The present invention relates to a novel pharmaceutical composition comprising combination of Olopatadine or salt thereof and Nepafenac or salt thereof, process for preparation thereof and use thereof for the treatment of ophthalmic disorders.

The present invention relates to a novel pharmaceutical composition comprising combination of Olopatadine or salt thereof and Nepafenac or salt thereof, process for preparation thereof and use thereof for the treatment of ophthalmic disorders.

The present invention relates to a novel pharmaceutical composition comprising combination of Olopatadine or salt thereof and Nepafenac or salt thereof, process for preparation thereof and use thereof for the treatment of ophthalmic disorders.

The present disclosure relates to the use of cannabidiol (CBD) for the reduction of total convulsive seizure frequency in the treatment of “treatment-resistant epilepsy” (TRE). In particular, the disclosure relates to the use of CBD of treating TRE when the TRE is Dravet syndrome; myoclonic absence seizures or febrile infection related epilepsy syndrome (FIRES). The disclosure further relates to the use of CBD in combination with one or more anti-epileptic drugs (AEDs).

The present disclosure relates to the use of cannabidiol (CBD) for the reduction of total convulsive seizure frequency in the treatment of “treatment-resistant epilepsy” (TRE). In particular, the disclosure relates to the use of CBD of treating TRE when the TRE is Dravet syndrome; myoclonic absence seizures or febrile infection related epilepsy syndrome (FIRES). The disclosure further relates to the use of CBD in combination with one or more anti-epileptic drugs (AEDs).

Disclosed are compounds of Formulas (I), (II), (III), (IV), and (V): ##STR00001##
and/or a salt thereof, wherein R.sub.1 is —OH or —OP(O)(OH).sub.2, and X.sub.1, X.sub.2, X.sub.3, R.sub.2, R.sub.2a, R.sub.a, R.sub.b, and R.sub.c are defined herein. Also disclosed are methods of using such compounds as selective agonists for G protein-coupled receptor S1P.sub.1, and pharmaceutical compositions comprising such compounds. These compounds are useful in treating, preventing, or slowing the progression of diseases or disorders in a variety of therapeutic areas, such as autoimmune diseases and vascular disease.

Disclosed are compounds of Formulas (I), (II), (III), (IV), and (V): ##STR00001##
and/or a salt thereof, wherein R.sub.1 is —OH or —OP(O)(OH).sub.2, and X.sub.1, X.sub.2, X.sub.3, R.sub.2, R.sub.2a, R.sub.a, R.sub.b, and R.sub.c are defined herein. Also disclosed are methods of using such compounds as selective agonists for G protein-coupled receptor S1P.sub.1, and pharmaceutical compositions comprising such compounds. These compounds are useful in treating, preventing, or slowing the progression of diseases or disorders in a variety of therapeutic areas, such as autoimmune diseases and vascular disease.

The present invention provides compositions for delivering cannabinoids to the nasal cavity. The subject invention utilizes a composition comprising one or more cannabinoids and an adjuvant mixture to enhance the delivery of the cannabinoid, benefitting the subject to whom the cannabinoid is delivered.

The present invention provides compositions for delivering cannabinoids to the nasal cavity. The subject invention utilizes a composition comprising one or more cannabinoids and an adjuvant mixture to enhance the delivery of the cannabinoid, benefitting the subject to whom the cannabinoid is delivered.

The present invention provides methods for improving or accelerating wound healing in a subject comprising administering to a wound of the subject in need thereof an agent that suppresses expression of a clock gene, wherein the clock gene is neuronal PAS domain protein 2 (Npas2). This invention also relates to methods for regenerating alveolar bone, regenerating connective tissue at a wound site, and for decreasing wound area size comprising administering to a bone loss site or a wound site, in particular, an open wound site, of a subject an agent that suppresses expression of Npas2.