Nutrabiotech Imatinib 99% Powder 1G, 99% high purity Imatinib powder, selective tyrosine kinase inhibitor, BCR-ABL pathway regulator, cell proliferation inhibition research raw material

Imatinib STI‑571 CAS 152459‑95‑5 High‑Purity Powder First‑Generation BCR‑ABL Tyrosine Kinase Inhibitor Oncological Biochemical Reagent

High‑purity Imatinib powder CAS 152459‑95‑5, also well‑known as STI‑571 and CGP‑57148B, is a classic first‑generation ATP‑competitive tyrosine kinase‑inhibitor small‑molecule compound. This off‑white crystalline reagent potently suppresses BCR‑ABL fusion‑kinase, c‑Kit and PDGFR‑α/β receptor‑kinase activity, blocks Ras‑MAPK and PI3K‑AKT tumour‑survival signalling pathways and induces cancer‑cell apoptosis. It is widely used for laboratory‑scale research on chronic myeloid leukemia (CML), gastrointestinal stromal tumour(GIST), mast‑cell disorder, hypereosinophilic‑syndrome and targeted‑anti‑cancer drug‑screening projects. Every‑batch completes strict HPLC purity inspection, bulk‑order service and customizable‑packaging are available for global oncology‑pharmacology research‑oriented purchasers.

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Imatinib Free Base (CAS 152459-95-5) BCR-ABL Tyrosine Kinase Inhibitor | STI571, c-KIT & PDGFR Inhibitor

Imatinib Free Base CAS 152459-95-5
BCR-ABL, c-KIT & PDGFR Tyrosine Kinase Inhibitor

Imatinib (STI571; the mesylate salt is marketed as Gleevec / Glivec) is the first rationally designed targeted cancer therapy and the compound that defined the modern kinase-inhibitor era. This 2-phenylaminopyrimidine binds the ATP pocket of BCR-ABL only in its inactive DFG-out conformation, and also potently inhibits c-KIT (CD117) and PDGFR-α/β — the molecular basis of its activity in Philadelphia-chromosome-positive leukaemia and in KIT-driven gastrointestinal stromal tumours.

BCR-ABL Inhibitor c-KIT / CD117 PDGFRA / PDGFRB ATP-Competitive DFG-Out Binder First-in-Class TKI CML & GIST Research
Request a Quote Technical Specs
493.60
MW (C29H31N7O)
3 Targets
BCR-ABL / c-KIT / PDGFR
≥98%
Purity (HPLC)

Molecular Information

Name: Imatinib (free base)
CAS: 152459-95-5
Formula: C29H31N7O
MW: 493.60 g/mol
Purity: ≥98% (HPLC)
SMILES: Cc1ccc(cc1Nc1nccc
  (n1)c1cccnc1)NC(=O)
  c1ccc(cc1)CN1CCN(C)CC1
InChIKey: KTUFNOKKBVMGRW
  -UHFFFAOYSA-N
MP: 208-210°C (dec.)
Appearance: White to off-white powder
Solubility: DMSO; methanol;
  water (pH-dependent)
Synonyms: STI571 / CGP 57148
Storage: -20°C, sealed, desiccated
🧪
CAS Number
152459-95-5
⚖️
Molecular Weight
493.60
🎯
Primary Target
BCR-ABL
✅
Purity
≥98%

Imatinib Technical Specifications & QC Parameters

Complete physicochemical data and quality-control profile for research-grade imatinib free base (CAS 152459-95-5)

📋 Physicochemical Properties

  • Product NameImatinib (free base)
  • IUPAC Name4-[(4-Methylpiperazin-1-yl)methyl]-N-(4-methyl-3-{[4-(pyridin-3-yl)pyrimidin-2-yl]amino}phenyl)benzamide
  • CAS Number152459-95-5
  • Mesylate Salt CAS220127-57-1
  • SynonymsSTI571 / CGP 57148 / CGP57148B
  • Molecular FormulaC29H31N7O
  • Molecular Weight493.60 g/mol
  • Exact Mass493.2590 Da
  • SMILESCc1ccc(cc1Nc1nccc(n1)c1cccnc1)NC(=O)c1ccc(cc1)CN1CCN(C)CC1
  • InChIKeyKTUFNOKKBVMGRW-UHFFFAOYSA-N
  • AppearanceWhite to off-white / pale beige powder
  • Melting Point208-210°C (dec.)
  • pKa8.07 / 3.73 / 2.56 / 1.52 (predicted, 25°C)
  • Chemical Class2-Phenylaminopyrimidine

