A method of treating or preventing adverse outcomes associated with tissue plasminogen activator (tPA) administration, cerebral edema-related side effects, cerebral edema associated with radiation therapy, or migraine headaches by administering an effective amount of a SUR1-TRPM4 channel inhibitor, such as glyburide, and optionally the co-administration of a second therapeutically active agent, to a subject in need thereof. Adverse outcomes associated with tPA include cerebral hemorrhage, cerebral edema, physical impairment or death. The administration of the SUR1-TRPM4 channel inhibitors occurs prior to the radiation therapy, during the radiation therapy, after the radiation therapy, or combinations thereof. The SUR1-TRPM4 channel inhibitor is administered prior to surgical excision of a brain tumor, CAR-T therapy, or administration of flutarabine. Alternatively, or in addition, the SUR1-TRPM4 channel inhibitor is administered prior the onset of the cerebral edema-related side effects.

A method of treating or preventing adverse outcomes associated with tissue plasminogen activator (tPA) administration, cerebral edema-related side effects, cerebral edema associated with radiation therapy, or migraine headaches by administering an effective amount of a SUR1-TRPM4 channel inhibitor, such as glyburide, and optionally the co-administration of a second therapeutically active agent, to a subject in need thereof. Adverse outcomes associated with tPA include cerebral hemorrhage, cerebral edema, physical impairment or death. The administration of the SUR1-TRPM4 channel inhibitors occurs prior to the radiation therapy, during the radiation therapy, after the radiation therapy, or combinations thereof. The SUR1-TRPM4 channel inhibitor is administered prior to surgical excision of a brain tumor, CAR-T therapy, or administration of flutarabine. Alternatively, or in addition, the SUR1-TRPM4 channel inhibitor is administered prior the onset of the cerebral edema-related side effects.

A method of treating or preventing adverse outcomes associated with tissue plasminogen activator (tPA) administration, cerebral edema-related side effects, cerebral edema associated with radiation therapy, or migraine headaches by administering an effective amount of a SUR1-TRPM4 channel inhibitor, such as glyburide, and optionally the co-administration of a second therapeutically active agent, to a subject in need thereof. Adverse outcomes associated with tPA include cerebral hemorrhage, cerebral edema, physical impairment or death. The administration of the SUR1-TRPM4 channel inhibitors occurs prior to the radiation therapy, during the radiation therapy, after the radiation therapy, or combinations thereof. The SUR1-TRPM4 channel inhibitor is administered prior to surgical excision of a brain tumor, CAR-T therapy, or administration of flutarabine. Alternatively, or in addition, the SUR1-TRPM4 channel inhibitor is administered prior the onset of the cerebral edema-related side effects.

The present invention relates to a pharmaceutical composition for preventing or treating acidosis. The pharmaceutical composition has a remarkable effect in decreasing the concentration of acid accumulated in an organism and thus is expected to be widely used in the fields of medicine and health.

A pharmaceutical composition and a method of administering the pharmaceutical composition to a patient suffering from edema, heart failure, kidney or liver disease or having symptoms thereof are disclosed. The pharmaceutical composition includes torsemide, or a pharmaceutically acceptable salt, hydrate or ester thereof and a cyclodextrin.

A pharmaceutical composition and a method of administering the pharmaceutical composition to a patient suffering from edema, heart failure, kidney or liver disease or having symptoms thereof are disclosed. The pharmaceutical composition includes torsemide, or a pharmaceutically acceptable salt, hydrate or ester thereof and a cyclodextrin.

Cannabidiol (CBD) based compositions for use in the treatment of angiogenesis in proliferative diabetic retinopathy (PDR) is provided. The invention also relates to methods and compositions for treating conditions associated with lymphangiogenesis using cannabidiol (CBD). Preferably the angiogenesis manifest as abnormal vascular lesions with visual impairment and the angiogenesis is treatment resistant.

Cannabidiol (CBD) based compositions for use in the treatment of angiogenesis in proliferative diabetic retinopathy (PDR) is provided. The invention also relates to methods and compositions for treating conditions associated with lymphangiogenesis using cannabidiol (CBD). Preferably the angiogenesis manifest as abnormal vascular lesions with visual impairment and the angiogenesis is treatment resistant.

An oral dosage form of an antidiabetic pharmaceutical composition comprises a core portion, an outer portion, and a controlled membrane film sandwiched therebetween. The core and outer portions respectively comprise a first antidiabetic agent and a second antidiabetic agent, such as metformin HCl and sitagliptin phosphate, each at a therapeutically effective amount. The controlled membrane film encapsulates the core portion and is provided with at least one passageway for allowing the first antidiabetic agent to release out when the oral dosage form is in an aqueous environment, such as in the gastrointestinal (GI) tract of a subject. The oral dosage form is configured, upon a single-dose oral administration, to provide a maximum plasma concentration of the first antidiabetic agent in the subject from approximately 7.5 to 15 hours after administration. A method for manufacturing the oral dosage form of the antidiabetic pharmaceutical composition is also provided.

An oral dosage form of an antidiabetic pharmaceutical composition comprises a core portion, an outer portion, and a controlled membrane film sandwiched therebetween. The core and outer portions respectively comprise a first antidiabetic agent and a second antidiabetic agent, such as metformin HCl and sitagliptin phosphate, each at a therapeutically effective amount. The controlled membrane film encapsulates the core portion and is provided with at least one passageway for allowing the first antidiabetic agent to release out when the oral dosage form is in an aqueous environment, such as in the gastrointestinal (GI) tract of a subject. The oral dosage form is configured, upon a single-dose oral administration, to provide a maximum plasma concentration of the first antidiabetic agent in the subject from approximately 7.5 to 15 hours after administration. A method for manufacturing the oral dosage form of the antidiabetic pharmaceutical composition is also provided.