The present invention relates to a method of converting human fibroblasts into neural stem cells, and more particularly, to a method of directly converting human fibroblasts into neural stem cells using only a combination of small-molecule compounds without any introduction of a foreign gene, and to the use of the neural stem cells. The method of directly converting human fibroblasts into neural stem cells using only small-molecule compounds without any introduction of a foreign gene makes it possible to obtain genetically stable neural stem cells in an amount sufficient for use in cell therapy by deriving them from human fibroblasts. The neural stem cells obtained according to the method of the present invention can differentiate into functional neural cells and are not tumorigenic. Thus, these neural stem cells are useful as cellular therapeutic agents for treatment of brain diseases.

The present invention provides compositions and methods for reducing inflammation in the lungs of a mammal that is afflicted by a condition that leads to inflammation in the lungs. The compositions and methods described herein include agents that inhibit inflammasome signaling in the mammal such as antibodies directed against inflammasome components used alone or in combination with extracellular vesicle uptake inhibitor(s).

The present invention provides compositions and methods for reducing inflammation in the lungs of a mammal that is afflicted by a condition that leads to inflammation in the lungs. The compositions and methods described herein include agents that inhibit inflammasome signaling in the mammal such as antibodies directed against inflammasome components used alone or in combination with extracellular vesicle uptake inhibitor(s).

The present invention provides oligomeric compounds. Certain such oligomeric compounds are useful for hybridizing to a complementary nucleic acid, including but not limited, to nucleic acids in a cell. In certain embodiments, hybridization results in modulation of the amount, activity, or expression of the target nucleic acid in a cell. In certain embodiments, hybridization results in selective modulation of the amount, activity, or expression of a target Huntingtin gene or Huntingtin transcript in a cell.

A method of promoting the generation of oligodendrocytes from oligodendrocyte precursor cells by enhancing their survival and/or maturation includes administering to the cell an effective amount of an agent that enhances and/or induces accumulation of Δ8,9-unsaturated sterol intermediates of the cholesterol biosynthesis pathway in the oligodendrocyte precursor cells.

A method of promoting the generation of oligodendrocytes from oligodendrocyte precursor cells by enhancing their survival and/or maturation includes administering to the cell an effective amount of an agent that enhances and/or induces accumulation of Δ8,9-unsaturated sterol intermediates of the cholesterol biosynthesis pathway in the oligodendrocyte precursor cells.

Substituted 1H-imidazo[4,5-b]pyridin-2(3H)-ones as NR2B receptor ligands. Such compounds may be used in NR2B receptor modulation and in pharmaceutical compositions and methods for the treatment of disease states, disorders, and conditions mediated by NR2B receptor activity.

Dysregulation of TAF1 function by various mechanisms can lead to disease in the central nervous system, such as the TAF1 Intellectual Disability (ID) Syndrome which currently has no therapeutic treatments. The present invention indicates that a novel T-type calcium channel enhancer, such as SAK3, has disease-modifying effects in animal models of TAF1 editing. In addition, the present invention provides insights into the molecular mechanism by which SAK3 exerts in pharmacologic effects. Moreover, the present findings imply that the T-Type voltage-gated calcium channels are novel molecular targets to develop therapeutics to treat TAF1 ID syndrome and that SAK3 is an attractive drug candidate to treat TAF1 associated neurologic disorders.

Dysregulation of TAF1 function by various mechanisms can lead to disease in the central nervous system, such as the TAF1 Intellectual Disability (ID) Syndrome which currently has no therapeutic treatments. The present invention indicates that a novel T-type calcium channel enhancer, such as SAK3, has disease-modifying effects in animal models of TAF1 editing. In addition, the present invention provides insights into the molecular mechanism by which SAK3 exerts in pharmacologic effects. Moreover, the present findings imply that the T-Type voltage-gated calcium channels are novel molecular targets to develop therapeutics to treat TAF1 ID syndrome and that SAK3 is an attractive drug candidate to treat TAF1 associated neurologic disorders.

The present invention provides a compound suitable for use as an acetyl CoA carboxylase (ACC) inhibitor, specifically, a thienopyridine derivative, and use of the compound in the preparation of drugs for treating metabolic disorders, cancers or other proliferative disorders, and nonalcoholic steatohepatitis (NASH).