Benzydamine HCl是一种局部非甾体抗炎药，具有抗炎、镇痛、解热和局部麻醉活性。
Cas No.:132-69-4
Sample solution is provided at 25 µL, 10mM.
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Benzydamine HCl is a topical non-steroidal anti-inflammatory drug with anti-inflammatory, analgesic, antipyretic, and local anesthetic activities[1-2]. Benzydamine HCl alleviates inflammatory responses by inhibiting prostaglandin synthesis, stabilizing cell membranes, and suppressing the production of pro-inflammatory cytokines. Benzydamine HCl is used in studies related to oropharyngeal inflammation, postoperative pain, and radiotherapy-induced oral mucositis[3-4].
In vitro, Benzydamine HCl (6–50μM) was co-treated with LPS for 24h in human peripheral blood mononuclear cells (PBMCs) or for 6–24h in mouse peritoneal macrophages. Benzydamine HCl significantly inhibited TNF-α production and mildly suppressed IL-1β production[5]. Benzydamine HCl (1.0mg/mL) was incubated with Pseudomonas aeruginosa (PA) for 24h. Benzydamine HCl significantly inhibited the proliferation of PA[6].
In vivo, Benzydamine HCl (10mg/kg; administered twice on day 0 and day 2) was locally injected into the calvaria of C57BL/6 mice in an LPS-induced inflammatory bone destruction model, or administered intraperitoneally (six times per week for three weeks) in an ovariectomy (OVX)-induced postmenopausal osteoporosis model in C57BL/6 mice. Benzydamine HCl significantly reduced inflammation-induced calvarial bone destruction and osteoclast number, and reversed OVX-induced decreases in bone mineral density, bone volume, and other bone loss parameters[7]. Benzydamine HCl (10 or 20mg/kg; single injection) was subcutaneously injected either concurrently with or after (30min or 4h) LPS administration in an endotoxemia model in female Balb/c mice. Benzydamine HCl significantly increased the median lethal dose of LPS and, when given 30min or 4h after LPS injection, significantly decreased LPS-induced mortality in mice[8].
References:
[1] Zhang Y, Yang L, Gan Y, et al. Benzydamine attenuates microglia-mediated neuroinflammation and ischemic brain injury by targeting cathepsin s. Int Immunopharmacol. 2025 Jan 27;146:113824.
[2] Modéer T, Yucel-Lindberg T. Benzydamine reduces prostaglandin production in human gingival fibroblasts challenged with interleukin-1 beta or tumor necrosis factor alpha. Acta Odontol Scand. 1999 Feb;57(1):40-5.
[3] Zhou Y, He X, Jiang Y, et al. Repurposed benzydamine targeting CDK2 suppresses the growth of esophageal squamous cell carcinoma. Front Med. 2023 Apr;17(2):290-303.
[4] Yamazaki-Nishioka M, Shimizu M, Suemizu H, et al. Human plasma metabolic profiles of benzydamine, a flavin-containing monooxygenase probe substrate, simulated with pharmacokinetic data from control and humanized-liver mice. Xenobiotica. 2018 Feb;48(2):117-123.
[5] Sironi M, Pozzi P, Polentarutti N, et al. Inhibition of inflammatory cytokine production and protection against endotoxin toxicity by benzydamine. Cytokine. 1996 Sep;8(9):710-6.
[6] Fanaki NH, el-Nakeeb MA. Antimicrobial activity of benzydamine, a non-steroid anti-inflammatory agent. J Chemother. 1992 Dec;4(6):347-52.
[7] Son HS, Lee J, Lee HI, et al. Benzydamine inhibits osteoclast differentiation and bone resorption via down-regulation of interleukin-1 β expression. Acta Pharm Sin B. 2020 Mar;10(3):462-474.
[8] Guglielmotti A, Aquilini L, Rosignoli MT, et al. Benzydamine protection in a mouse model of endotoxemia. Inflamm Res. 1997 Sep;46(9):332-5.