🔬 Quality Control & Handling

  • Purity (HPLC)≥98%
  • FormCrystalline powder
  • Kinase TargetsBCR-ABL / v-ABL, c-KIT (CD117), PDGFRA, PDGFRB
  • Typical PotencyIC50 ≈ 0.1-0.6 µM (cellular ABL, c-KIT, PDGFR)
  • Binding ModeATP-competitive, inactive DFG-out conformation
  • SolubilityDMSO (warm/sonicate); methanol; water pH-dependent — mesylate freely soluble below pH 5.5
  • Storage Condition-20°C, sealed, desiccated, dark
  • Stock Solution Storage-20°C to -80°C, aliquoted, avoid freeze-thaw
  • QC DocumentationCOA / HPLC / NMR / MS / MSDS
  • Pack Sizes1g / 5g / 10g / 100g / 1KG
  • Stock StatusIn Stock
  • Use StatementResearch use only; not for human or clinical use

Kinase Target Profile & Downstream Signalling

Imatinib is remarkably selective for a small family of structurally related tyrosine kinases — the reason it became the template for rational kinase drug design

🎯 BCR-ABL1 (p210 / p190) 🎯 c-ABL / v-ABL 🎯 c-KIT (CD117) 🎯 PDGFRA 🎯 PDGFRB 🧬 ARG (ABL2) 🧬 DDR1 / DDR2 🧬 CSF1R 🔻 RAS / MAPK Cascade 🔻 PI3K / AKT Survival 🔻 STAT5 Transcription 🔻 CRKL Phosphorylation

Imatinib Mechanism of Action: Conformational Selection at the ATP Pocket

From Philadelphia chromosome to apoptosis — how one molecule shut down an oncogenic kinase and created targeted oncology

1

The Oncogenic Driver

The t(9;22) Philadelphia translocation fuses BCR to ABL1, producing a constitutively active cytoplasmic tyrosine kinase that autophosphorylates without any upstream signal — the single genetic lesion sufficient to cause chronic myeloid leukaemia.

2

Conformational Selection

Imatinib does not bind the active kinase. It engages only the closed, inactive DFG-out state, in which the Asp-Phe-Gly motif flips outward and opens an adjacent hydrophobic allosteric pocket. This conformational requirement is the origin of its selectivity.

3

ATP-Pocket Occupancy

The pyridinyl-pyrimidine hydrogen bonds to hinge residue Met318; the anilino NH contacts the gatekeeper Thr315; the amide bridges to Glu286 and Asp381; and the N-methylpiperazine picks up ionic contacts at the solvent front — six hydrogen bonds in total.

4

Signal Shutdown

With ATP excluded, BCR-ABL can no longer phosphorylate CRKL, GAB2, STAT5 and other substrates. The RAS/MAPK proliferative arm, the PI3K/AKT survival arm and STAT5-driven transcription all collapse within hours of exposure.

5

Apoptosis in Driver-Dependent Cells

Because Ph-positive cells are addicted to BCR-ABL signalling, loss of the survival signal releases BIM and BAD, triggering mitochondrial apoptosis. Normal haematopoietic cells lacking the fusion are largely spared — the therapeutic index of targeted therapy.

6

Parallel c-KIT and PDGFR Blockade

c-KIT and PDGFRA/B share the same DFG-out-accessible architecture, so the same molecule shuts down KIT exon 11-mutant GIST, PDGFRA-rearranged myeloid neoplasms and PDGFR-driven fibrotic signalling — the basis of imatinib's second and third indications.

