G-36是一种具有细胞渗透性的G蛋白偶联雌激素受体（GPER/GPR30）拮抗剂，可抑制雌激素介导的钙动员（IC50=112nM）。
Cas No.:1392487-51-2
Sample solution is provided at 25 µL, 10mM.
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G-36 is a cell-permeable G protein-coupled estrogen receptor (GPER/GPR30) antagonist that inhibits estrogen-mediated calcium mobilization (IC50=112nM)[1-2]. G-36 can be used in research on cancer-related signaling pathways[3-4].
In vitro, pretreatment of human umbilical vein endothelial cells (HUVECs) with G-36 (1μM) completely blocked the ethinylestradiol (EE) and estetrol (E4) (1nM–100nM)-induced cell migration and inhibited the accumulation of phosphorylated focal adhesion kinase at tyrosine 397 (FAK Y397)[5]. Treatment of human cervical squamous cell carcinoma (CSCC) cell lines SiHa and C33A with G-36 (1–5μM) for 3 to 7 days had no significant effect on cell migration, colony formation, or tumor spheroid formation; however, treatment of SiHa cells with 2.5μM G-36 significantly increased the protein expression of plasminogen activator inhibitor-1 (PAI-1)[6].
In vivo, G-36 (0.5mg/kg) was co-administered with G-1 via intraperitoneal injection to high-fat diet (HFD)-fed C57BL/6 male mice (5 times per week for 5 weeks). G-36 blocked the protective effects of G-1 against HFD-induced obese asthma, reversing G-1's effects on airway hyperresponsiveness (AHR), pulmonary immune cell infiltration, tissue inflammation, fibrosis, mucus hypersecretion, increases in pro-inflammatory M1 macrophages, and decreases in anti-inflammatory M2 macrophages[7]. In ovariectomized C57Bl6 female mice, a single subcutaneous injection of G-36 (50μg/kg) blocked the G-1 (10μg/kg)-induced proliferation of uterine epithelial cells and significantly reduced the 17β-estradiol (E2; 10μg/kg)-induced proliferation[8].
References:
[1] Meyer MR, Barton M. GPER blockers as Nox downregulators: A new drug class to target chronic non-communicable diseases. J Steroid Biochem Mol Biol. 2018 Feb;176:82-87.
[2] Yu X, Stallone JN, Heaps CL, et al. The activation of G protein-coupled estrogen receptor induces relaxation via cAMP as well as potentiates contraction via EGFR transactivation in porcine coronary arteries. PLoS One. 2018 Jan 23;13(1):e0191418.
[3] Sharma G, Mauvais-Jarvis F, Prossnitz ER. Roles of G protein-coupled estrogen receptor GPER in metabolic regulation. J Steroid Biochem Mol Biol. 2018 Feb;176:31-37.
[4] Evans PD. Rapid signalling responses via the G protein-coupled estrogen receptor, GPER, in a hippocampal cell line. Steroids. 2019 Dec;152:108487.
[5] Dama A, Baggio C, Trevisi L, et al. Regulation of human endothelial cell migration by oral contraceptive estrogen receptor ligands. Eur J Pharmacol. 2023 Apr 15;945:175591.
[6] Rörig L, Ruckriegl S, Gallwas J, et al. G Protein-coupled Estrogen Receptor 1 (GPER1) Regulates Expression of SERPINE1/PAI-1 and Inhibits Tumorigenic Potential of Cervical Squamous Cell Carcinoma Cells In Vitro. Cancer Genomics Proteomics. 2025 Jan-Feb;22(1):13-23.
[7] Son SE, Im DS. Activation of G Protein-Coupled Estrogen Receptor 1 (GPER) Attenuates Obesity-Induced Asthma by Switching M1 Macrophages to M2 Macrophages. Int J Mol Sci. 2024 Sep 2;25(17):9532.
[8] Dennis MK, Field AS, Burai R, et al. Identification of a GPER/GPR30 antagonist with improved estrogen receptor counterselectivity. J Steroid Biochem Mol Biol. 2011 Nov;127(3-5):358-66.
