Abstract: The present disclosure describes methods of treating a central nervous system condition associated with oxidative stress using a 5-lipoxigenase activating protein (FLAP) inhibitor, for example, N-acetylcysteine or nordihydroguaiaretic acid. The present disclosure also describes methods of treating a central nervous system condition with N-acetylcysteine and a second therapeutic agent such as prostaglandin E2.

Abstract: The present disclosure describes methods of treating a central nervous system condition caused by a traumatic brain injury using a 5-lipoxigenase activating protein (FLAP) inhibitor, for example, N-acetylcysteine or nordihydroguaiaretic acid.

Abstract: This invention relates to methods of administering compounds containing selenium, selenocysteine, or a selenocysteine peptide to treat, for example, conditions associated with selenium deficiency, or ferroptoptic, parthanototic, and endoplasmic reticulum stress, and/or cancer. The methods of treatment may activate or inhibit (via TFAP2C and Sp1 proteins) the adaptive homeostatic response of the selenome. The compounds may contain a targeting sequence that causes them to be delivered to specific organs and/or tissues. The compounds may be administered, for example, orally, intranasally, intravenously, or by a minimally invasive catheter or BrainPath.

Abstract: The present disclosure describes methods of treating a central nervous system condition associated with oxidative stress using a 5-lipoxigenase activating protein (FLAP) inhibitor, for example, N-acetylcysteine or nordihydroguaiaretic acid. The present disclosure also describes methods of treating a central nervous system condition with N-acetylcysteine and a second therapeutic agent such as prostaglandin E2.

Abstract: The present disclosure describes methods of treating a central nervous system condition associated with oxidative stress using a 5-lipoxigenase activating protein (FLAP) inhibitor, for example, N-acetylcysteine or nordihydroguaiaretic acid. The present disclosure also describes methods of treating a central nervous system condition with N-acetylcysteine and a second therapeutic agent such as prostaglandin E2.

Abstract: This invention relates to methods of administering compounds containing selenium, selenocysteine, or a selenocysteine peptide to treat, for example, conditions associated with selenium deficiency, or ferroptoptic, parthanototic, and endoplasmic reticulum stress, and/or cancer. The methods of treatment may activate or inhibit (via TFAP2C and Sp1 proteins) the adaptive homeostatic response of the selenome. The compounds may contain a targeting sequence that causes them to be delivered to specific organs and/or tissues. The compounds may be administered, for example, orally, intranasally, intravenously, or by a minimally invasive catheter or BrainPath.

Abstract: This invention relates to methods of administering compounds containing selenium, selenocysteine, or a selenocysteine peptide to treat, for example, conditions associated with selenium deficiency, or ferroptoptic, parthanototic, and endoplasmic reticulum stress, and/or cancer. The methods of treatment may activate or inhibit (via TFAP2C and Sp1 proteins) the adaptive homeostatic response of the selenome. The compounds may contain a targeting sequence that causes them to be delivered to specific organs and/or tissues. The compounds may be administered, for example, orally, intranasally, intravenously, or by a minimally invasive catheter or BrainPath.

Abstract: The present disclosure describes methods of administering N-acetylcysteine (NAC) via intranasal nose-to-brain administration. The effect of intranasal NAC nose-to-brain administration can be monitored using an analytical technique, for example, magnetic resonance spectroscopy (MRS). In some embodiments, intranasal nose-to-brain NAC can be used to treat a condition, for example, a brain injury.

Abstract: Methods for treating a patient suffering from neural cell injury, the method comprising administering to the patient an effective amount of a HIE prolyl-4-hydroxylase inhibiting compound having the following general formula (1) wherein R1 is a cyclic group containing at least three and up to seven carbon atoms and optionally containing one or more heteroatoms selected from O, N, and S, and optionally attached to the shown carbon atom by a linking group; R2 is independently selected from said cyclic groups of R1 and a cyclic hydrocarbon groups R5 containing up to twenty carbon atoms; R3 is selected from hydrogen atom and hydrocarbon groups containing up to six carbon atoms; R6 and R7 are independently selected from hydrogen atom, hydrocarbon groups containing up to three carbon atoms, halogen atom, and polar groups, as well as methylene-linked versions thereof; and t is 0 or 1.

Abstract: The present disclosure describes methods of treating a central nervous system condition associated with oxidative stress using a 5-lipoxigenase activating protein (FLAP) inhibitor, for example, N-acetylcysteine or nordihydroguaiaretic acid. The present disclosure also describes methods of treating a central nervous system condition with N-acetylcysteine and a second therapeutic agent such as prostaglandin E2.

Abstract: Methods for treating a patient suffering from neural cell injury, the method comprising administering to the patient an effective amount of a HIF prolyl-4-hydroxylase inhibiting compound having the following general formula (1) wherein R1 is a cyclic group containing at least three and up to seven carbon atoms and optionally containing one or more heteroatoms selected from O, N, and S, and optionally attached to the shown carbon atom by a linking group; R2 is independently selected from said cyclic groups of R1 and acyclic hydrocarbon groups R5 containing up to twenty carbon atoms; R3 is selected from hydrogen atom and hydrocarbon groups containing up to six carbon atoms; R6 and R7 are independently selected from hydrogen atom, hydrocarbon groups containing up to three carbon atoms, halogen atom, and polar groups, as well as methylene-linked versions thereof; and t is 0 or 1.

Abstract: The present disclosure describes methods of treating a central nervous system condition associated with oxidative stress using a 5-lipoxigenase activating protein (FLAP) inhibitor, for example, N-acetylcysteine or nordihydroguaiaretic acid. The present disclosure also describes methods of treating a central nervous system condition with N-acetylcysteine and a second therapeutic agent such as prostaglandin E2.

