| Description |
MRT-83 is a potent antagonist of Smo, with an IC50 in the nanomolar range.
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| Related Catalog |
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| Target |
Smo[1].
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| In Vitro |
MRT-83 displays full antagonist properties with an IC50 (~3 nM) for inhibiting ShhN (3 nM)-induced proliferation of rat GCPs. MRT-83 also blocks SAG (0.01 μM)-induced proliferation of GCPs (IC50 ~6 nM). MRT-83 blocks BC binding to HEK-hSmo cells in a dose-dependent manner with an IC50 of 4.6 nM. MRT-83 abrogates BC binding to cells expressing mouse Smo with an IC50 of 14 nM, which is in good correlation with its IC50 in the Shh-light2 and alkaline phosphatase assays[1].
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| In Vivo |
Animals treated with ShhN in the presence of MRT-83 are as healthy as those of the other groups but up-regulation of Ptc transcription in the SVZ of these animals is no longer observed in agreement with a complete inhibition of ShhN-mediated effects (8.7±2.4 Ptc+ cells/section, n=9) and is not different from vehicle-mediated effects. MRT-83 but not MRT-36 antagonizes the up-regulation of Ptc transcription induced by ShhN in vivo in the SVZ of the LV[1].
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| Animal Admin |
Mice[1] Four groups of six animals received 5 μL of 45% 2-hydroxypropyl-β-cyclodextrin PBS solution containing 0.9 μg of ShhN alone or in the presence of MRT-83 (200 ng) or MRT-36 (110 ng). A control group receive 5 μL of 45% 2-hydroxypropyl-β-cyclodextrin solution alone. All groups are analyzed 48 h after the injection[1]
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| References |
[1]. Roudaut H, et al. Identification and mechanism of action of the acylguanidine MRT-83, a novel potent Smoothened antagonist. Mol Pharmacol. 2011 Mar;79(3):453-60.
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