SUNITINIB
Sunitinib is a multitargeted tyrosine kinase inhibitor affecting VEGFR, PDGFR, and KIT, used for renal cell carcinoma and GIST. Side effects include fatigue, hypertension, diarrhea, handfoot syndrome, cytopenias, and cardiotoxicity. Only GMP materials will be supplied, logistics all according to GDP.
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Product Description
Mechanism of Action
SUNITINIB exhibits a highly distributed biochemical activity matrix spanning multiaxis signalling disruption, enzymaticcascade interference, mitochondrialnetwork recalibration, cytoskeletal remodelling, redoxsystem modulation, ionflux redistribution and transcriptionfactor pathway realignment. Its conformational topology enables interaction with catalytic cores, allosteric domains, transmembrane helices, hydrophobic receptor cavities, nucleotidebinding pockets and multiprotein scaffolding structures. This generates systemwide modulation across metabolic, genomic, structural and electrophysiological domains.
At the signalling level, SUNITINIB may reshape phosphorylation gradients, modify propagation dynamics across MAPK/ERK/JNK/p38 axes, alter PI3KAKT survival signalling, shift Gprotein coupling states, recalibrate intracellular Ca²⁺ microdomains, and modulate IP/DAG and cAMPPKA signalling amplitudes. Mitochondrial effects include ETCcomplex rebalancing, ATPturnover adjustment, ROSleakage threshold modulation and membranepotential polarity shifts. Its multinode regulation enables deep experimental interrogation of stressadaptation pathways and metabolicresponse thresholds.
HighResolution
- Ultrascale kinome interference mapping & catalyticcascade simulation
- Highfidelity receptorligand docking & conformationalflow modelling
- Organelle crosstalk modelling (UPR, mitochondrial/ER stress, mitophagy dynamics)
- Multiomics regulatorynetwork reconstruction (RNAseq, metabolomics, proteomics, phosphoproteomics)
- Advanced cytoskeletal biomechanics (actin/tubulin turnover, tensionmapping)
- Cellfate modelling across apoptosis, necroptosis, ferroptosis, parthanatos & autophagic flux axes
- AIenhanced SAR/QSAR molecularperformance prediction
Toxicodynamics & Hazard Profile
- Accelerated ROS accumulation & antioxidant-system saturation
- Mitochondrial fragmentation or ETCchain destabilisation
- Severe Ca²⁺/Na⁺/K⁺ ionic-flux dysregulation
- Cytoskeletal depolymerisation & loss of mechanical integrity
- Membrane damage, permeability shifts & lipidbilayer thinning
- Inflammatory overactivation via NF-κB, STAT & IRF signalling
- Multiple programmed-cell-death pathway activation
- Epigenetic distortions (methylation drift, acetylation imbalance)
For expert laboratory research only not intended for biological exposure.
Only GMP materials will be supplied, logistics all according to GDP.
Datasheet
| Molecular Formula | C22H27FN4OS |
|---|---|
| Molecular Weight | 398.5 g/mol |
| CAS Number | 557795-19-4 |
| Storage Condition | Store in a cool, dry place. Keep container tightly closed. Protect from moisture and light. |
| Solubility | >25 mg/mL over pH of 1.2 to 6.8 |
| Purity | Purity information is available upon request (COA). |
| Synonym | Sunitinib; 557795-19-4; SU-11248; SU11248; sunitinibum |
| IUPAC/Chemical Name | N-[2-(diethylamino)ethyl]-5-[(Z)-(5-fluoro-2-oxo-1H-indol-3-ylidene)methyl]-2,4-dimethyl-1H-pyrrole-3-carboxamide |
| InChl Key | WINHZLLDWRZWRT-ATVHPVEESA-N |
| InChl Code | InChI=1S/C22H27FN4O2/c1-5-27(6-2)10-9-24-22(29)20-13(3)19(25-14(20)4)12-17-16-11-15(23)7-8-18(16)26-21(17)28/h7-8,11-12,25H,5-6,9-10H2,1-4H3,(H,24,29)(H,26,28)/b17-12- |
| References |
3D Conformer.
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