- ￥553 - 840
- AmBeed
- A423772
- 2026年05月28日
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- 技术资料
- 英文名：
(S)-2-((4-((2-Fluorobenzyl)oxy)benzyl)amino)propanamide methanesulfonate
- 供应商：
上海安毕达生物科技有限公司
- CAS号：
202825-45-4
- 规格：
50mg/100mg
| 规格： | 50mg | 产品价格： | ￥553.0 |
|---|---|---|---|
| 规格： | 100mg | 产品价格： | ￥840.0 |
Ralfinamide mesylate is an orally available Na+ channel blocker derived from α-aminoamide, with function of suppressing pain. Ralfinamide (30 mg/kg, 60 mg/kg; p.o.; twice daily; 42 days) treated with Ralfinamide (80 mg/kg; p.o.; twice daily; 7 days) preoperatively suppresses neuropathic pain1. Ralfinamide inhibition was voltage-dependent showing highest potency towards inactivated channels. IC50 values for tonic block of half-maximal inactivated tetrodotoxin-resistant and tetrodotoxin-sensitive currents were 10 microM and 22 microM2. Oral ralfinamide dose-dependently alleviated spared nerve injury-induced allodynia in rats and mice. Ralfinamide increased mechanical withdrawal thresholds in oxaliplatin-induced and paclitaxel-induced neuropathic pain. Ralfinamide did not affect physiological pain, locomotion, or cardiovascular function3. Ralfinamide (25 microM) suppressed afferent hyperexcitability selectively in capsaicin-responsive, presumably nociceptive neurons, but had no measurable effects on firing in CAPS-unresponsive neurons4.
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文献和实验Stummann TC, Salvati P, Fariello RG, Faravelli L. The anti-nociceptive agent ralfinamide inhibits tetrodotoxin-resistant and tetrodotoxin-sensitive Na+ currents in dorsal root ganglion neurons. Eur J Pharmacol. 2005 Mar 14;510(3):197-208
Liang X, Yu G, Su R. Effects of ralfinamide in models of nerve injury and chemotherapy-induced neuropathic pain. Eur J Pharmacol. 2018 Mar 15;823:27-34
Yamane H, de Groat WC, Sculptoreanu A. Effects of ralfinamide, a Na+ channel blocker, on firing properties of nociceptive dorsal root ganglion neurons of adult rats. Exp Neurol. 2007 Nov;208(1):63-72
Detection of BCR-ABL Mutations and Resistance to Imatinib Mesylate
The major mechanism of imatinib resistance for patients with chronic myeloid leukemia (CML) is clonal expansion of leukemic cells with mutations in the Bcr-Abl fusion tyrosine kinase that reduce the capacity of imatinib to inhibit kinase
-4 and C-5 centers ( 3 ). After formatron of the mesylate, from the recycled material the amine function is introduced through azrde displacement of the mesylate, followed by reduction ( 4 ) and protectron with the t -BOC group. Finally, the lactone
Inhibitors of Cellular Signaling Targets: Designs and Limitations
. Because of their central role in cellular signaling, as well as their primary role in disease progression, protein kinases are attractive therapeutic targets (2 ,3 ). Seven molecules targeting protein kinases, imatinib mesylate (Gleevec) and trastuzumab (Herceptin
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