Nilotinib (AMN-107)

Catalog No.S1033

Nilotinib (AMN-107) is a Bcr-Abl inhibitor with IC50 less than 30 nM in Murine myeloid progenitor cells.

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Nilotinib (AMN-107) Chemical Structure

Nilotinib (AMN-107) Chemical Structure
Molecular Weight: 529.52

Validation & Quality Control

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Related Compound Libraries

Bcr-Abl Inhibitors with Unique Features

  • Pan Bcr-Abl Inhibitor

    Imatinib Mesylate (STI571) Multi-target inhibitor of v-Abl, c-Kit and PDGFRIC50=0.6 μM/0.1 μM/0.1 μM.

  • Most Potent Bcr-Abl Inhibitor

    GZD824 Bcr-Abl(WT), IC50=0.34 nM; Bcr-Abl(T315I), IC50=0.68 nM.

  • FDA-approved Bcr-Abl Inhibitor

    Dasatinib Approved by FDA for CML and Ph+ ALL.

  • Newest Bcr-Abl Inhibitor

    GZD824 Orally bioavailable Bcr-Abl inhibitor for Bcr-Abl(WT) and Bcr-Abl(T315I) with IC50 of 0.34 nM and 0.68 nM, respectively.

Product Information

  • Compare Bcr-Abl Inhibitors
    Compare Bcr-Abl Products
  • Research Area
  • Combination Therapy
    Combination Therapy

Product Description

Biological Activity

Description Nilotinib (AMN-107) is a Bcr-Abl inhibitor with IC50 less than 30 nM in Murine myeloid progenitor cells.
Targets Bcr-Abl [1]
(Murine myeloid progenitor cells)
IC50 <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]
Cell Data
Cell LinesAssay TypeConcentrationIncubation TimeFormulationActivity DescriptionPMID
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... Click to View More Cell Line Experimental Data

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(Only for 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
Formulation 10% NMP-90% PEG300, PEG300
Dosages 75 mg/kg, 100 mg/kg
Administration Oral administration

Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)

SpeciesMouseRatRabbitGuinea pigHamsterDog
Weight (kg)0.020.151.80.40.0810
Body Surface Area (m2)0.0070.0250.150.050.020.5
Km factor36128520
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.

Rat dose (mg/kg) = mouse dose (22.4 mg/kg) ×  mouse Km(3)  = 11.2 mg/kg
rat Km(6)
1

References

[1] Weisberg E, et al. Blood. 2007, 109(5), 2112-2120.

[2] Liu Y, et al. J Hepatol. 2011, 55(3), 612-625.

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Clinical Trial Information( data from http://clinicaltrials.gov, updated on 2016-07-30)

NCT Number Recruitment Conditions Sponsor
/Collaborators
Start Date Phases
NCT02709083 Not yet recruiting Chronic Myelogenous Leukemia|Chronic Myeloid Leukemia|Leukemia Emory University December 2016 Phase 2
NCT01887522 Recruiting Refractory Low-grade Gliomas|Recurrent Low-grade Gliomas Gustave Roussy, Cancer Campus, Grand Paris|Innovative The  ...more Gustave Roussy, Cancer Campus, Grand Paris|Innovative Therapies For Children with Cancer Consortium June 2016 Phase 2
NCT02774512 Not yet recruiting Colon Cancer Institut Bergonié|Novartis Pharmaceuticals May 2016 Phase 0
NCT02611492 Recruiting Philadelphia Chromosome Positive Adult Acute Lymphoblastic Leukemia Assistance Publique - Hôpitaux de Paris April 2016 Phase 3
NCT02602314 Not yet recruiting Chronyc Myeloid Leukemia Gruppo Italiano Malattie EMatologiche dellAdulto March 2016 Phase 4

view more

Chemical Information

Download Nilotinib (AMN-107) SDF
Molecular Weight (MW) 529.52
Formula

C28H22F3N7O

CAS No. 641571-10-0
Storage 3 years -20℃powder
6 months-80℃in solvent
Synonyms N/A
Solubility (25°C) * In vitro DMSO 27 mg/mL (50.98 mM)
Water <1 mg/mL (<1 mM)
Ethanol <1 mg/mL (<1 mM)
In vivo 4% DMSO+30% PEG 300+5% Tween 80+ddH2O 3mg/mL
* <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.
Chemical Name 4-methyl-N-(3-(4-methyl-1H-imidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-(4-(pyridin-3-yl)pyrimidin-2-ylamino)benzamide

Tech Support

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    Features:WP1130 has an advantage over imatinib mesylate in that its activity is not inhibited by a variety of Abl kinase mutations, including T315I.

  • DCC-2036 (Rebastinib)

    DCC-2036 (Rebastinib) is a conformational control Bcr-Abl inhibitor for Abl1(WT) and Abl1(T315I) with IC50 of 0.8 nM and 4 nM, also inhibits SRC, LYN, FGR, HCK, KDR, FLT3, and Tie-2, and low activity to seen towards c-Kit. Phase 1.

    Features:A conformational control inhibitor of Abl1 and T315I Abl1.

  • GZD824 Dimesylate

    GZD824 Dimesylate is a novel orally bioavailable Bcr-Abl inhibitor for Bcr-Abl(WT) and Bcr-Abl(T315I) with IC50 of 0.34 nM and 0.68 nM, respectively.

  • GNF-2

    GNF-2 is a highly selective non-ATP competitive inhibitor of Bcr-Abl, shows no activity to Flt3-ITD, Tel-PDGFR, TPR-MET and Tel-JAK1 transformed tumor cells.

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