BI-9627

BI-9627, a chemical probe, is a potent sodium-hydrogen exchanger isoform 1 (NHE1) inhibitor (IC50 = 6 and 31 nM in intracellular pH recovery (pHi) and human platelet swelling assays) . BI-9627 displays >30-fold selectivity against NHE2 and with no measurable inhibitory activity against the NHE3 isoform. BI-9627 decreases autophagy in HTR-8/SVneo cells. BI-9627 can significantly reduce the pHi of human sperm and partially reverse the effect of DMA. BI-9627 prolongs Ca2+ recovery time in KO hiPSC-CMs. BI-9627 shows low DDI (agent-agent interaction) potential, excellent pharmacokinetics in rat and dog, and remarkably potent activity in the isolated heart model of ischemia-reperfusion injury[1][2][3][4].

Product Specifications

CAS Number

[1204329-34-9]

UNSPSC

12352005

Target

Autophagy; Na+/H+ Exchanger (NHE)

Type

Reference compound

Related Pathways

Autophagy; Membrane Transporter/Ion Channel

Applications

Neuroscience-Neuromodulation

Field of Research

Cardiovascular Disease

Assay Protocol

https://www.medchemexpress.com/bi-9627.html

Concentration

10mM

Purity

99.71

Solubility

DMSO : 100 mg/mL (ultrasonic)

Smiles

NC(NC(C1=CC=C(C2CCN(C(C)=O)CC2)C(C(F)(F)F)=C1)=O)=N

Molecular Formula

C16H19F3N4O2

Molecular Weight

356.34

References & Citations

[1]Huber JD, et al. Identification of a potent sodium hydrogen exchanger isoform 1 (NHE1) inhibitor with a suitableprofile for chronic dosing and demonstrated cardioprotective effects in a preclinical model of myocardial infarction in the rat. J Med Chem. 2012 Aug 23;55 (16) :7114-40.|[2]Chen, M., et al., (2023) . An abnormal LPA/LPAR1-NHE1 axis leads to the autophagy deficiency of trophoblast cells in recurrent spontaneous abortion. Reproduction (Cambridge, England), 166 (5), 357–368.|[3]Liang, M., et al., (2024) . Flagellar pH homeostasis mediated by Na+/H+ exchangers regulates human sperm functions through coupling with CatSper and KSper activation. Human reproduction (Oxford, England), 39 (4), 674–688.|[4]Li, S., et al., (2024) . Mitochondrial transplantation rescues Ca2+ homeostasis imbalance and myocardial hypertrophy in SLC25A3-related hypertrophic cardiomyopathy. Cell reports, 43 (12), 115065.