Research Applications of the BCR-ABL Inhibitor Imatinib

A reference tyrosine kinase inhibitor across oncology, resistance biology, fibrosis and beyond

🩸

Chronic Myeloid Leukaemia (CML)

The canonical BCR-ABL model system. Imatinib is the benchmark comparator in K562, KU812, KCL-22 and BaF3/BCR-ABL assays, in colony-forming and apoptosis studies, and in molecular-response work tracking BCR-ABL transcript levels and CRKL phosphorylation.

Haematologic Oncology
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Gastrointestinal Stromal Tumour & c-KIT Biology

About 80% of GIST is driven by activating KIT mutations, most often exon 11. Imatinib is the standard tool for probing genotype-dependent sensitivity in GIST-T1 and GIST882 lines, for studying mast-cell and interstitial-cell-of-Cajal biology, and for CD117-directed research.

c-KIT / GIST
🧬

TKI Resistance & the T315I Gatekeeper

Imatinib underpins the entire field of kinase-inhibitor resistance: kinase-domain point mutations (T315I, E255K, Y253H, M351T), BCR-ABL amplification, efflux via ABCB1/ABCG2 and BCR-ABL-independent bypass signalling are all mapped against imatinib as the reference agent.

Resistance Biology
🔬

Structural Biology & Rational Drug Design

The ABL–imatinib co-crystal structure is one of the most reproduced images in medicinal chemistry and remains the teaching example of type II, DFG-out kinase inhibition. Widely used in docking validation, fragment-growing exercises and conformational-selection studies.

Structure-Based Design
🫁

PDGFR-Driven Fibrosis & Vascular Remodelling

PDGF signalling drives fibroblast proliferation and myofibroblast transition. Imatinib is applied in pulmonary fibrosis, systemic sclerosis, hepatic stellate cell activation, pulmonary arterial hypertension and vascular restenosis models as a PDGFR-blockade tool.

Fibrosis Research
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Myeloproliferative & Eosinophilic Neoplasms

FIP1L1-PDGFRA fusion hypereosinophilic syndrome, PDGFRB-rearranged chronic myelomonocytic leukaemia, dermatofibrosarcoma protuberans (COL1A1-PDGFB) and systemic mastocytosis are all imatinib-sensitive fusion-driven models used in translational research.

Fusion-Driven Disease
💊

Pharmacokinetics, Transporters & Drug Interactions

Imatinib is a CYP3A4 substrate and inhibitor, an OCT1 influx substrate and an ABCB1/ABCG2 efflux substrate, making it a standard probe compound in transporter, DDI, plasma-protein-binding (AGP) and therapeutic-drug-monitoring method development.

DMPK / ADME
🧠

Repurposing & Off-Oncology Research

Explored in type 1 and type 2 diabetes, graft-versus-host disease, pulmonary hypertension, atherosclerosis, neuroinflammation and antiviral/antibacterial ABL-dependent entry pathways — imatinib's clean selectivity makes it a favoured repurposing probe.

Drug Repurposing
📈

Analytical Reference & Impurity Profiling

Used as a working reference standard for HPLC/UPLC-MS method development, imatinib and imatinib mesylate assay validation, dissolution testing, salt-form and polymorph characterisation, and as the parent for the active metabolite CGP74588.

Analytical Standard

Landmark Publications on Imatinib (STI571)

The papers that established targeted kinase therapy and defined resistance biology

