SR 59230A hydrochloride
目录号 : GC12227
SR 59230A hydrochloride是一种高效、选择性的β3-肾上腺素受体拮抗剂，对β3、β1和β2受体的IC50值分别为40nM、408nM和648nM。
Cas No.:1135278-41-9
Sample solution is provided at 25 µL, 10mM.
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SR 59230A hydrochloride is a potent and selective β3-adrenoceptor antagonist, with IC50 values of 40, 408, and 648nM for β3-, β1-, and β2-receptors, respectively [1]. SR 59230A hydrochloride is a novel inhibitor of the Kir2.1 channel, with an IC50 value of 33μM[2]. SR 59230A hydrochloride inhibits the phosphorylation and thereby the activation of the mTOR/p70S6K pathway, crosses the blood-brain barrier, and acts on β3 adrenoceptors[3-4]. SR 59230A hydrochloride has been widely used to inhibit cancer cell progression and to develop novel combination therapies[5].
In vitro, SR 59230A hydrochloride treatment for 72 hours significantly inhibited the proliferation of HUVEC, BRAF mutated 8505 C thyroid carcinoma cells, and U-87 cells with IC50 values of 6.45µM, 13.09µM, and 18.21µM, respectively[6]. Treatment with 10µM SR 59230A hydrochloride for 48 hours induced apoptosis in K562, KCL22, HEL and HL60 cells under hypoxic conditions (1% O2)[7].
In vivo, SR 59230A hydrochloride treatment via continuous intratumoral injection at a dose of 5mg/kg for 8 consecutive days led to a significant reduction in tumor volume and weight in the melanoma mouse model, and inhibited angiogenesis[8]. For a period of 5 weeks, 50µg of SR 59230A hydrochloride (dissolved in DMSO) was injected into the tail vein every 3 days, which significantly inhibited the growth of breast cancer xenograft tumors in mice and reduced the expressions of p-mTOR S2448, p-4E-BP1 (T37/46), and p-mTOR S2481[9].
References:
[1] Kanzler S A, Januario A C, Paschoalini M A. Involvement of β3-adrenergic receptors in the control of food intake in rats[J]. Brazilian Journal of Medical and Biological Research, 2011, 44: 1141-1147.
[2] Kulzer M, Seyler C, Welke F, et al. Inhibition of cardiac Kir2. 1–2.3 channels by beta3 adrenoreceptor antagonist SR 59230A[J]. Biochemical and Biophysical Research Communications, 2012, 424(2): 315-320.
[3] Deng J, Jiang P, Yang T, et al. Targeting β3-adrenergic receptor signaling inhibits neuroblastoma cell growth via suppressing the mTOR pathway[J]. Biochemical and Biophysical Research Communications, 2019, 514(1): 295-300.
[4] Lob H E, Song J, Hurr C, et al. Deletion of p22phox-dependent oxidative stress in the hypothalamus protects against obesity by modulating β3-adrenergic mechanisms[J]. JCI insight, 2017, 2(2): e87094.
[5] Ascone M, Banella C, Amato R, et al. Abstract A048 SR 59230A hydrochloride-induced ferroptosis sensitization of Ewing sarcoma cells via Beta-3 adrenergic receptor modulation: A novel therapeutic target[J]. Cancer Research, 2024, 84(17_Supplement): A048-A048.
[6] Bandini A, Biso L, Viaggi C, et al. Synergistic combination of the adrenergic antagonist SR 59230A hydrochloride with common chemotherapeutic drugs and target therapies in cancer and endothelial cells[J]. Investigational New Drugs, 2025: 1-11.
[7] Calvani M, Dabraio A, Bruno G, et al. β3-adrenoreceptor blockade reduces hypoxic myeloid leukemic cells survival and Chemoresistance[J]. International Journal of Molecular Sciences, 2020, 21(12): 4210.
[8] Dal Monte M, Casini G, Filippi L, et al. Functional involvement of β3-adrenergic receptors in melanoma growth and vascularization[J]. Journal of molecular medicine, 2013, 91(12): 1407-1419.
[9] Zhou Z, Zhan J, Luo Q, et al. ADRB3 induces mobilization and inhibits differentiation of both breast cancer cells and myeloid-derived suppressor cells[J]. Cell Death & Disease, 2022, 13(2): 141.
