374933-30-9
Chemical Structure
Calindol
- CAS No.: 374933-30-9
- Formula:C21H20N2
- Molecular Weight:300.41
IUPAC Name: (R)-N-((1H-indol-2-yl)methyl)-1-(naphthalen-1-yl)ethan-1-amine
InChIKey: JLPWXRZETODYFC-OAHLLOKOSA-N
SMILES: [C@@H](NCC1=CC=2C(N1)=CC=CC2)(C)C=3C4=C(C=CC3)C=CC=C4
Biological Activity: Calindol is a positive allosteric modulator of the calcium-sensing receptor and a selective calcimimetic agonist. Calindol couples K+ efflux with KIR channels and Na+/K+-ATPase by opening endothelial IKCa channels, producing endothelium-dependent cardiomyocyte hyperpolarization and vasodilation, and directly blocks whole-cell VGCC currents to inhibit vascular tone through a mechanism independent of CaSR and the endothelium. Calindol activates the CaSR-PLC/IP3-calmodulin (calmodulin) signaling pathway and upregulates cystathionine-γ-lyase/H2S, reducing vascular smooth muscle cell viability and migration under hyperhomocysteinemia conditions; it also promotes neutrophil NLRP3 inflammasome activation and IL-1β release, neutrophil-mediated cardiomyocyte apoptosis (Apoptosis) and cardiac fibroblast fibrosis/inflammation, and promotes GLP-1 secretion. Calindol can be used for research on acute myocardial infarction, intrahepatic cholangiocarcinoma, hyperhomocysteinemia, and type II diabetes[1][2][3][4][5][6][7][8][9].
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Calindol | Calindol is a positive allosteric modulator of the calcium-sensing receptor and a selective calcimimetic agonist. Calindol couples K+ efflux with KIR channels and Na+/K+-ATPase by opening endothelial IKCa channels, producing endothelium-dependent cardiomyocyte hyperpolarization and vasodilation, and directly blocks whole-cell VGCC currents to inhibit vascular tone through a mechanism independent of CaSR and the endothelium. Calindol activates the CaSR-PLC/IP3-calmodulin (calmodulin) signaling pathway and upregulates cystathionine-γ-lyase/H2S, reducing vascular smooth muscle cell viability and migration under hyperhomocysteinemia conditions; it also promotes neutrophil NLRP3 inflammasome activation and IL-1β release, neutrophil-mediated cardiomyocyte apoptosis (Apoptosis) and cardiac fibroblast fibrosis/inflammation, and promotes GLP-1 secretion. Calindol can be used for research on acute myocardial infarction, intrahepatic cholangiocarcinoma, hyperhomocysteinemia, and type II diabetes. | |||||||||||||||||||||
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References
- [1]. Weston AH, et al. Evidence in favor of a calcium-sensing receptor in arterial endothelial cells: studies with calindol and Calhex 231. Circulation research. 2005 Aug 19;97(4):391-8.
- [2]. Tokonami N, et al. The excretion of uromodulin is modulated by the calcium-sensing receptor. Kidney international. 2018 Nov 1;94(5):882-6.
- [3]. Ren Z, et al. Calcium-sensing receptor on neutrophil promotes myocardial apoptosis and fibrosis after acute myocardial infarction via NLRP3 inflammasome activation. Canadian Journal of Cardiology. 2020 Jun 1;36(6):893-905.
- [4]. Fang Y, et al. Calcium-sensing receptor promotes tumor proliferation and migration in human intrahepatic cholangiocarcinoma by targeting ERK signaling pathway. European journal of pharmacology. 2020 Apr 5;872:172915.
- [5]. Greenberg HZ, et al. The calcilytics Calhex-231 and NPS 2143 and the calcimimetic Calindol reduce vascular reactivity via inhibition of voltage-gated Ca2+ channels. European journal of pharmacology. 2016 Nov 15;791:659-68. [Content Brief]
- [6]. Wang Y, et al. Inhibition of hydrogen sulfide on the proliferation of vascular smooth muscle cells involved in the modulation of calcium sensing receptor in high homocysteine. Experimental cell research. 2016 Sep 10;347(1):184-191.
- [7]. Weston AH, et al. The expression and function of Ca2+‐sensing receptors in rat mesenteric artery; comparative studies using a model of type II diabetes. British Journal of Pharmacology. 2008 Jun;154(3):652-62.
- [8]. Guo S, et al. Matrine, as a CaSR agonist promotes intestinal GLP-1 secretion and improves insulin resistance in diabetes mellitus. Phytomedicine : international journal of phytotherapy and phytopharmacology. 2021 Apr;84:153507. [Content Brief]
- [9]. Mohammed SH, et al. Non-Genomic Actions of Testosterone Metabolites on Uterine Contractility in Rats. Pharmaceutics. 2026 Aug 26;18(9):1063.
