Disclosed herein are methods and kits for treating or preventing a heart condition, e.g., cardiac arrhythmia, e.g., atrial arrhythmia, using potassium channel inhibitors and class I antiarrhythmic agents. Also disclosed herein are methods and kits for treating a heart condition via an intravenously, orally, or inhalationally administered fixed-dose combination of a sodium channel blocker and a class I antiarrhythmic agent.

The present invention relates to the treatment of pancreatic cancer. In this study, the results of the inventors led them to highlight the non-explored but relevant pathway in the pancreatic cancer field, the Fatty Acid Oxidation (FAO) pathway. Interestingly, they found that the mitochondrial respiration of PDAC cells depends mostly on this pathway. Thus they hypothesized that inhibition of FAO could be an effective therapeutic strategy against PDAC. 10 Their data support the hypothesis that this metabolic pathway plays a crucial role in PDAC, as it has been reported in other types of cancer. Thus, the invention relates to an inhibitor of fatty acid oxidation (FAO) for use in the treatment of pancreatic cancer in a patient in need thereof.

The present invention relates to the treatment of pancreatic cancer. In this study, the results of the inventors led them to highlight the non-explored but relevant pathway in the pancreatic cancer field, the Fatty Acid Oxidation (FAO) pathway. Interestingly, they found that the mitochondrial respiration of PDAC cells depends mostly on this pathway. Thus they hypothesized that inhibition of FAO could be an effective therapeutic strategy against PDAC. 10 Their data support the hypothesis that this metabolic pathway plays a crucial role in PDAC, as it has been reported in other types of cancer. Thus, the invention relates to an inhibitor of fatty acid oxidation (FAO) for use in the treatment of pancreatic cancer in a patient in need thereof.

The present invention relates to the treatment of pancreatic cancer. In this study, the results of the inventors led them to highlight the non-explored but relevant pathway in the pancreatic cancer field, the Fatty Acid Oxidation (FAO) pathway. Interestingly, they found that the mitochondrial respiration of PDAC cells depends mostly on this pathway. Thus they hypothesized that inhibition of FAO could be an effective therapeutic strategy against PDAC. 10 Their data support the hypothesis that this metabolic pathway plays a crucial role in PDAC, as it has been reported in other types of cancer. Thus, the invention relates to an inhibitor of fatty acid oxidation (FAO) for use in the treatment of pancreatic cancer in a patient in need thereof.

It is proposed that dissipation of relative benefit during long-term treatment is due to long-term tolerance to stimulant medications. To improve adherence and persistence of medication use, it is advantageous to develop medications that are not undermined by long-term tolerance. Disclosed herein in certain implementations are formulations and methods relating to an alternative formulation of medication for the treatment of ADHD based on two principles: (a) retaining the initial immediate-release component of controlled-release formulations that targets a neural mechanism, which elicits acute tolerance, and (b) replacing the subsequent sustained-release component with a medication that maintains the initial benefit by targeting a different neural mechanism does not elicit tolerance, thus allowing more time for acute tolerance elicited by the initial bolus dose of stimulant medication to dissipate completely each day and avoid carry-over and accumulation that results in long-term tolerance.

It is proposed that dissipation of relative benefit during long-term treatment is due to long-term tolerance to stimulant medications. To improve adherence and persistence of medication use, it is advantageous to develop medications that are not undermined by long-term tolerance. Disclosed herein in certain implementations are formulations and methods relating to an alternative formulation of medication for the treatment of ADHD based on two principles: (a) retaining the initial immediate-release component of controlled-release formulations that targets a neural mechanism, which elicits acute tolerance, and (b) replacing the subsequent sustained-release component with a medication that maintains the initial benefit by targeting a different neural mechanism does not elicit tolerance, thus allowing more time for acute tolerance elicited by the initial bolus dose of stimulant medication to dissipate completely each day and avoid carry-over and accumulation that results in long-term tolerance.

It is proposed that dissipation of relative benefit during long-term treatment is due to long-term tolerance to stimulant medications. To improve adherence and persistence of medication use, it is advantageous to develop medications that are not undermined by long-term tolerance. Disclosed herein in certain implementations are formulations and methods relating to an alternative formulation of medication for the treatment of ADHD based on two principles: (a) retaining the initial immediate-release component of controlled-release formulations that targets a neural mechanism, which elicits acute tolerance, and (b) replacing the subsequent sustained-release component with a medication that maintains the initial benefit by targeting a different neural mechanism does not elicit tolerance, thus allowing more time for acute tolerance elicited by the initial bolus dose of stimulant medication to dissipate completely each day and avoid carry-over and accumulation that results in long-term tolerance.

Provided is a Withania somnifera extract composition contains at least one of withaferin A, withanoside IV, withanoside V, withanoside VI, withanolide A, withanolide B, anaferine, anahygrine, 12-deoxywithastromonolide, sitoindoside X, sitoindoside IX, cuscohygrine, isopelletierine, bracteosin A, bracteosin B, or bracteosin C, or a salt or solvate of any one thereof. Related compositions, methods, and processes are also provided.

Provided is a Withania somnifera extract composition contains at least one of withaferin A, withanoside IV, withanoside V, withanoside VI, withanolide A, withanolide B, anaferine, anahygrine, 12-deoxywithastromonolide, sitoindoside X, sitoindoside IX, cuscohygrine, isopelletierine, bracteosin A, bracteosin B, or bracteosin C, or a salt or solvate of any one thereof. Related compositions, methods, and processes are also provided.

The present invention relates to MEK inhibitors that are capable of displaying one or more beneficial therapeutic effects. The MEK inhibitors can be used in the prevention and/or treatment of viral infection. MEK inhibitors in combination with a cap-dependent endonuclease inhibitor are capable of displaying one or more beneficial therapeutic effects in the treatment of viral diseases.