Benzydamine HCl是一种局部非甾体抗炎药，具有抗炎、镇痛、解热和局部麻醉活性[1-2]。Benzydamine HCl可通过抑制前列腺素合成、稳定细胞膜并抑制促炎细胞因子产生来减轻炎症反应。Benzydamine HCl可用于口腔咽喉炎症、术后疼痛以及放疗引起的口腔黏膜炎的相关研究[3-4]。
在体外，Benzydamine HCl（6-50μM）与LPS共同处理人外周血单个核细胞（PBMC）24小时，或处理小鼠腹腔巨噬细胞6-24小时。Benzydamine HCl显著抑制TNF-α的产生，对IL-1β的产生有轻度抑制[5]。Benzydamine HCl（1.0mg/mL）孵育Pseudomonas aeruginosa（PA）24小时。Benzydamine HCl显著抑制PA的增殖[6]。
在体内，Benzydamine HCl（10mg/kg；在第0天和第2天共两次注射）通过颅骨局部注射于LPS诱导的炎症性骨破坏模型中的C57BL/6小鼠，或通过腹腔注射（每周六次；持续三周）于卵巢切除（OVX）诱导的绝经后骨质疏松模型中的C57BL/6小鼠。Benzydamine HCl显著减少了炎症引起的颅骨骨破坏和破骨细胞数量，并逆转了卵巢切除引起的骨密度下降、骨体积减少等骨质流失现象[7]。Benzydamine HCl（10或20mg/kg；单次注射）通过皮下注射，在LPS注射的同时或之后（30分钟或4小时）用于处理内毒素血症模型中的雌性Balb/c小鼠。Benzydamine HCl能显著提高LPS的半数致死剂量，并在LPS注射后30分钟或4小时给药，显著降低LPS诱导的小鼠死亡率[8]。
| Cell experiment [1]: | |
Cell lines | Human peripheral blood mononuclear cells (PBMC) and mouse peritoneal macrophages |
Preparation Method | Human PBMC were cultured in RPMI + 1% fetal calf serum (FCS). Mouse peritoneal macrophages were cultured in RPMI-1640 medium + 1% FCS. Cells were treated with Benzydamine HCl (6-50μM) simultaneously with the stimulus (LPS or inactivated streptococci). |
Reaction Conditions | 6-50μM; 6-24 hours. |
Applications | Benzydamine HCl significantly inhibited the production of tumour necrosis factor-alpha (TNF-α) by LPS-stimulated human monocytes. Benzydamine HCl showed a modest or no effect on the production of interleukin (IL)-1, IL-6 and IL-8. Benzydamine HCl also significantly inhibited TNF-α and IL-6 production by mouse peritoneal macrophages stimulated with LPS in vitro. The inhibition of TNF-α production was associated with a modest reduction of its mRNA level, but no alteration of its mRNA half-life. |
| Animal experiment [2]: | |
Animal models | Female Balb/c mice (18-20g) |
Preparation Method | Endotoxic shock was induced by an intraperitoneal (i.p.) injection of Lipopolysaccharide (LPS). For therapeutic studies, Benzydamine HCl (10-20mg/kg) was administered subcutaneously (s.c.) either 30min or 4 hours after the endotoxin injection. Mortality was assessed daily and mice were followed for 8 days |
Dosage form | 10-20mg/kg; s.c.; single injection at specified time points after LPS. |
Applications | Benzydamine HCl administered simultaneously with LPS, significantly increased the LPS LD50. When administered 30min or 4 hours after an LD100 dose of LPS, Benzydamine HCl significantly protected mice against LPS-induced lethality. Therapeutic administration (4 hours post-LPS) also significantly reduced TNFα and IL-1β levels in serum and TNFα levels in lung homogenate. |
References: | |
| Cas No. | 132-69-4 | SDF | |
| 别名 | 盐酸苄达明 | ||
| 化学名 | 3-(1-benzylindazol-3-yl)oxy-N,N-dimethylpropan-1-amine;hydrochloride | ||
| Canonical SMILES | CN(C)CCCOC1=NN(C2=CC=CC=C21)CC3=CC=CC=C3.Cl | ||
| 分子式 | C19H23N3O.HCl | 分子量 | 345.87 |
| 溶解度 | ≥ 17.05mg/mL in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.8913 mL | 14.4563 mL | 28.9126 mL |
| 5 mM | 578.3 μL | 2.8913 mL | 5.7825 mL |
| 10 mM | 289.1 μL | 1.4456 mL | 2.8913 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
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- Purity: >98.00% Appearance: A solid
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