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R0658

RN-1734

≥98% (HPLC)

Synonym(s):

2,4-Dichloro-N-isopropyl-N-(2-isopropylaminoethyl)benzenesulfonamide

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About This Item

Empirical Formula (Hill Notation):
C14H22Cl2N2O2S
CAS Number:
946387-07-1
Molecular Weight:
353.31
NACRES:
NA.77
PubChem Substance ID:
329823990
UNSPSC Code:
12352200
MDL number:
MFCD00129453
Assay:
≥98% (HPLC)
Form:
powder
Quality level:
100
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Quality Level

100

assay

≥98% (HPLC)

form

powder

color

white to off-white

solubility

DMSO: >20 mg/mL

storage temp.

2-8°C

SMILES string

ClC1=C(S(N(C(C)C)CCNC(C)C)(=O)=O)C=CC(Cl)=C1

InChI

1S/C14H22Cl2N2O2S/c1-10(2)17-7-8-18(11(3)4)21(19,20)14-6-5-12(15)9-13(14)16/h5-6,9-11,17H,7-8H2,1-4H3

InChI key

IHYZMEAZAIFMTN-UHFFFAOYSA-N

Application

RN-1734 has been used as a transient receptor potential vanilloid 4 (TRPV4) blocker to study its effects on differentiation of a corneal epithelial cell model, RCE1(5T5) cells.

Biochem/physiol Actions

RN-1734 is a selective TRPV4 antagonist.

Storage Class

11 - Combustible Solids

wgk

nwg

flash_point_f

Not applicable

flash_point_c

Not applicable

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Jacqueline Martínez-Rendón et al.
Journal of cellular physiology, 232(7), 1794-1807 (2016-11-22)
TRPV4 (transient receptor potential vanilloid 4) is a cation channel activated by hypotonicity, moderate heat, or shear stress. We describe the expression of TRPV4 during the differentiation of a corneal epithelial cell model, RCE1(5T5) cells. TRPV4 is a late differentiation
Vittorio Abbonante et al.
Haematologica, 102(7), 1150-1160 (2017-04-16)
Megakaryocytes (MK) in the bone marrow (BM) are immersed in a network of extracellular matrix components that regulates platelet release into the circulation. Combining biological and bioengineering approaches, we found that the activation of transient receptor potential cation channel subfamily
Hitesh Soni et al.
American journal of physiology. Renal physiology, 313(5), F1136-F1148 (2017-08-05)
Myogenic response, a phenomenon in which resistance size arteries and arterioles swiftly constrict or dilate in response to an acute elevation or reduction, respectively, in intravascular pressure is a key component of renal autoregulation mechanisms. Although it is well established
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