RN 1734 |
Catalog No.GC17267 |
RN 1734 es un antagonista selectivo del canal TRPV4, antagoniza por completo la activación de TRPV4 mediada por 4αPDD con IC50 micromolares bajos comparables para las tres especies (hTRPV4: 2,3 μM, mTRPV4: 5,9 μM, rTRPV4: 3,2 μM).
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 946387-07-1
Sample solution is provided at 25 µL, 10mM.
RN-1734 is selective antagonist of the TRPV4 channel, completely antagonizes 4αPDD-mediated activation of TRPV4 with comparable, low micromolar IC50s for all three species (hTRPV4: 2.3 μM, mTRPV4: 5.9 μM, rTRPV4: 3.2 μM)[1]. RN-1734 clearly decreases the production of tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) without altering the number of olig2-positive cells[2].
RN-1734 (27 hours; 10μM) reverses the increase in the apoptotic rate of oligodendrocytes induced by CM (LPS-activated microglia group) apoptosis[2].RN-1734 (27 hours; 10μM) alleviates CM-induced decreases in CNP[2].
RN-1734 (0.5 μl; microinjector pump; daily for 5 weeks) significantly reverses the decrease in CNP protein and improves myelination in CPZ-induced demyelination mouse[2].
References:
[1]. Kato K, et al. Acidosis environment promotes osteoclast formation by acting on the last phase of preosteoclast differentiation: a study to elucidate the action points of acidosis and search for putative target molecules. Eur J Pharmacol. 2011 Aug 1;663(1-3):27-39.
[2]. Liu M, et al. TRPV4 Inhibition Improved Myelination and Reduced Glia Reactivity and Inflammation in a Cuprizone-Induced Mouse Model of Demyelination. Front Cell Neurosci. 2018 Nov 5;12:392.
[3]. Vincent F, et al. Identification and characterization of novel TRPV4 modulators. Biochem Biophys Res Commun. 2009 Nov 20;389(3):490-4.
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