Abstract: This invention relates to methods of administering compounds containing selenium, selenocysteine, or a selenocysteine peptide to treat, for example, conditions associated with selenium deficiency, or ferroptoptic, parthanototic, and endoplasmic reticulum stress, and/or cancer. The methods of treatment may activate or inhibit (via TFAP2C and Sp1 proteins) the adaptive homeostatic response of the selenome. The compounds may contain a targeting sequence that causes them to be delivered to specific organs and/or tissues. The compounds may be administered, for example, orally, intranasally, intravenously, or by a minimally invasive catheter or BrainPath.

Abstract: The present invention relates to methods for enhancing Hypoxia inducible factor-1 (HIF) activity in a cell by contacting the cell with any one of the following compounds: 3,6-bis[2-(dimethylamino)ethoxy]-9h-xanthen-9-onedihydrochloride, 2,8-bis[dimethylaminoacetyl]dibenzofurin dihydrochloride hydrate, tilorone analog R-9536-DA, indoprofen, ciclopiroxolamine, tryptophan, ansindione, nabumetone, oxybendazole, albendazole, tropicamide, pramoxine hydrochloride, atenolol, mebendazole, carbetapentane citrate, monensin sodium, methoxyvone, hydroxyzine, phenazopyridine, clofoctol, ipraflavone, zomepirac, biochanin A, xylometazoline hydrochloride, fenbendazole, pirenzepine, triprolidine hydrochloride, daidzein, tripelennamine citrate, colchicines, aminopyridine, trimethoprim, helenine, hydroxyurea, amiodarone hydrochloride, clindamycin hydrochloride, sulfachlorpyridazine, mephenesin, semustine, clofivric acid, clofibrate, ibuprofen, hyoscyamime, nafcillin sodium, piperin, clidinium bromide, trioxsalen, hydralazine and

Abstract: Compounds for inhibiting hypoxia inducible factor (HIF) prolyl-4-hydroxylases (PHDs) having the general formula (1). Methods of using these and related compounds for treating a patient having a condition that would benefit from inhibiting HIF PHD are also described herein.

Abstract: Methods for treating a patient suffering from neural cell injury, the method comprising administering to the patient an effective amount of a HIF prolyl-4-hydroxylase inhibiting compound having the following general formula (1) wherein R1 is a cyclic group containing at least three and up to seven carbon atoms and optionally containing one or more heteroatoms selected from O, N, and S, and optionally attached to the shown carbon atom by a linking group; R2 is independently selected from said cyclic groups of R1 and acyclic hydrocarbon groups R5 containing up to twenty carbon atoms; R3 is selected from hydrogen atom and hydrocarbon groups containing up to six carbon atoms; R6 and R7 are independently selected from hydrogen atom, hydrocarbon groups containing up to three carbon atoms, halogen atom, and polar groups, as well as methylene-linked versions thereof; and t is 0 or 1.

Abstract: The present invention relates to a method for enhancing arginase activity in a damaged or injured cell. In other aspects, the invention provides a method for treating a disorder that can be treated by enhancing arginase activity in a human in need thereof, the method comprising administering to the human an effective amount of a compound that enhances arginase activity. Such disorders include ischemia, hypoxia, neurodegenerative disease or condition, stroke or trauma of the nervous system. In yet another aspect, the invention provides methods for promoting regeneration of a neural cell in a human in need thereof.

Abstract: The present invention relates to methods for enhancing Hypoxia inducible factor-1 (HIF) activity in a cell by contacting the cell with any one of the following compounds: 3,6-bis[2-(dimethylamino)ethoxy]-9h-xanthen-9-onedihydrochloride, 2,8-bis[dimethylaminoacetyl]dibenzofurin dihydrochloride hydrate, tilorone analogue R-9536-DA, indoprofen, ciclopiroxolamine, tryptophan, ansindione, nabumetone, oxybendazole, albendazole, tropicamide, pramoxine hydrochloride, atenolol, mebendazole, carbetapentane citrate, monensin sodium, methoxyvone, hydroxyzine, phenazopyridine, clofoctol, ipraflavone, zomepirac, biochanin A, xylometazoline hydrochloride, fenbendazole, pirenzepine, triprolidine hydrochloride, daidzein, tripelennamine citrate, colchicines, aminopyridine, trimethoprim, helenine, hydroxyurea, amiodarone hydrochloride, clindamycin hydrochloride, sulfachlorpyridazine, mephenesin, semustine, clofivric acid, clofibrate, ibuprofen, hyoscyamime, nafcillin sodium, piperin, clidinium bromide, trioxsalen, hydralazine a

Abstract: In one aspect, the invention relates to a method for identifying a drug candidate with activity as a neuroprotective agent. The method includes determining whether a compound reduces ATF4 activity; and identifying the compound that reduces ATF4 activity as a drug candidate.

Abstract: The present invention relates to a method for identifying a drug candidate for enhancing expression of p21cip1/waf1 in a human patient suffering from a medical condition that can be treated by enhancing expression of p21C?1/waf1. The method includes (a) providing a cell line comprising a nucleic acid sequence that comprises a p21cip1/waf1 promoter operationally ligated to a reporter domain; (b) exposing the cell line to a compound; and (c) identifying a compound that induces expression of the reporter domain. The compound that induces expression of the reporter domain is a drug candidate for treating a medical condition that can be treated by enhancing expression of p21cip1/waf1.