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| Targets |
G-1 targets the G protein-coupled estrogen receptor 1 (GPER/GPR30), a membrane receptor that mediates estrogen signaling. GPER is involved in various physiological processes, including cell proliferation, migration, and apoptosis. By binding to GPER with a Ki of 11 nM, G-1 activates downstream signaling pathways, including calcium mobilization and MAPK activation. Its selectivity for GPER over classical estrogen receptors makes it a valuable tool for studying GPER biology.
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| ln Vitro |
G-1 is a selective GPR30 coagulant that has a high affinity and is nonsteroidal, with a Ki of 11 nM [1]. G-1 treatment (10 μM and 100 μM) for 48 and 72 hours dramatically inhibited cell proliferation (P<0.001). G-1's IC50 value at 72 hours was determined to be 20 μM. G-1 treatment of A549 cells at a dose of 20 μM resulted in a considerable increase in cells and a persistent anti-proliferative impact (P<0.001). After receiving G-1 therapy for 24 hours, cell cycle examination of H295R cells revealed that the cells were in the G2 phase of their life cycle. G-1 decreases Bcl-2 while also expressing Bax[3].
In vitro, G-1 is a potent and selective GPER agonist with a Ki of 11 nM and an EC50 of 2 nM. It increases cytosolic Ca2+ and inhibits migration of SKBr3 and MCF-7 cells in response to chemoattractants with IC50s of 0.7 and 1.6 nM, respectively. G-1 treatment (10 and 100 μM) for 48 and 72 hours significantly inhibits cell proliferation. It induces cell cycle arrest, DNA damage, and cell death by activating the intrinsic apoptotic mechanism in H295R cells. |
| ln Vivo |
The Basso S Scale (BMS) score of the G-1 group was substantially greater (P<0.05) than that of the other groups, according to the results obtained 14 days after the injury. This group had fewer positive cells than the other groups (P<0.05), and there was no difference when compared (P>0.05)[1]. Beginning on day 14 of therapy, the G-1 medication resulted in a statistically significant decrease in the volume of the tumor, and after three weeks of treatment, the tumor weight of transplanted tumors was significantly lower than that of animals receiving a vehicle treatment [3].
In vivo, G-1 has demonstrated antineoplastic, antihypertensive, and anti-obesity effects. As a GPER agonist, it modulates estrogen signaling through this receptor. Its effects on cancer cell growth and migration have been observed in preclinical models. The compound's in vivo efficacy supports its potential for therapeutic applications. Specific dosing regimens and detailed efficacy data are available in the scientific literature. |
| Enzyme Assay |
In vitro receptor binding assays for G-1 involve measuring its binding affinity to GPER using radioligand binding assays. Membranes from cells expressing GPER are incubated with radiolabeled estradiol and varying concentrations of G-1. The Ki value of 11 nM is determined from competition binding curves. Selectivity against ERα and ERβ is assessed using similar assays. Functional activity is assessed by measuring calcium mobilization or other downstream signaling events.
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| Cell Assay |
In vitro cell-based assays for G-1 involve treating cells expressing GPER with the compound to assess its effects on cell proliferation, migration, and signaling. Cell migration is assessed using Transwell or wound healing assays. Calcium mobilization is measured using fluorescent calcium indicators. Cell proliferation is measured using MTT or similar assays. Apoptosis is quantified by flow cytometry. These assays characterize the compound's GPER agonist activity.
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| Animal Protocol |
In vivo animal experiments for G-1 have been conducted in models of cancer, hypertension, and obesity. The compound is typically administered via injection. Efficacy endpoints depend on the specific model being studied. Its effects on tumor growth, blood pressure, and body weight have been evaluated. These studies support the compound's potential therapeutic applications.
