
  • Animal Models

    Systemic 32D Bcr-Abl leukemia model in Female BALB/c mice, Bioluminescent Bcr-Abl model of CML in Female NOD-SCID mice and Bone marrow transplant Bcr-Abl model of CML in syngeneic Balb/c recipient mice

  • Dosages

    75 mg/kg, 100 mg/kg

  • Administration

    Oral administration

References

  • https://pubmed.ncbi.nlm.nih.gov/17068153/
  • https://pubmed.ncbi.nlm.nih.gov/21251937/
  • https://pubmed.ncbi.nlm.nih.gov/21220945/
  • https://pubmed.ncbi.nlm.nih.gov/21727212/
  • https://pubmed.ncbi.nlm.nih.gov/21659722/
  • https://pubmed.ncbi.nlm.nih.gov/15710326/

Customer Product Validation

<p>Effect of nilotinib on Bcr-Abl kinase activity in ABCB1- and ABCG2- overexpressing CD34<sup>+</sup>CD38<sup>-</sup> cells. K562 parental cells and CD34<sup>+</sup>CD38<sup>-</sup> subpopulation isolated from K562 cells were treated with nilotinib at 0.01, 0.1 and 1.0 umol/L for 12 h. Equal amount of protein was loaded for western blot analysis as described in the Experimental section. The experiments were repeated at least three times independently, and a representative experiment is shown.</p>

Data from [ Molecules , 2014 , 19, 3356-75 ]

<p>Nilotinib up-regulates the ERK survival signal in prostate cancer cells. (B and C) Immunoblot analyses of DU-145 cells (B) or DU-145 cells in comparison with LNCaP and PC-3 cells (C) treated with nilotinib for the expression of phospho-ERK1/2 T202/Y204 and total ERK. Immunoblot for GAPDH is shown as a loading control.</p>

Data from [ Urol Oncol , 2014 , 0.1016/j.urolonc.2014.06.001 ]

<p>Immunohistochemical staining of xenografted DU-145 cells after 21 days of treatment with 75 mg/kg/d of nilotinib for phospho-ERK1/2 T202/Y204 expression. It can be noted that tumors explanted from vehicle-treated mice showed mostly positivity at the tumor periphery, whereas tumors explanted from nilotinib-treated mice showed a more evenly distributed phospho-ERK immunostaining (left panels). Quantification of phospho-ERK-positive DU-145 xenografts explanted after 21 days of treatment. Mean and standard errors of positive cells per high-power field (HPF; x40) from at least 3 tumors are given (right panel).</p>

Data from [ Urol Oncol , 2014 , 0.1016/j.urolonc.2014.06.001 ]

<p> </p><p>Inhibition of thymidine (a and b) and cytarabine (c and d) uptake with nilotinib. The legend is similar to Fig. 1, except that imatinib was replaced by nilotinib.</p>

Data from [ Leukemia Res , 2012 , 36, 1311-1314 ]

Selleck's Nilotinib has been cited by 158 publications

Nilotinib attenuates vascular pathology in experimental cerebral malaria [ Blood Adv, 2025, bloodadvances.2024015364] PubMed: 39993234
CDK8/19 inhibition attenuates G1 arrest induced by BCR-ABL antagonists and accelerates death of chronic myelogenous leukemia cells [ Cell Death Discov, 2025, 11(1):62] PubMed: 39955308
Electrochemical assay for the quantification of anticancer drugs and their inhibition mechanism [ Methods, 2025, 241:13-23] PubMed: 40345605
Discovery of non-steroidal aldo-keto reductase 1D1 inhibitors through automated screening and in vitro evaluation [ Toxicol Lett, 2025, 406:31-37] PubMed: 39988211
Structural Identification of Major Molecular Determinants for Phosphotyrosine Recognition in Tyrosine Kinases Reveals Tumour Promoting and Suppressive Functions [ bioRxiv, 2025, 2025.06.10.658871] PubMed: 40661594
Activating p53 abolishes self-renewal of quiescent leukaemic stem cells in residual CML disease [ Nat Commun, 2024, 15(1):651] PubMed: 38246924
Comprehensive multi-omics analysis reveals WEE1 as a synergistic lethal target with hyperthermia through CDK1 super-activation [ Nat Commun, 2024, 15(1):2089] PubMed: 38453961
The molecular basis of Abelson kinase regulation by its αI-helix [ Elife, 2024, 12RP92324] PubMed: 38588001
Satellite cell-derived TRIM28 is pivotal for mechanical load- and injury-induced myogenesis [ EMBO Rep, 2024, 10.1038/s44319-024-00227-1] PubMed: 39143258
Patient-derived rhabdomyosarcoma cells recapitulate the genetic and transcriptomic landscapes of primary tumors [ iScience, 2024, 27(10):110862] PubMed: 39319271

RETURN POLICY
Selleck Chemical’s Unconditional Return Policy ensures a smooth online shopping experience for our customers. If you are in any way unsatisfied with your purchase, you may return any item(s) within 7 days of receiving it. In the event of product quality issues, either protocol related or product related problems, you may return any item(s) within 365 days from the original purchase date. Please follow the instructions below when returning products.

SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

NOT FOR HUMAN, VETERINARY DIAGNOSTIC OR THERAPEUTIC USE.