SR 59230A hydrochloride是一种高效、选择性的β3-肾上腺素受体拮抗剂，对β3、β1和β2受体的IC50值分别为40nM、408nM和648nM[1]。SR 59230A hydrochloride是Kir2.1通道的新型抑制剂，IC50值为33μM[2]。SR 59230A hydrochloride能通过抑制mTOR/p70S6K通路的磷酸化以阻断活化，并能穿过血脑屏障，作用于β3 肾上腺素受体[3-4]。SR 59230A hydrochloride已广泛应用于抑制癌细胞进展及开发新型联合疗法[5]。
在体外，SR 59230A hydrochloride处理72小时可显著抑制HUEVC、BRAF突变甲状腺癌细胞和U-87细胞的增殖，IC50值分别为6.45µM、13.09µM和18.21µM[6]。在低氧条件下，使用10µM的SR 59230A hydrochloride处理K562、KCL22、HEL和HL60细胞48小时，能在缺氧条件下（1% O2）诱导细胞凋亡[7]。
在体内，连续9日每日瘤内注射5mg/kg剂量的SR 59230A hydrochloride，可显著缩小黑色素瘤小鼠模型的肿瘤体积和重量，并抑制血管生成[8]。每3日尾静脉注射50µg剂量的的SR 59230A hydrochloride（溶于DMSO）连续5周，能显著抑制乳腺癌移植瘤在小鼠体内的生长，并降低p-mTOR S2448、p-4E-BP1(T37/46)和p-mTOR S2481的表达水平[9]。
| Cell experiment [1]: | |
Cell lines | Human umbilical vein endothelial cells (HUVECs) |
Preparation Method | HUVECs were cultured in MCDB131 medium supplemented with 10% heat-inactivated fetal bovine serum, 2mM L-glutamine, 10U/ml heparin, 10ng/ml epidermal growth factor (EGF), and 5ng/ml basic fibroblast growth factor, at 37 °C, 5% CO2, and 95% humidity. The cells (2×104) were seeded in 24-well sterile plastic plates and allowed to adhere overnight. The cells were treated with SR 59230A hydrochloride (0.001, 0.1, 1, 10, and 100μM) for 72 hours, or treated with solvent as a control to assess cell viability. |
Reaction Conditions | 0.001, 0.1, 1, 10, and 100μM; 72h |
Applications | SR 59230A hydrochloride treatment inhibited the cell viability of HUVECs cells in a dose-dependent manner. |
| Animal experiment [2]: | |
Animal models | Male C57BL/6J mice |
Preparation Method | Fifty male C57BL/6J mice (8 weeks old) were raised in a standard environment. The mice were injected with B16F10 cells and then received either SR 59230A hydrochloride or L-748,337 treatment. SR 59230A hydrochloride and L-748,337 were injected intratumorally at a dose of 5mg/kg/day. The treatment began on the 10th day (D10) after tumor cell injection and continued until D18. The length (L) and width (W) of the tumors were measured daily using a vernier caliper, and the tumor volume was calculated as the formula L×W2×0.5. |
Dosage form | 5mg/kg/day for 9 days; intratumoral injection |
Applications | SR 59230A hydrochloride treatment decreases the growth of melanoma in xenograft mouse model of B16F10 cells. |
References: | |
| Cas No. | 1135278-41-9 | SDF | |
| 化学名 | (S)-1-(2-ethylphenoxy)-3-(((S)-1,2,3,4-tetrahydronaphthalen-1-yl)amino)propan-2-ol hydrochloride | ||
| Canonical SMILES | O[C@H](COC1=CC=CC=C1CC)CN[C@H]2CCCC3=CC=CC=C23.Cl | ||
| 分子式 | C21H27NO2.HCl | 分子量 | 361.91 |
| 溶解度 | DMSO: 100 mM,Water: 10 mM | 储存条件 | Store at 4°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 | 2.7631 mL | 13.8156 mL | 27.6312 mL |
| 5 mM | 552.6 μL | 2.7631 mL | 5.5262 mL |
| 10 mM | 276.3 μL | 1.3816 mL | 2.7631 mL |
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| 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。
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- Purity: >98.00%
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