97075-46-2
Chemical Structure
AMN082
- CAS No.: 97075-46-2
- Formula:C28H30Cl2N2
- Molecular Weight:465.46
IUPAC Name: N1,N2-dibenzhydrylethane-1,2-diamine dihydrochloride
InChIKey: YRQCDCNQANSUPB-UHFFFAOYSA-N
SMILES: [H]Cl.[H]Cl.C(NCCNC(C1=CC=CC=C1)C2=CC=CC=C2)(C3=CC=CC=C3)C4=CC=CC=C4
Biological Activity: AMN082, a selective, orally active, and brain penetrant mGluR7 agonist, directly activates receptor signaling via an allosteric site in the transmembrane domain. AMN082 potently inhibits cAMP accumulation and stimulates GTPγS binding (EC50 values, 64-290 nM) at transfected mammalian cells expressing mGluR7. AMN082 shows selectivity over other mGluR subtypes and selected ionotropic glutamate receptors. Antidepressant effects[1][2].
| Cat. No. | Nom du produit | Pureté | Description | Pricing | |||||||||||||||||||
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AMN082 | 99.73% | AMN082, a selective, orally active, and brain penetrant mGluR7 agonist, directly activates receptor signaling via an allosteric site in the transmembrane domain. AMN082 potently inhibits cAMP accumulation and stimulates GTPγS binding (EC50 values, 64-290 nM) at transfected mammalian cells expressing mGluR7. AMN082 shows selectivity over other mGluR subtypes and selected ionotropic glutamate receptors. Antidepressant effects. | ||||||||||||||||||||
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AMN082 (Standard) | ≥98% | AMN082 (Standard) is the analytical standard of AMN082. This product is intended for research and analytical applications. AMN082, a selective, orally active, and brain penetrant mGluR7 agonist, directly activates receptor signaling via an allosteric site in the transmembrane domain. AMN082 potently inhibits cAMP accumulation and stimulates GTPγS binding (EC50 values, 64-290 nM) at transfected mammalian cells expressing mGluR7. AMN082 shows selectivity over other mGluR subtypes and selected ionotropic glutamate receptors. Antidepressant effects. | ||||||||||||||||||||
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Cetirizine Impurity D (Standard) | ≥98% | Cetirizine Impurity D (Standard) is the analytical standard of Cetirizine Impurity D. This product is intended for research and analytical applications. Cetirizine Impurity D is an impurity of Cetirizine. Cetirizine, a second-generation antihistamine, is a specific, orally active and long-acting histamine H1-receptor antagonist. Cetirizine marks antiallergic properties and inhibits eosinophil chemotaxis during the allergic response. | ||||||||||||||||||||
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AMN082 free base (Standard) | ≥98% | AMN082 (free base) (Standard) is the analytical standard of AMN082 (free base). This product is intended for research and analytical applications. AMN082 free base, a selective, orally active, and brain penetrant mGluR7 agonist, directly activates receptor signaling via an allosteric site in the transmembrane domain. AMN082 free base potently inhibits cAMP accumulation and stimulates GTPγS binding (EC50 values, 64-290 nM) at transfected mammalian cells expressing mGluR7. AMN082 free base shows selectivity over other mGluR subtypes and selected ionotropic glutamate receptors. Antidepressant effects. | ||||||||||||||||||||
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UCL 2077 | 98.91% | UCL 2077 is a potassium channel and slow afterhyperpolarization (sAHP) inhibitor. UCL 2077 selectively blocks sAHP channels without affecting L-type Ca2+ currents. UCL 2077 blocks KCNQ1- and KCNQ2-containing K+ channels, decreases erg current amplitude, increases erg deactivation rate. UCL 2077 can be used for the research of hippocampus-dependent memory retrieval deficit and cardiac arrhythmias. | ||||||||||||||||||||
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NP118809 | 98.73% | NP118809 is a potent N-type calcium channel blocker, with an IC50 of 0.11 μM; also less potently inhibits L-type calcium channel with an IC50 of 12.2 μM. | ||||||||||||||||||||
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Fendiline | 99.41% | Fendiline, a diphenylalkylamine type of antianginal agent, is an L-type calcium channel blocker (IC50 of 17 µM). Fendiline is also a selective K-Ras inhibitor, and has no effect on H-Ras and N-Ras. Fendiline inhibits K-Ras plasma membrane localization (IC50 of 9.64 μM), inhibits K-Ras signal output and blocks the proliferation of pancreatic, colon, lung, and endometrial cancer cell lines expressing oncogenic mutant K-Ras. Fendiline is a STING agonist and is able to inhibit the growth of multiple refractory cold tumors (MC38, CT26 and B16F10). | ||||||||||||||||||||
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Fendiline hydrochloride (Standard) | 99.76% | Fendiline (hydrochloride) (Standard) is the analytical standard of Fendiline (hydrochloride). This product is intended for research and analytical applications. Fendiline hydrochloride, a diphenylalkylamine type of antianginal agent, is an L-type calcium channel blocker (IC50 of 17 µM). Fendiline hydrochloride is also a selective K-Ras inhibitor, and has no effect on H-Ras and N-Ras. Fendiline hydrochloride inhibits K-Ras plasma membrane localization (IC50 of 9.64 μM), inhibits K-Ras signal output and blocks the proliferation of pancreatic, colon, lung, and endometrial cancer cell lines expressing oncogenic mutant K-Ras. Fendiline hydrochloride is a STING agonist and is able to inhibit the growth of multiple refractory cold tumors (MC38, CT26 and B16F10). | ||||||||||||||||||||
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Cinnarizine (Standard) | 99.01% | Cinnarizine (Standard) is the analytical standard of Cinnarizine. This product is intended for research and analytical applications. | ||||||||||||||||||||
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Triphenylmethane | 99.88% | Triphenylmethane is a biochemical reagent that can be used as a biological material or organic compound for life science related research. | ||||||||||||||||||||
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Trt-Gly-OH | 95.19% | Trt-Gly-OH is a Glycine (HY-Y0966) derivative. | ||||||||||||||||||||
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Cetirizine impurity D hydrochloride | Cetirizine impurity D hydrochloride is an impurity of Cetirizine D hydrochloride. | |||||||||||||||||||||
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References
- [1]. Mitsukawa K, et al. A selective metabotropic glutamate receptor 7 agonist: activation of receptor signaling via an allosteric site modulates stress parameters in vivo. Proc Natl Acad Sci U S A. 2005;102(51):18712-18717. [Content Brief]
- [2]. Wang CC, et al. Metabotropic glutamate 7 receptor agonist AMN082 inhibits glutamate release in rat cerebral cortex nerve terminal. Eur J Pharmacol. 2018;823:11-18. [Content Brief]