Skip to Content
Merck
All Photos(1)

Key Documents

SML0143

Sigma-Aldrich

HC-067047

≥98% (HPLC)

Synonym(s):

2-Methyl-1-[3-(4-morpholinyl)propyl]-5-phenyl-N-[3-(trifluoromethyl)phenyl]-1H-pyrrole-3-carboxamide

Sign Into View Organizational & Contract Pricing


About This Item

Empirical Formula (Hill Notation):
C26H28F3N3O2
CAS Number:
Molecular Weight:
471.51
MDL number:
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77

Quality Level

Assay

≥98% (HPLC)

form

powder

storage condition

desiccated

color

white to tan

solubility

DMSO: ≥15 mg/mL

storage temp.

2-8°C

SMILES string

CC1=C(C(NC2=CC(C(F)(F)F)=CC=C2)=O)C=C(C3=CC=CC=C3)N1CCCN4CCOCC4

InChI

1S/C26H28F3N3O2/c1-19-23(25(33)30-22-10-5-9-21(17-22)26(27,28)29)18-24(20-7-3-2-4-8-20)32(19)12-6-11-31-13-15-34-16-14-31/h2-5,7-10,17-18H,6,11-16H2,1H3,(H,30,33)

InChI key

NCZYSQOTAYFTNM-UHFFFAOYSA-N

Application

HC-067047 has been used as a transient receptor potential cation channel subfamily V member 4 (TRPV4) inhibitor:
  • to study its effects on organoid formation and proliferation in human endometrial tissues
  • to determine its effects on neuronal survival after intracerebral hemorrhage (ICH)
  • to study its effects on TRPV4 regulation of angiotensin II receptor type 1 (AT1R) task, phosphorylation and β-arrestin recruitment in choroid plexus

Biochem/physiol Actions

HC-067047 is a potent, selective inhibitor of hTRPV4. The compound inhibits human, rat and mouse TRPV4 with IC50 values of 48, 133 and 17 nM, respectively. HC-067047 does not inhibit other TRPV isoforms at concentrations up to 5 μM. HC-067047 inhibits hERG channel and the menthol receptor TRPM8 with IC50 values of 370 and 780 nM, respectively.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

Already Own This Product?

Find documentation for the products that you have recently purchased in the Document Library.

Visit the Document Library

Lihua Ying et al.
Science translational medicine, 7(319), 319ra204-319ra204 (2015-12-25)
The importance of gaining insight into the mechanisms underlying uterine quiescence and contractility is highlighted by the absence of an effective strategy to prevent or treat preterm labor, the greatest cause of perinatal mortality and morbidity worldwide. Although current evidence
Zhihua Yu et al.
Frontiers in pharmacology, 8, 559-559 (2017-10-04)
Airway smooth muscle cells (SMC) proliferation contributes to the airways remodeling and irreversible airway obstruction during severe asthma, but the mechanisms of airway SMC proliferation are poorly understood. Intracellular Ca
Gisela Di Giusto et al.
Journal of cellular physiology, 235(5), 4443-4454 (2019-10-20)
Aquaporin-2 (AQP2) promotes renal cell migration by the modulation of integrin β1 trafficking and the turnover of focal adhesions. The aim of this study was to investigate whether AQP2 also works in cooperation with Na+ /H+ exchanger isoform 1 (NHE1)
Philipp P Prosseda et al.
Science advances, 6(18), eaay8699-eaay8699 (2020-06-05)
Glaucoma is a group of progressive optic neuropathies that cause irreversible vision loss. Although elevated intraocular pressure (IOP) is associated with the development and progression of glaucoma, the mechanisms for its regulation are not well understood. Here, we have designed
Osama F Harraz et al.
eLife, 7 (2018-08-08)
We recently reported that the inward-rectifier Kir2.1 channel in brain capillary endothelial cells (cECs) plays a major role in neurovascular coupling (NVC) by mediating a neuronal activity-dependent, propagating vasodilatory (hyperpolarizing) signal. We further demonstrated that Kir2.1 activity is suppressed by

Our team of scientists has experience in all areas of research including Life Science, Material Science, Chemical Synthesis, Chromatography, Analytical and many others.

Contact Technical Service