SB-206553

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SB-206553.svg

SB-206553 is a chemical compound that acts as a selective antagonist of the 5-HT2B receptor and 5-HT2C receptor. It is commonly used in scientific research to study the roles of these receptors in various physiological and pathological processes.

Chemical Properties[edit | edit source]

SB-206553 has the chemical formula C19H18F3N3O2 and a molecular weight of 377.36 g/mol. It is a member of the phenylpiperazine class of compounds, which are known for their activity on serotonin receptors.

Pharmacology[edit | edit source]

SB-206553 exhibits high affinity for the 5-HT2B receptor and 5-HT2C receptor, with a lower affinity for the 5-HT2A receptor. By blocking these receptors, SB-206553 can modulate various neurotransmitter systems, including the serotonergic system, which plays a crucial role in mood regulation, anxiety, and other central nervous system functions.

Research Applications[edit | edit source]

SB-206553 is widely used in neuroscience and pharmacology research. It has been employed in studies investigating the role of 5-HT2B receptors in cardiovascular diseases, pulmonary hypertension, and fibrosis. Additionally, its effects on the 5-HT2C receptor have been explored in the context of obesity, anxiety disorders, and schizophrenia.

Mechanism of Action[edit | edit source]

As an antagonist, SB-206553 binds to the 5-HT2B and 5-HT2C receptors without activating them, thereby preventing the natural ligand, serotonin, from binding and exerting its effects. This blockade can lead to alterations in downstream signaling pathways, affecting various physiological responses.

Safety and Toxicology[edit | edit source]

The safety profile of SB-206553 has been evaluated in preclinical studies. While it is generally well-tolerated in experimental settings, the long-term effects and potential toxicity in humans are not well-documented. Researchers using SB-206553 should follow appropriate safety guidelines and protocols.

See Also[edit | edit source]

References[edit | edit source]



External Links[edit | edit source]

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