Druker BJ, Talpaz M, Resta DJ, et al. Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. New England Journal of Medicine. 2001;344(14):1031-1037. [Practice-defining CML trial]
doi: 10.1056/NEJM200104053441401
Demetri GD, von Mehren M, Blanke CD, et al. Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors. New England Journal of Medicine. 2002;347(7):472-480. [GIST / c-KIT]
doi: 10.1056/NEJMoa020461
Capdeville R, Buchdunger E, Zimmermann J, Matter A. Glivec (STI571, imatinib), a rationally developed, targeted anticancer drug. Nature Reviews Drug Discovery. 2002;1(7):493-502.
doi: 10.1038/nrd839
Schindler T, Bornmann W, Pellicena P, et al. Structural mechanism for STI-571 inhibition of Abelson tyrosine kinase. Science. 2000;289(5486):1938-1942. [DFG-out co-crystal structure]
doi: 10.1126/science.289.5486.1938
Gorre ME, Mohammed M, Ellwood K, et al. Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification. Science. 2001;293(5531):876-880. [Origin of T315I resistance biology]
doi: 10.1126/science.1062538
Hochhaus A, Larson RA, Guilhot F, et al. Long-term outcomes of imatinib treatment for chronic myeloid leukemia (IRIS, 10-year follow-up). New England Journal of Medicine. 2017;376(10):917-927.
doi: 10.1056/NEJMoa1609324

Imatinib Pack Sizes & Ordering Information

Research-grade imatinib free base (CAS 152459-95-5) supplied with full QC documentation — available in 1g / 5g / 10g / 100g / 1KG

TierPack SizeStock StatusTypical Use CaseShipping Notes
Standard1 gIn StockKinase assays, cell viability and apoptosis panels, IC50 determinationSame/next-day dispatch; amber vial with desiccant
Medium5 gIn StockResistance-mutant screening, xenograft pilot studies, combination workSame/next-day dispatch; sealed foil pouch, ambient shipping
Large10 gIn StockIn vivo oncology cohorts, analytical reference standard qualification1-2 business days; double-sealed, light-protected
Bulk100 gIn StockFormulation and salt-form development, polymorph and dissolution studiesQuote to confirm; HDPE container, cool-chain option available
Industrial1 KGMade to orderPilot-scale campaigns, CRO/CMO supply agreements, salt conversion to mesylateBatch delivery on campaign schedule; per-lot COA and export documents

💡 Reference pack sizes shown above; for current pricing, lot availability and bulk imatinib quotations please contact us for a quote. Tiered discounts apply to 100 g and 1 KG orders.

Imatinib Frequently Asked Questions (FAQ)

