上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白,专注于信号通路和疾病研究领域。
PrNMI
PrNMI 是一种有效的、具有口服活性的外周限制性大麻素 1 受体 (CB1R) 激动剂。PrNMI 可抑制化疗引起的周围神经病变疼痛症状,并且还可作为癌症引起的骨痛的镇痛剂。
PrNMI Chemical Structure
CAS No. : 1541244-33-0
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是否有货 |
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100 mg |
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询价 |
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250 mg |
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询价 |
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500 mg |
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询价 |
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* Please select Quantity before adding items.
生物活性 |
PrNMI is a potent and orally active agonist of peripherally restricted cannabinoid 1 receptor (CB1R). PrNMI suppresses chemotherapy-induced peripheral neuropathy pain symptoms and also acts as an analgesic in cancer-induced bone pain[1][2].
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IC50 & Target |
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体外研究 (In Vitro) |
PrNMI (1 nM-1 μM; 24 hours) shows no effects on viability of 66.1 breast tumor cells in vitro[2].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[2]
Cell Line: |
66.1 breast cancer cell |
Concentration: |
1 nM, 10 nM, 100 nM, and 1 μM |
Incubation Time: |
24 hours |
Result: |
Showed no effects on viability of 66.1 breast tumor cells in vitro. |
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体内研究 (In Vivo) |
PrNMI (0.25 mg/kg; Intraplantar ipsilateral administration; i.p.) causes significantly greater suppression in mechanical but not cold allodynia on the ipsilateral paw compared to contralateral paw or systemic administration at 2 h post-PrNMI[1]. PrNMI (3.0 mg/kg; i.g.; 48 hours) dose-dependently suppresses CIPN symptoms in both male and female rats and is equally effective in male and female rats after oral administration[1]. PrNMI (1 mg/kg; p.o.; 48 hours) exhibits anti-allodynic effects in CIPN mediated mainly by CB1Rs[1]. PrNMI (1 mg/kg; p.o.; daily for two weeks) shows no significant tolerance to suppression of both mechanical and cold allodynia during the two-week testing period[1]. PrNMI (0.1, 0.3, and 0.6 mg/kg; i.p.) results in a significant, time-related reduction of flinching but not guarding in a dose-dependent manner. This suppression of flinching starts 1-hour post-injection and persists for at least 5 hours[2].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model: |
Chemotherapy-induced peripheral neuropathy (CIPN) rat model (Cisplatin; i.p.; daily 3 mg/kg for 4 weeks)[1] |
Dosage: |
0.25 mg/kg |
Administration: |
Intraplantar ipsilateral administration; i.p. |
Result: |
At 2 h post-PrNMI, mechanical but not cold allodynia suppression was significantly greater on the ipsilateral paw compared to contralateral paw or systemic administration. |
Animal Model: |
Chemotherapy-induced peripheral neuropathy (CIPN) rat model (i.p.; daily 3 mg/kg for 4 weeks)[1] |
Dosage: |
1 mg/kg |
Administration: |
p.o.; daily for two weeks |
Result: |
Suppressed mechanical and cold allodynia CIPN symptoms. |
Animal Model: |
18–20 g female BALB/cAnNHsd mice (bearing murine mammary tumor line, 66.1; CIBP model)[2] |
Dosage: |
0.1, 0.3, and 0.6 mg/kg |
Administration: |
i.p. |
Result: |
Resulted in a significant, time-related reduction of flinching but not guarding in a dose-dependent manner. This suppression of flinching started 1-hour post-injection and persisted for at least 5 hours. |
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Formula |
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运输条件 |
Room temperature in continental US; may vary elsewhere.
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储存方式 |
Please store the product under the recommended conditions in the Certificate of Analysis.
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参考文献 |
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[1]. Mulpuri Y, et al. Synthetic peripherally-restricted cannabinoid suppresses chemotherapy-induced peripheral neuropathy pain symptoms by CB1 receptor activation. Neuropharmacology. 2018;139:85-97.
[2]. Zhang H, et al. Peripherally restricted cannabinoid 1 receptor agonist as a novel analgesic in cancer-induced bone pain. Pain. 2018;159(9):1814-1823.
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