Calhex 231 

Calhex 231 is a potent negative allosteric modulator that blocks (IC₅₀ = 0.39 μM) increases in [³H]inositol phosphates elicited by activating the human wild-type CaSR transiently Ca²⁺-sensing receptor. Calhex 231 can be used in the study of traumatic hemorrhagic shock (THS) and diabetic cardiomyopathy (DCM)^[1].

CaSR^[1]
IC50: 0.39 μM (Inositol phosphate)^[1]

Calhex 231 dose-dependently inhibited the IP response induced by 10 mM Ca²⁺ with a potency in the T764A (IC₅₀ = 0.28 ± 0.05 μM) and H766A (IC₅₀ = 0.64 ± 0.03 μM) mutant receptors similar to that in the WT receptor^[1]. Calhex 231 treatment significantly downregulates the CaSR, α-SMA, Col-I/III, MMP2/9 expresses. Calhex231 alleviates high glucose-induced myocardial fibrosis in cardiac fibroblasts^[2].
Calhex 231 could inhibit Itch (atrophin-1 interacting protein 4)-ubiquitin proteasome and TGF-β1/Smads pathways, and then depress the proliferation of cardiac fibroblasts, along with the reduction deposition of collagen, alleviate glucose-induced myocardial fibrosis^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Calhex 231 (4.07 mg/kg (10 µmol/kg); intraperitoneal injection; daily; for 12 weeks; male Wistar rats) treatment ameliorates diabetic myocardial fibrosis in type 1 diabetic model (T1D) rats^[2].
Calhex-231 (Cal, 0.1-1 mg/kg) has a mitigating effect on traumatic hemorrhagic shock by improving vascular hyporesponsiveness and reducing mitochondrial dysfunction^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

406.95

C₂₅H₂₇ClN₂O

652973-93-8

O=C(N[C@@H]1[C@@H](N[C@@H](C2=C3C=CC=CC3=CC=C2)C)CCCC1)C4=CC=C(Cl)C=C4

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Christophe Petrel, et al. Modeling and mutagenesis of the binding site of Calhex 231, a novel negative allosteric modulator of the extracellular Ca(2+)-sensing receptor. J Biol Chem. 2003 Dec 5;278(49):49487-94.  [Content Brief]

  [2]. Petrel C1, et al. Modeling and mutagenesis of the binding site of Calhex 231, a novel negative allosteric modulator of the extracellular Ca(2+)-sensing receptor. J Biol Chem. 2003 Dec 5;278(49):49487-94.  [Content Brief]

  [3]. Yan Lei, et al. The Calcilytic Drug Calhex-231 Ameliorates Vascular Hyporesponsiveness in Traumatic Hemorrhagic Shock by Inhibiting Oxidative Stress and miR-208a-Mediated Mitochondrial Fission. Oxid Med Cell Longev. 2020 Dec 3:2020:4132785.  [Content Brief]