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	<title>2-Cl-IB-MECA - Revision history</title>
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	<updated>2026-04-27T05:11:49Z</updated>
	<subtitle>Revision history for this page on the wiki</subtitle>
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		<id>https://wikimd.org/index.php?title=2-Cl-IB-MECA&amp;diff=6021840&amp;oldid=prev</id>
		<title>Prab: CSV import</title>
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		<updated>2024-12-01T21:12:13Z</updated>

		<summary type="html">&lt;p&gt;CSV import&lt;/p&gt;
&lt;p&gt;&lt;b&gt;New page&lt;/b&gt;&lt;/p&gt;&lt;div&gt;{{DISPLAYTITLE:2-Cl-IB-MECA}}&lt;br /&gt;
&lt;br /&gt;
&amp;#039;&amp;#039;&amp;#039;2-Cl-IB-MECA&amp;#039;&amp;#039;&amp;#039; (2-chloro-N6-(3-iodobenzyl)adenosine-5&amp;#039;-N-methyluronamide) is a synthetic compound that acts as a selective agonist for the [[adenosine A3 receptor]]. This compound is of significant interest in the field of [[pharmacology]] and [[medicine]] due to its potential therapeutic applications, particularly in [[inflammation]], [[cancer]], and [[cardioprotection]].&lt;br /&gt;
&lt;br /&gt;
==Chemical Structure and Properties==&lt;br /&gt;
2-Cl-IB-MECA is a modified adenosine derivative. Its chemical structure includes a chlorine atom at the 2-position and an iodine-substituted benzyl group at the N6 position, along with a methyluronamide group. These modifications confer high selectivity and affinity for the adenosine A3 receptor.&lt;br /&gt;
&lt;br /&gt;
* &amp;#039;&amp;#039;&amp;#039;IUPAC Name&amp;#039;&amp;#039;&amp;#039;: 2-chloro-N6-(3-iodobenzyl)adenosine-5&amp;#039;-N-methyluronamide&lt;br /&gt;
* &amp;#039;&amp;#039;&amp;#039;Molecular Formula&amp;#039;&amp;#039;&amp;#039;: C17H17ClIN5O4&lt;br /&gt;
* &amp;#039;&amp;#039;&amp;#039;Molecular Weight&amp;#039;&amp;#039;&amp;#039;: 517.71 g/mol&lt;br /&gt;
&lt;br /&gt;
==Mechanism of Action==&lt;br /&gt;
2-Cl-IB-MECA binds to the adenosine A3 receptor, a G protein-coupled receptor (GPCR) that is involved in various physiological processes. Upon activation, the A3 receptor can influence the activity of adenylate cyclase, leading to changes in intracellular cyclic AMP levels. This can result in a variety of downstream effects, including modulation of [[inflammatory pathways]], [[apoptosis]], and [[cell proliferation]].&lt;br /&gt;
&lt;br /&gt;
==Therapeutic Applications==&lt;br /&gt;
&lt;br /&gt;
===Inflammation===&lt;br /&gt;
2-Cl-IB-MECA has been shown to have anti-inflammatory effects. It can reduce the production of pro-inflammatory cytokines and inhibit the activation of inflammatory cells. This makes it a potential candidate for the treatment of inflammatory diseases such as [[rheumatoid arthritis]] and [[inflammatory bowel disease]].&lt;br /&gt;
&lt;br /&gt;
===Cancer===&lt;br /&gt;
Research has indicated that 2-Cl-IB-MECA may have anti-cancer properties. It can induce apoptosis in certain cancer cell lines and inhibit tumor growth in animal models. The compound&amp;#039;s ability to selectively target cancer cells while sparing normal cells is of particular interest in [[oncology]].&lt;br /&gt;
&lt;br /&gt;
===Cardioprotection===&lt;br /&gt;
The adenosine A3 receptor is involved in cardioprotection, particularly during ischemic events. 2-Cl-IB-MECA has been studied for its potential to reduce myocardial injury during [[ischemia-reperfusion]] events, which could be beneficial in conditions such as [[myocardial infarction]].&lt;br /&gt;
&lt;br /&gt;
==Research and Development==&lt;br /&gt;
Ongoing research is focused on understanding the full range of biological effects of 2-Cl-IB-MECA and its potential clinical applications. Studies are also exploring its pharmacokinetics, safety profile, and efficacy in various disease models.&lt;br /&gt;
&lt;br /&gt;
==Also see==&lt;br /&gt;
* [[Adenosine receptor]]&lt;br /&gt;
* [[GPCR signaling]]&lt;br /&gt;
* [[Anti-inflammatory drugs]]&lt;br /&gt;
* [[Cancer therapeutics]]&lt;br /&gt;
* [[Cardioprotection]]&lt;br /&gt;
&lt;br /&gt;
{{Receptor agonists}}&lt;br /&gt;
{{Pharmacology}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Pharmacology]]&lt;br /&gt;
[[Category:Receptor agonists]]&lt;br /&gt;
[[Category:Experimental drugs]]&lt;/div&gt;</summary>
		<author><name>Prab</name></author>
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