Sorafenib tosylate
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| Category | Antineoplastic |
| Catalog number | BBF-05857 |
| CAS | 475207-59-1 |
| Molecular Weight | 637.03 |
| Molecular Formula | C28H24ClF3N4O6S |
| Purity | ≥ 95% |
Ordering Information
| Catalog Number | Size | Price | Stock | Quantity |
|---|---|---|---|---|
| BBF-05857 | 50 g | $199 | In stock |
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Add to cartDescription
Sorafenib Tosylate (Bay 43-9006) is a multikinase inhibitor of Raf-1, B-Raf and VEGFR-2 with IC50 of 6 nM, 22 nM and 90 nM, respectively.
Specification
| Related CAS | 284461-73-0 (free base) |
| Synonyms | Sorafenib p-toluenesulfonate; BAY 43-9006 Mono-p-tosylate; BAY 54-9085; Nexavar(R); 1-(4-Chloro-3-(trifluoromethyl)phenyl)-3-(4-((2-(methylcarbamoyl)pyridin-4-yl)oxy)phenyl)urea mono(4-methylbenzenesulfonate); 2-Pyridinecarboxamide, 4-(4-((((4-chloro-3-(trifluoromethyl)phenyl)amino)carbonyl)amino)phenoxy)-N-methyl-, mono(4-methylbenzenesulfonate); Bay 43-9006 |
| Storage | 2-8 °C |
| IUPAC Name | 4-[4-[[4-chloro-3-(trifluoromethyl)phenyl]carbamoylamino]phenoxy]-N-methylpyridine-2-carboxamide;4-methylbenzenesulfonic acid |
| Canonical SMILES | CC1=CC=C(C=C1)S(=O)(=O)O.CNC(=O)C1=NC=CC(=C1)OC2=CC=C(C=C2)NC(=O)NC3=CC(=C(C=C3)Cl)C(F)(F)F |
| InChI | InChI=1S/C21H16ClF3N4O3.C7H8O3S/c1-26-19(30)18-11-15(8-9-27-18)32-14-5-2-12(3-6-14)28-20(31)29-13-4-7-17(22)16(10-13)21(23,24)25;1-6-2-4-7(5-3-6)11(8,9)10/h2-11H,1H3,(H,26,30)(H2,28,29,31);2-5H,1H3,(H,8,9,10) |
| InChI Key | IVDHYUQIDRJSTI-UHFFFAOYSA-N |
Properties
| Appearance | White to Off-white Solid |
| Antibiotic Activity Spectrum | Neoplastics (Tumor) |
| Boiling Point | 523.3 °C at 760 mmHg |
| Melting Point | 229-232 °C |
| Density | 1.454 g/cm3 (Predicted) |
| Solubility | Soluble in Methanol, DMSO, DMF |
Reference Reading
1.Targeted therapy for renal cell carcinoma: a new treatment paradigm.
Hutson TE Proc (Bayl Univ Med Cent). 2007 Jul;20(3):244-8.
Metastatic clear cell renal cell cancer has traditionally been treated with cytokines (interferon or interleukin-2). Improved understanding of biology has engendered novel targeted therapeutic agents that have altered the natural history of this disease. The vascular endothelial growth factor and its related receptor and the mTOR signal transduction pathway have particularly been exploited. Sunitinib malate, sorafenib tosylate, temsirolimus, and bevacizumab have improved clinical outcomes in randomized trials. Other multitargeted tyrosine kinase inhibitors (lapatinib, axitinib, pazopanib) and antiangiogenic agents (VEGF Trap, lenalidomide) have also demonstrated activity in early studies. Combinations of these agents are being evaluated. The future of the therapy of renal cancer appears promising owing to the efficacy of these novel agents.
2.Sorafenib and rapamycin induce growth suppression in mouse models of hepatocellular carcinoma.
Huynh H;Ngo VC;Koong HN;Poon D;Choo SP;Thng CH;Chow P;Ong HS;Chung A;Soo KC J Cell Mol Med. 2009 Aug;13(8B):2673-83. doi: 10.1111/j.1582-4934.2009.00692.x. Epub 2009 Feb 9.
Hepatocellular carcinoma (HCC) is the fifth most common malignancy worldwide. Vascular endothelial growth factor, platelet derived growth factor and the Raf/mitogen-activated protein kinase/extracellular signal regulated kinase (Raf/MEK/ERK) signalling pathway regulates the growth, neovascularization, invasiveness and metastatic potential of HCC. In this study, we investigated the in vivo antitumour activity and mechanisms of action of sorafenib tosylate on four patient-derived HCC xenografts. Sorafenib dosed at 50 mg/kg and 100 mg/kg inhibited tumour growth by 85% and 96%, respectively. Sorafenib-induced growth suppression and apoptosis were associated with inhibition of angiogenesis, down-regulation of phospho-platelet-derived growth factor receptor beta Tyr1021, phospho-eIF4E Ser209, phospho-c-Raf Ser259, c-Raf, Mcl-1, Bcl-2, Bcl-x and positive cell cycle regulators, up-regulation of apoptosis signalling kinase-1, p27 and p21. Expression of IGF-1Rbeta and phosphorylation of c-Raf Ser338, MEK1/2 Ser217/221 and ERK1/2 Thr202/Tyr204 were increased by sorafenib treatment. Phosphorylation of mammalian target-of-rapamycin (mTOR) targets (p70S6K, S6R and 4EBP1) was reduced by sorafenib in sorafenib-sensitive lines but activated in sorafenib-less-sensitive 10-0505 xenograft.
3.Renal cell carcinoma with an emphasis on drug therapy of advanced disease, part 1.
Cersosimo RJ Am J Health Syst Pharm. 2009 Sep 1;66(17):1525-36. doi: 10.2146/ajhp080387.p1.
PURPOSE: ;The diagnosis, staging, and management of renal cell carcinoma (RCC) are reviewed. The mechanism, pharmacokinetics, toxicity, clinical activity, and application of molecularly targeted agents in RCC are emphasized.;SUMMARY: ;RCC is the eighth most commonly diagnosed malignancy in the United States. The most common signs and symptoms are gross hematuria, flank pain, and the presence of a flank mass. Localized disease is found in about 55% of patients, 19% of patients have locally advanced disease, and 20% of patients have metastatic disease. Surgical resection is the mainstay of therapy for stage I-III RCC. The pharmacotherapy of RCC is undergoing significant change. Standard therapy used to include the cytokines interferon alfa and aldesleukin. High-dose aldesleukin is used to treat select patients. Its major value is the durability of responses in the few patients who achieve a complete remission. However, cytokines have been largely displaced by sorafenib tosylate, sunitinib malate, and temsirolimus due to their lower rates of toxicity and positive effects on progression-free survival. Bevacizumab has also shown activity in patients with advanced disease. Estimated five-year survival rates for patients with RCC are 89.
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