What is imatinib and why is it historically important?
Imatinib (originally STI571 / CGP 57148) is a 2-phenylaminopyrimidine tyrosine kinase inhibitor with formula C29H31N7O and molecular weight 493.60 g/mol. It was the first small molecule deliberately designed against a known oncogenic driver — the BCR-ABL fusion kinase created by the Philadelphia chromosome — and its clinical success transformed chronic myeloid leukaemia from a fatal disease into a chronically managed one. Every subsequent kinase-inhibitor programme is measured against the imatinib template.
What is the difference between imatinib free base and imatinib mesylate?
The free base (CAS 152459-95-5, C29H31N7O, MW 493.60) is the neutral parent molecule supplied here. The mesylate (CAS 220127-57-1, MW ≈589.7) is the methanesulfonic acid salt used in the commercial drug product because it is freely soluble in aqueous media below about pH 5.5, while the free base is only sparingly water soluble. The active pharmacophore is identical, but you must apply a 493.60 / 589.7 ≈ 0.837 conversion factor when comparing salt and base weights so that molar dosing is equivalent.
How exactly does imatinib inhibit BCR-ABL?
Imatinib is an ATP-competitive type II inhibitor: it binds the ATP cleft only when the kinase adopts the inactive DFG-out conformation, in which the Asp-Phe-Gly motif rotates outward and exposes an adjacent hydrophobic pocket. The pyridinyl-pyrimidine hydrogen bonds to hinge residue Met318, the anilino NH engages the gatekeeper Thr315, the amide bridges Glu286 and Asp381, and the N-methylpiperazine makes solvent-front contacts. Trapping the kinase in this closed state abolishes autophosphorylation and substrate phosphorylation, collapsing RAS/MAPK, PI3K/AKT and STAT5 signalling and inducing apoptosis in driver-addicted cells.
Why does the T315I gatekeeper mutation abolish imatinib activity?
Threonine 315 guards the entrance to the hydrophobic back pocket and donates a key hydrogen bond to imatinib's anilino NH. Replacing it with isoleucine both removes that hydrogen bond and adds a bulky β-branched side chain that sterically blocks the binding pose. The result is profound resistance that dasatinib and nilotinib also cannot overcome. T315I is the textbook gatekeeper mutation in kinase pharmacology and motivated the development of ponatinib (a type II inhibitor with a triple-bond linker that threads past Ile315) and asciminib (an allosteric myristoyl-pocket binder).
How does imatinib compare with dasatinib and nilotinib?
Nilotinib is a structure-guided optimisation of imatinib: same DFG-out requirement, roughly 10-30 fold more potent, and active against many imatinib-resistant ABL mutants. Dasatinib is a chemically unrelated thiazolecarboxamide that binds both the active and inactive conformations, is substantially more potent, and additionally inhibits SRC-family kinases, BTK and TEC — broader coverage at the cost of selectivity. Imatinib remains the reference agent because of its narrow, well-mapped target spectrum and unmatched depth of clinical and mechanistic data. None of the three is active against T315I.
Why is imatinib active in GIST, and does the KIT genotype matter?
c-KIT (CD117) is structurally related to ABL and can also adopt the DFG-out state, so imatinib inhibits it directly. Roughly 80% of gastrointestinal stromal tumours carry activating KIT mutations and a further subset carry PDGFRA mutations. Genotype strongly predicts sensitivity: KIT exon 11 mutants are the most imatinib-sensitive, exon 9 mutants respond less well and often require higher exposure, and the PDGFRA D842V substitution is intrinsically resistant because it stabilises the active conformation that imatinib cannot bind.
How should imatinib free base be dissolved for in vitro work?
The free base dissolves in DMSO — gentle warming to 37 °C and brief sonication help — and in methanol; both are typically used for 10-50 mM stocks. It is only sparingly soluble in neutral water, so for aqueous work either use the mesylate salt or acidify the vehicle below pH 5.5. Dilute DMSO stocks into medium immediately before use and keep final DMSO ≤0.1% v/v. Note that imatinib binds strongly to alpha-1 acid glycoprotein, so serum content in the medium can shift apparent potency — keep serum concentration constant across comparisons.
What concentrations of imatinib are typically used in cell assays?
In BCR-ABL-driven lines such as K562 or BaF3/BCR-ABL, growth inhibition is usually seen between 0.1 and 1 µM, with complete CRKL dephosphorylation typically by 1 µM. For c-KIT and PDGFR readouts the working range is similar, around 0.1-1 µM. Concentrations above 10 µM begin to produce off-target effects and should be interpreted cautiously. Always include a BCR-ABL-negative control line to distinguish on-target from general cytotoxicity, and confirm target engagement by phospho-CRKL or phospho-KIT immunoblot.
What are the main mechanisms of imatinib resistance studied in the laboratory?
Four categories dominate: (1) kinase-domain point mutations — T315I, E255K/V, Y253H, M351T, F317L and others; (2) BCR-ABL gene amplification or overexpression; (3) altered drug transport, with reduced OCT1 (SLC22A1) influx and increased ABCB1/ABCG2 efflux; and (4) BCR-ABL-independent bypass signalling through SRC-family kinases, JAK/STAT, or leukaemic stem cell quiescence and bone-marrow niche protection. Imatinib is the standard selection agent used to generate and characterise resistant sublines.
What QC documentation is supplied, and are bulk quantities available?
Every lot ships with a Certificate of Analysis (COA) reporting HPLC purity (≥98%), 1H NMR structural confirmation and MS identity data; MSDS/SDS, residual-solvent data, water content and Certificates of Origin are available on request. Pack sizes run 1 g, 5 g, 10 g, 100 g and 1 KG, with the 1 KG tier produced to order on a campaign basis; conversion to the mesylate salt can be discussed for bulk programmes. For custom specifications or long-term supply agreements please contact our technical sales team.

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The reference BCR-ABL, c-KIT and PDGFR tyrosine kinase inhibitor — request your quote today

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