G-36是一种具有细胞渗透性的G蛋白偶联雌激素受体（GPER/GPR30）拮抗剂，可抑制雌激素介导的钙动员（IC50=112nM）[1-2]。G-36可用于癌症相关的信号通路研究[3-4]。
在体外，G-36（1μM）预处理人脐静脉内皮细胞（HUVECs）6小时，可完全阻断由炔雌醇（EE）和雌四醇（E4）（1nM–100nM）所诱导的细胞迁移，并抑制磷酸化蛋白酪氨酸激酶2在酪氨酸397位点（FAK Y397）的积累[5]。G-36（1–5μM）处理人宫颈鳞状细胞癌（CSCC）细胞系SiHa和C33A细胞30至7天，对细胞的迁移能力、克隆形成以及肿瘤球形成均无显著影响；使用2.5μM G-36处理SiHa细胞，可显著增加其纤溶酶原激活物抑制剂-1（PAI-1）的蛋白表达[6]。
在体内，G-36（0.5mg/kg）与G-1共同腹腔注射处理高脂饮食（HFD）喂养的C57BL/6雄性小鼠（每周5次，持续5周）。G-36可阻断G-1对HFD诱导的肥胖性哮喘的保护作用，逆转G-1对气道高反应性（AHR）、肺部免疫细胞浸润、组织炎症、纤维化、粘液高分泌、促炎性M1巨噬细胞增多、抗炎性M2巨噬细胞减少[7]。G-36（50μg/kg；单次注射）通过皮下注射处理卵巢切除的C57Bl6雌性小鼠，可阻断G-1（10μg/kg）诱导的子宫上皮细胞增殖，并显著降低17β-雌二醇（E2；10μg/kg）诱导的增殖 [8]。
| Cell experiment [1]: | |
Cell lines | Human umbilical vein endothelial cells |
Preparation Method | HUVECs were grown in M199 medium supplemented with 15% FBS, ECGS, heparin, glutamine, and gentamicin. For experiments, cells were switched to phenol-free M199 medium with 5% FBS, ECGS, and heparin. HUVECs were treated with G-36 (1μM). |
Reaction Conditions | 1μM; 6h. |
Applications | G-36 completely abolished the enhancement of HUVEC migration induced by ethinylestradiol (EE) and estetrol (E4) in both scratch and Boyden chamber assays. G-36 also blocked the accumulation of phosphorylated FAK at tyrosine 397 (FAK Y397) induced by EE and E4. |
| Animal experiment [2]: | |
Animal models | Ovariectomized C57Bl6 female mice |
Preparation Method | Mice were ovariectomized at 10 weeks of age. At 12 days post-ovariectomy, mice were subcutaneously injected with G-36 (50μg/kg). Mice were sacrificed 18 hours after injection, and uterine epithelial proliferation was quantified by Ki-67 immunofluorescence. |
Dosage form | 50μg/kg; s.c.; single injection. |
Applications | G-36 completely abolished the G-1-induced proliferation of uterine epithelial cells and significantly reduced the E2-induced proliferation. G-36 alone had no effect on proliferation. |
References: | |
| Cas No. | 1392487-51-2 | SDF | |
| 化学名 | (3aS,4R,9bR)-4-(6-bromobenzo[d][1,3]dioxol-5-yl)-8-isopropyl-3a,4,5,9b-tetrahydro-3H-cyclopenta[c]quinoline | ||
| Canonical SMILES | CC(C1=CC([C@]2([H])C=CC[C@]2([H])[C@]3([H])C4=CC(OCO5)=C5C=C4Br)=C(N3)C=C1)C | ||
| 分子式 | C22H22BrNO2 | 分子量 | 412.33 |
| 溶解度 | 1/mL in ethanol, 20mg/mL in DMSO, 30mg/mL in DMF | 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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1 mg | 5 mg | 10 mg |
| 1 mM | 2.4252 mL | 12.1262 mL | 24.2524 mL |
| 5 mM | 485 μL | 2.4252 mL | 4.8505 mL |
| 10 mM | 242.5 μL | 1.2126 mL | 2.4252 mL |
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动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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