A61K31/4468

THERAPEUTICS FOR TREATMENT OF COVID-19 SYMPTOMS

The present disclosure relates to methods of treating Coronavirus-Associated Lung Damage (CALD) and cytokine storm using CALD-treating compounds. The methods can involve administering CALD-treating compounds to a patient suffering from CALD or cytokine storm.

THERAPEUTICS FOR TREATMENT OF COVID-19 SYMPTOMS

The present disclosure relates to methods of treating Coronavirus-Associated Lung Damage (CALD) and cytokine storm using CALD-treating compounds. The methods can involve administering CALD-treating compounds to a patient suffering from CALD or cytokine storm.

Combination of low dose IL-2 and an inhibitor of Treg IL-2R desensitization to treat autoimmune and allergic inflammatory diseases

Provided herein are methods and compositions for treating inflammatory disease by the administration, to a patient in need thereof, of an inhibitor of IL-2R desensitization in combination with a low dose of IL-2. A low dose of interleukin-2 (IL-2) is sufficient to stimulate regulatory T lymphocytes (Tregs) without substantially inducing effector T lymphocytes (Teffs). In some embodiments, the inhibitor of IL-2R desensitization is a small molecule or drug. Is some embodiments the inhibitor is a NEDD8 activating enzyme (NAE) inhibitor. In some embodiments a combination therapy provides for a synergistic effect, where the combination of the inhibitor of IL-2R desensitization and low dose IL-2 provides an effect that is greater than the sum of either the inhibitor or low dose IL-2 administered as a single agent.

Combination of low dose IL-2 and an inhibitor of Treg IL-2R desensitization to treat autoimmune and allergic inflammatory diseases

Provided herein are methods and compositions for treating inflammatory disease by the administration, to a patient in need thereof, of an inhibitor of IL-2R desensitization in combination with a low dose of IL-2. A low dose of interleukin-2 (IL-2) is sufficient to stimulate regulatory T lymphocytes (Tregs) without substantially inducing effector T lymphocytes (Teffs). In some embodiments, the inhibitor of IL-2R desensitization is a small molecule or drug. Is some embodiments the inhibitor is a NEDD8 activating enzyme (NAE) inhibitor. In some embodiments a combination therapy provides for a synergistic effect, where the combination of the inhibitor of IL-2R desensitization and low dose IL-2 provides an effect that is greater than the sum of either the inhibitor or low dose IL-2 administered as a single agent.

Combination of low dose IL-2 and an inhibitor of Treg IL-2R desensitization to treat autoimmune and allergic inflammatory diseases

Provided herein are methods and compositions for treating inflammatory disease by the administration, to a patient in need thereof, of an inhibitor of IL-2R desensitization in combination with a low dose of IL-2. A low dose of interleukin-2 (IL-2) is sufficient to stimulate regulatory T lymphocytes (Tregs) without substantially inducing effector T lymphocytes (Teffs). In some embodiments, the inhibitor of IL-2R desensitization is a small molecule or drug. Is some embodiments the inhibitor is a NEDD8 activating enzyme (NAE) inhibitor. In some embodiments a combination therapy provides for a synergistic effect, where the combination of the inhibitor of IL-2R desensitization and low dose IL-2 provides an effect that is greater than the sum of either the inhibitor or low dose IL-2 administered as a single agent.

Prevention of the risks associated with drug-induced QT interval prolongation by using a specific inhibitor of the production of ROS of miochondrial origin

A method of treating a subject for reducing the risk of QT space prolongation associated with the intake of a drug known to prolong QT space includes administering to the subject at least one specific inhibitor of mitochondrial ROS production selected from among anethole trithione (ATT), 4-OH-anethole trithione (ATX), and an ATX ester, and administering to the subject the drug known to prolong QT space.

Prevention of the risks associated with drug-induced QT interval prolongation by using a specific inhibitor of the production of ROS of miochondrial origin

A method of treating a subject for reducing the risk of QT space prolongation associated with the intake of a drug known to prolong QT space includes administering to the subject at least one specific inhibitor of mitochondrial ROS production selected from among anethole trithione (ATT), 4-OH-anethole trithione (ATX), and an ATX ester, and administering to the subject the drug known to prolong QT space.

Substituted Alkynylene Compounds As Anticancer Agents

The present invention relates to substituted alkynylene compounds represented by the compounds of formula (I), pharmaceutically acceptable salts and stereoisomers thereof. The present invention further provides the therapeutic uses of the compounds of formula (I) as anti-cancer agents.

Substituted Alkynylene Compounds As Anticancer Agents

The present invention relates to substituted alkynylene compounds represented by the compounds of formula (I), pharmaceutically acceptable salts and stereoisomers thereof. The present invention further provides the therapeutic uses of the compounds of formula (I) as anti-cancer agents.