Abstract: Activation of 5-HT2A receptors using agonists at surprisingly low concentrations was shown to potently inhibit TNF-?-induced inflammation in multiple cell types. Significantly, proinflammatory markers were also inhibited by the agonist, (R)-DOI, even many hours after treatment with TNF-?. With the exception of a few natural toxins, no current drugs or small molecule therapeutics demonstrate a comparable potency for any physiological effect. TNF-? and TNF-? receptor mediated inflammatory pathways have been strongly implicated in a number of diseases, including atherosclerosis, asthma, rheumatoid arthritis, psoriasis, type II diabetes, depression, schizophrenia, and Alzheimer's disease. Importantly, because (R)-DOI can significantly inhibit the effects of TNF-? many hours after the administration of TNF-?, potential therapies could be aimed not only at preventing inflammation, but also treating inflammatory injury that has already occurred or is ongoing.

Abstract: Activation of 5-HT2A receptors using agonists at surprisingly low concentrations was shown to potently inhibit TNF-?-induced inflammation in multiple cell types. Significantly, proinflammatory markers were also inhibited by the agonist, (R)-DOI, even many hours after treatment with TNF-?. With the exception of a few natural toxins, no current drugs or small molecule therapeutics demonstrate a comparable potency for any physiological effect. TNF-? and TNF-? receptor mediated inflammatory pathways have been strongly implicated in a number of diseases, including atherosclerosis, asthma, rheumatoid arthritis, psoriasis, type II diabetes, depression, schizophrenia, and Alzheimer's disease. Importantly, because (R)-DOI can significantly inhibit the effects of TNF-? many hours after the administration of TNF-?, potential therapies could be aimed not only at preventing inflammation, but also treating inflammatory injury that has already occurred or is ongoing.

Abstract: The present invention is directed to a method for the treatment of an inflammatory disorder in a mammal, said method comprising administering to a mammal in need of such treatment a therapeutically effective amount of (R)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane ((R)-DOI) in a pharmaceutically acceptable carrier or salt thereof, wherein said inflammatory disorder is associated with a disease selected from asthma, rheumatoid arthritis, irritable bowel syndrome, and Crohn's disease.

Abstract: Activation of 5-HT2A receptors using agonists at surprisingly low concentrations was shown to potently inhibit TNF-?-induced inflammation in multiple cell types. Significantly, proinflammatory markers were also inhibited by the agonist, (R)-DOI, even many hours after treatment with TNF-?. With the exception of a few natural toxins, no current drugs or small molecule therapeutics demonstrate a comparable potency for any physiological effect. TNF-? and TNF-? receptor mediated inflammatory pathways have been strongly implicated in a number of diseases, including atherosclerosis, asthma, rheumatoid arthritis, psoriasis, type II diabetes, depression, schizophrenia, and Alzheimer's disease. Importantly, because (R)-DOI can significantly inhibit the effects of TNF-? many hours after the administration of TNF-?, potential therapies could be aimed not only at preventing inflammation, but also treating inflammatory injury that has already occurred or is ongoing.