Abstract: This document provides methods and materials involved in identifying and/or treating mammals having a treatment-resistant prostate cancer (e.g., an enzalutamide-resistant, castration-resistant prostate cancer). For example, methods and materials for identifying a mammal (e.g., a human) having treatment-resistant prostate cancer (e.g., an enzalutamide-resistant, castration-resistant prostate cancer) as having an elevated level of one or more polypeptides (e.g., one or more of a CXXC5, a CXXC4, a TET2, an ID1, an ID3, and/or a PFN2 polypeptide) in treatment-resistant prostate tissue are provided. Methods and materials for administering one or more targeted therapies with or without one or more chemotherapeutic agents to a mammal having treatment-resistant prostate cancer identified as having an elevated level of one or more polypeptides (e.g., one or more of a CXXC5, a CXXC4, a TET2, an ID1, an ID3, and/or a PFN2 polypeptide) in treatment-resistant prostate tissue also are provided.

Abstract: A tampon and therapeutic delivery device is disclosed and includes a generally cylindrical applicator tube defining a cartridge within which a tampon is slidably received for ejection through one end of the cartridge. A generally hollow cylindrical plunger member is slidably received within an opposite end of the cartridge for ejecting the tampon therefrom. A cannabinoid-infused disintegrable carrier material is partially embedded in and movably held by the tampon for intravaginal delivery when ejected from the cartridge, whereupon the cannabinoid agent is released into the vagina and absorbed through the vaginal mucosa to provide relief of dysmenorrhea. The cartridge has a plurality of slots to permit pre-lubrication of the tampon, if desired, prior to insertion into the vaginal cavity. The system delivers a higher concentration to the muscle of the uterus, the primary site for the dyskinetic muscle contraction, which is the pathophysiologic cause of dysmenorrhea.

Abstract: Provided are methods for treatment of Fabry disease in patients having HEK assay amenable mutations in ?-galactosidase A. Certain methods comprise administering migalastat or a salt thereof every other day, such as administering about 150 mg of migalastat hydrochloride every other day.

Abstract: Dosage forms, drug delivery systems, and methods related to sustained release of dextromethorphan or improved therapeutic effects are disclosed. Typically, bupropion or a related compound is orally administered to a human being to be treated with, or being treated with, dextromethorphan.

Abstract: The present invention includes compositions and methods for treating and delivering medicinal formulations using an inhaler. The composition includes a space filled flocculated suspension having one or more flocculated particles of one or more active agents and a hydrofluoroalkane propellant. A portion of the one or more flocculated particles is templated by the formation of hydrofluoroalkane droplets upon atomization and the templated floc compacts upon the evaporation of the hydrofluoroalkane propellant to form a porous particle for deep lung delivery.

Abstract: Provided are methods for treatment of Fabry disease in patients having HEK assay amenable mutations in ?-galactosidase A. Certain methods comprise administering migalastat or a salt thereof every other day, such as administering about 150 mg of migalastat hydrochloride every other day.

Abstract: Provided are methods for treatment of Fabry disease in patients having HEK assay amenable mutations in ?-galactosidase A. Certain methods comprise administering migalastat or a salt thereof every other day, such as administering about 150 mg of migalastat hydrochloride every other day.

Abstract: The technology described herein is directed to methods of treating lung infections and/or lung inflammation (e.g, pneumonia) by inhibiting IP6K1.

Abstract: The present disclosure relates to methods, uses, pharmaceutical compositions and kits comprising an sGC stimulator or a pharmaceutically acceptable salt thereof, alone or in combination with one or more additional therapeutic agents, for the treatment of Nonalcoholic Steatohepatitis (NASH).

Abstract: Provided are methods for treatment of Fabry disease in patients having HEK assay amenable mutations in ?-galactosidase A. Certain methods comprise administering migalastat or a salt thereof every other day, such as administering about 150 mg of migalastat hydrochloride every other day.

Abstract: The present invention relates to a crystalline form of Compound I, a salt, a solvate, or a solvate salt thereof or an amorphous form of Compound I, a salt, a solvate, or a solvate salt thereof. The present invention also provides compositions comprising the crystalline form and/or the amorphous form, therapeutic uses of the crystalline forms and/or the amorphous forms, and the compositions thereof.

Abstract: Provided are methods for treatment of Fabry disease in patients having HEK assay amenable mutations in ?-galactosidase A. Certain methods comprise administering migalastat or a salt thereof every other day, such as administering about 150 mg of migalastat hydrochloride every other day.

Abstract: Provided are methods for treatment of Fabry disease in patients having HEK assay amenable mutations in ?-galactosidase A. Certain methods comprise administering migalastat or a salt thereof every other day, such as administering about 150 mg of migalastat hydrochloride every other day.

Abstract: The present disclosure provides for methods of treating a patient with a CYP3A4 substrate drug, wherein the patient is treated with posaconazole. In some embodiments, the patient stops posaconazole treatment, waits for at least 2 days, and then is treated with the CYP3A4 substrate drug as soon as it is safe to do so. In some embodiments, treatment with the CYP3A4 substrate drug is delayed for about 2-42 days after stopping posaconazole. In some embodiments, the patient is treated with a reduced dose of the CYP3A4 substrate drug for about 2-42 days.

Abstract: The disclosure is directed to methods of treating cancer in subjects with a combination of a monoclonal antibody and (R)-N-(4-chlorophenyl)-2-(cis-4-(6-fluoroquinolin-4-yl)cyclohexyl)propanamide, or a salt thereof.

Abstract: This invention relates to compounds that are useful for inhibiting the secretion of secretory leukocyte protease inhibitor (SLPI) in a subject. Methods of inhibiting metastasis of cancer and methods of treating cancer in a subject are also provided.

Abstract: The disclosed embodiments relate to methods of initiating aripiprazole treatment in a patient who is a CYP2D6 poor metabolizer or a CYP3A4 poor metabolizer, or both.

Abstract: Systems, methods, and kits for treating, preventing, and diagnosing viral infection using an androgen mediated pathway are described. Additionally, methods and kits for guiding treatment of viral respiratory disease are described by a method for testing for polymorphisms in the androgen receptor gene. Further, systems and methods for treatment of viral respiratory disease with various anti-androgens is detailed. Finally, systems, methods, and kits for treating, preventing, and diagnosing SARS-CoV-2 (COVID-19) are presented.

Abstract: The present invention is directed to stable lyophilisates comprising 5,10-methylene-(6R)-tetrahydrofolic acid or a pharmaceutically acceptable salt thereof and a dicarboxylic acid, or a salt thereof, as well as, a processes of obtaining the same, and the use of such products.

Abstract: Given its various activities in the brain, nitric oxide (NO) has been associated with various neuropsychiatric diseases and/or neuropsychiatric disorders, including schizophrenia. In fact, evidence has been accumulating to show that abnormalities in NO levels are associated with schizophrenia. Among a number of NO's neural mechanisms associated with schizophrenia, its role as a second messenger of NMDA receptor activation, which interacts with both dopaminergic and serotonergic pathways, has been of particular focus. It demonstrated herein that a combined administration of nitric oxide synthase substrates and co-factors display antineuropsychiatric activity and cognitive benefit by re-establishing homeostatic nitric oxide production.