Methylthiouracil - CAS 56-04-2
Catalog number:
56-04-2
Category:
Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C5H6N2OS
Molecular Weight:
142.18
COA:
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Targets:
Others
Description:
Methylthiouracil is an antithyroid preparation.The drug acts to decrease the formation of stored thyroid hormone, as thyroglobulin in the thyroid gland.
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Purity:
>98%
Synonyms:
NSC-193526, NSC-9378
MSDS:
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1.Methylthiouracil, a new treatment option for sepsis.
Kwak S1, Ku SK2, Kang H1, Baek MC3, Bae JS4. Vascul Pharmacol. 2015 Aug 1. pii: S1537-1891(15)00173-1. doi: 10.1016/j.vph.2015.07.013. [Epub ahead of print]
The screening of bioactive compound libraries can be an effective approach for repositioning FDA-approved drugs or discovering new treatments for human diseases. Inhibition of high mobility group box 1 (HMGB1) and restoration of endothelial integrity are emerging as an attractive therapeutic strategies in the management of severe sepsis or septic shock. Here, we examined the effects of methylthiouracil (MTU), used as antithyroid drug, by monitoring the effects on lipopolysaccharide (LPS)- or cecal ligation and puncture (CLP)-mediated release of HMGB1, and on the modulation of HMGB1-mediated inflammatory responses. The anti-inflammatory activities of MTU were determined by measuring permeability, leukocyte adhesion and migration, and the activation of pro-inflammatory proteins in HMGB1-activated HUVECs and mice. MTU inhibited the release of HMGB1 and downregulated HMGB1-dependent inflammatory responses in human endothelial cells. MTU also inhibited HMGB1-mediated hyperpermeability and leukocyte migration in mice.
2.Ameliorative effect of methylthiouracil on TGFBIp-induced septic responses.
Jung B1, Ku SK2, Bae JS3. Biochem Biophys Res Commun. 2015 Aug 7;463(4):661-6. doi: 10.1016/j.bbrc.2015.05.120. Epub 2015 Jun 2.
The screening of bioactive compound libraries can be an effective approach for repositioning FDA-approved drugs or discovering new treatments for human diseases. Transforming growth factor β-induced protein (TGFBIp) is an extracellular matrix protein whose expression in several cell types is greatly increased by TGF-β. TGFBIp is released by human umbilical vein endothelial cells (HUVECs), and functions as a mediator of experimental sepsis. Here, we investigated the anti-septic effects and underlying mechanisms of methylthiouracil (MTU), used as antithyroid drug, against TGFBIp-mediated septic responses in HUVECs and mice. The anti-inflammatory activities of MTU were determined by measuring permeability, human neutrophils adhesion and migration, and activation of pro-inflammatory proteins in TGFBIp-activated HUVECs and mice. According to the results, MTU effectively inhibited lipopolysaccharide-induced release of TGFBIp, and suppressed TGFBIp-mediated septic responses, such as hyperpermeability, adhesion and migration of leukocytes, and expression of cell adhesion molecules.
3.Novel insight into drug repositioning: Methylthiouracil as a case in point.
Baek MC1, Jung B2, Kang H2, Lee HS3, Bae JS4. Pharmacol Res. 2015 Sep;99:185-93. doi: 10.1016/j.phrs.2015.06.008. Epub 2015 Jun 25.
Drug repositioning refers to the development of existing drugs for new indications. These drugs may have (I) failed to show efficacy in late stage clinical trials without safety issues; (II) stalled in the development for commercial reasons; (III) passed the point of patent expiry; or (IV) are being explored in new geographic markets. Over the past decade, pressure on the pharmaceutical industry caused by the 'innovation gap' owing to rising development costs and stagnant product output have become major reasons for the growing interest in drug repositioning. Companies that offer a variety of broad platforms for identifying new indications have emerged; some have been successful in building their own pipelines of candidates with reduced risks and timelines associated with further clinical development. The business models and platforms offered by these companies will be validated if they are able to generate positive proof-of-concept clinical data for their repositioned compounds.
4.Anti-inflammatory effects of methylthiouracil in vitro and in vivo.
Ku SK1, Baek MC2, Bae JS3. Toxicol Appl Pharmacol. 2015 Nov 1;288(3):374-86. doi: 10.1016/j.taap.2015.08.009. Epub 2015 Aug 20.
The screening of bioactive compound libraries can be an effective approach for repositioning FDA-approved drugs or discovering new treatments for human diseases. Here, methylthiouracil (MTU), an antithyroid drug, was examined for its effects on lipopolysaccharide (LPS)-mediated vascular inflammatory responses. The anti-inflammatory activities of MTU were determined by measuring permeability, human neutrophil adhesion and migration, and activation of pro-inflammatory proteins in LPS-activated human umbilical vein endothelial cells and mice. We found that post-treatment with MTU inhibited LPS-induced barrier disruption, expression of cell adhesion molecules (CAMs), and adhesion/transendothelial migration of human neutrophils to human endothelial cells. MTU induced potent inhibition of LPS-induced endothelial cell protein C receptor (EPCR) shedding. It also suppressed LPS-induced hyperpermeability and neutrophil migration in vivo. Furthermore, MTU suppressed the production of tumor necrosis factor-α (TNF-α) and interleukin (IL)-6, and the activation of nuclear factor-κB (NF-κB) and extracellular regulated kinases (ERK) 1/2 by LPS.
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CAS 56-04-2 Methylthiouracil

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