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| ADME/Pharmacokinetics |
G-1 has a molecular weight of 392.27 and a molecular formula of C21H18BrNO2. It is a nonsteroidal, high-affinity, and selective GPER agonist. The compound is typically dissolved in DMSO for in vitro studies and formulated for in vivo administration. Its pharmacokinetic properties have been characterized in preclinical studies. It is typically stored under recommended conditions for research compounds.
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| Toxicity/Toxicokinetics |
Specific toxicity data for G-1 is not extensively reported. As a GPER agonist, its safety profile is related to its effects on estrogen signaling through this receptor. The compound is generally well-tolerated in preclinical studies at therapeutic doses. Comprehensive toxicological studies would be required for therapeutic development. Standard safety precautions should be taken when handling the compound.
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| References |
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| Additional Infomation |
G-1 is an agonist. LNS8801, a G protein-coupled estrogen receptor agonist, is a highly bioavailable, selective G protein-coupled estrogen receptor (G protein-coupled estrogen receptor 1; GPER; GPER1; GPR30) agonist with potential immunomodulatory and antitumor activities. After oral administration, LNS8801 targets, binds to, and activates GPER. This activates GPER-mediated signaling pathways and inhibits the expression of various tumor-related genes, such as c-Myc and programmed death-ligand 1 (PD-L1). This leads to suppression of tumor cell proliferation. Activation of GPER may also induce immune memory. GPER is a membrane protein belonging to the G protein-coupled receptor (GPCR) family, which is widely distributed in various tissues. GPER plays a tumor-suppressive role in various cell carcinoma types.
G-1 is a potent and selective GPER/GPR30 agonist with a Ki of 11 nM and an EC50 of 2 nM. It is a nonsteroidal compound that displays no activity at ERα and ERβ. G-1 increases cytosolic Ca2+, inhibits cell migration, and induces apoptosis. It has antineoplastic, antihypertensive, and anti-obesity effects. The compound is a valuable tool for studying GPER biology. |
| Molecular Formula |
C21H18BRNO3
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| Molecular Weight |
412.28
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| Exact Mass |
411.046
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| Elemental Analysis |
C, 61.18; H, 4.40; Br, 19.38; N, 3.40; O, 11.64
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| CAS # |
881639-98-1
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| PubChem CID |
5322399
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| Appearance |
White to off-white solid powder
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| Density |
1.5±0.1 g/cm3
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| Boiling Point |
529.6±50.0 °C at 760 mmHg
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| Flash Point |
274.1±30.1 °C
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| Vapour Pressure |
0.0±1.4 mmHg at 25°C
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| Index of Refraction |
1.637
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| LogP |
4.37
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
4
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| Rotatable Bond Count |
2
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| Heavy Atom Count |
26
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| Complexity |
596
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| Defined Atom Stereocenter Count |
3
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| SMILES |
BrC1C=C2OCOC2=CC=1[C@@H]1NC2C=CC(=CC=2[C@@H]2C=CC[C@H]12)C(=O)C
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| InChi Key |
VHSVKVWHYFBIFJ-HKZYLEAXSA-N
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| InChi Code |
InChI=1S/C21H18BrNO3/c1-11(24)12-5-6-18-15(7-12)13-3-2-4-14(13)21(23-18)16-8-19-20(9-17(16)22)26-10-25-19/h2-3,5-9,13-14,21,23H,4,10H2,1H3/t13-,14+,21-/m1/s1
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| Chemical Name |
1-[(3aS,4R,9bR)-4-(6-bromo-1,3-benzodioxol-5-yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta[c]quinolin-8-yl]ethanone
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| Synonyms |
G1; G 1; G-1
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| HS Tariff Code |
2934.99.03.00
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~50 mg/mL (~121.28 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (6.06 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: 2.5 mg/mL (6.06 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (6.06 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.4255 mL | 12.1277 mL | 24.2554 mL | |
| 5 mM | 0.4851 mL | 2.4255 mL | 4.8511 mL | |
| 10 mM | 0.2426 mL | 1.2128 mL | 2.4255 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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