Sunitinib malate is the salt form of SU11248, the oxindole kinase inhibitor Pfizer sells as Sutent. CAS 341031-54-7 belongs to the salt; the free base has its own number, and confusing them is the first trap.
The Sunitinib malate chemical structure pairs one molecule of drug with one of L-malic acid. A fluorinated oxindole joins through a Z-configured methylidene bridge to a dimethylpyrrole carboxamide ending in a basic diethylaminoethyl tail, pKa near 8.95, which takes the malate counterion.
Salt formation is not cosmetic: it lifts aqueous solubility above 25 mg/mL from pH 1.2 to 6.8, which is why an oral drug exists. Sunitinib malate has an average molecular weight of approximately 532.56 g/mol, compared with 398.48 g/mol for the Sunitinib free base, making the salt only about 75% drug by mass. Catalogs cross-reference it as PF-00262192.
Application of Sunitinib malate
Most orders come down to two motives: a dependable antiangiogenic control, or the material that went into patients.
As a control it is hard to beat: two decades of published data anchor its behaviour, so any xenograft or endothelial proliferation assay including it carries a built-in sanity check.
The salt form matters for anyone modelling clinical exposure, since this is what Sutent is. Which leads to the error worth flagging. Weighing 50 mg/kg of the malate delivers only about 37 mg/kg of drug; hitting 50 mg/kg of base takes roughly 67 mg/kg of salt. Skip that arithmetic and you underdose by a quarter.
Breadth is the other double edge. Hitting VEGFR, PDGFR, KIT, FLT3, CSF1R and RET at once is why the compound works clinically and why it cannot tell you which kinase produced your phenotype, so pair it with a selective inhibitor when that matters. Groups working on ER stress should note an off-target hit on IRE1alpha autophosphorylation. It also ships as a dangerous good, so order early.
In Vitro
Binding sits low nanomolar across the panel: Ki values of 2, 9 and 17 nM for VEGFR-1, -2 and -3, 8 nM for PDGFRbeta, 4 nM for KIT. In cells, Sunitinib malate blocks VEGF-driven VEGFR2 and PDGF-driven PDGFRbeta phosphorylation near 10 nM. FLT3 needs about 250 nM, yet the ITD mutant falls at 50 nM. HUVEC proliferation supplies an internal control: VEGF-driven growth stops near 30 nM, FGF-driven needs 700 nM, so the effect tracks the pathway, not toxicity.
In Vivo
Oral dosing at 20 to 80 mg/kg daily slows tumour growth in many mouse xenografts. The Mendel work behind them did more than report efficacy: it tied plasma exposure to receptor phosphorylation in tumour tissue, giving a pharmacokinetic and pharmacodynamic relationship later studies could dose against. Sunitinib malate went on to approval in renal cell carcinoma, GIST after imatinib failure, and pancreatic neuroendocrine tumours.
Biochemical and Physiological Actions
The oxindole of the Sunitinib malate structure fills the ATP pocket and hydrogen bonds to the hinge, making inhibition ATP-competitive. Its targets cluster in the class III and IV split-kinase-domain receptors, sharing enough pocket architecture to be caught together. EGFR, CDK2, MET, IGF1R, ABL and SRC are tenfold less sensitive at least.
That set produces two effects at once. On tumour cells driven by mutant KIT or FLT3 it hits the oncogene directly; on endothelium and pericytes it starves the tumour by cutting VEGFR and PDGFR signalling. Renal cell carcinoma responds because both arms apply.
Features and Benefits of Sunitinib malate
Sunitinib malate earns shelf space on concrete grounds:
- Nanomolar potency across a defined receptor panel.
- Aqueous solubility that supports oral dosing.
- The clinical salt form, matching decades of translational work.
- Supplied at 95% purity, with purity validated by NMR and/or LCMS methods for research use under agreement with Pfizer Inc.
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