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.

A compound of Formula (I), or a pharmaceutically acceptable salt thereof, is described, wherein the substituents are as defined herein. Pharmaceutical compositions comprising the same and method of using the same are also described.

##STR00001##

A compound of Formula (I), or a pharmaceutically acceptable salt thereof, is described, wherein the substituents are as defined herein. Pharmaceutical compositions comprising the same and method of using the same are also described.

##STR00001##

A kit or composition for in situ simultaneously derivatization of 14 phenol and carboxylic acid metabolites of benzene, toluene, ethyl benzene, and xylene (BTEX) in a urine sample is disclosed. The derivatization imparts a positive charge to phenol and carboxylic acid for subsequent LC-MS analysis. Limit of detection reached part-per-trillion levels for o-Cresol and part-per-billion levels for the remaining BTEX metabolites. BTEX metabolites can be detected in less than 35 mins according to one embodiment of the invention. Methods, kits and compositions disclosed herein can be used for in situ simultaneous derivatization of phenol and carboxylic acid in aqueous solution in general.

A kit or composition for in situ simultaneously derivatization of 14 phenol and carboxylic acid metabolites of benzene, toluene, ethyl benzene, and xylene (BTEX) in a urine sample is disclosed. The derivatization imparts a positive charge to phenol and carboxylic acid for subsequent LC-MS analysis. Limit of detection reached part-per-trillion levels for o-Cresol and part-per-billion levels for the remaining BTEX metabolites. BTEX metabolites can be detected in less than 35 mins according to one embodiment of the invention. Methods, kits and compositions disclosed herein can be used for in situ simultaneous derivatization of phenol and carboxylic acid in aqueous solution in general.

AKR1C3-activated prodrugs of Formula (I), pharmaceutical compositions comprising prodrugs of Formula (I), and their use in the treatment of hyperproliferative diseases such as cancer and for cell ablation. The compounds of the invention are able to penetrate neoplasm tissue and be selectively reduced to an active (cytotoxic) form by contact with an AKR1C3 enzyme found in the neoplasm. This active form is therefore able to ablate AKR1C3-expressing target cells of the neoplasm and therefore has particular utility in the treatment of cancer and other hyperproliferative disorders. ##STR00001##

Provided are compounds that inhibit ferroptosis activity, or modulate or inhibit a disease associated with ferroptosis dysregulation, such as neuropathy, ischemia reperfusion injury, acute kidney failure and cancer, including corresponding sulfonamides, and pharmaceutically acceptable salts, hydrates and stereoisomers thereof. The compounds are employed in pharmaceutical compositions, and methods of making and use, including treating a person in need thereof with an effective amount of the compound or composition, and detecting a resultant improvement in the person's health or condition.

The present invention relates to guanidine compounds for inhibiting mitochondrial oxidative phosphorylation (OXPHOS) and use thereof. More specifically, the present invention relates to a pharmaceutical composition for preventing or treating a OXPHOS-related disease, particularly cancer, by inhibiting mitochondrial oxidative phosphorylation and reprogramming cellular metabolism.

The present invention relates to guanidine compounds for inhibiting mitochondrial oxidative phosphorylation (OXPHOS) and use thereof. More specifically, the present invention relates to a pharmaceutical composition for preventing or treating a OXPHOS-related disease, particularly cancer, by inhibiting mitochondrial oxidative phosphorylation and reprogramming cellular metabolism.

The present disclosure describes an electroluminescent material which is formed of a compound having a structure of Formula (I), an OLED display panel utilizing the compound and an electronic device having the OLED display panel. The OLED display panel includes a first electrode, a second electrode, and an organic thin film layer disposed between the first electrode and the second electrode. The organic thin film layer comprises an electron transport layer which comprises any one or a combination of at least two of the compounds. The electroluminescent material has a triplet energy level E.sub.T of ≥2.7 eV, a HOMO energy level of ≤−5.85 eV, and a glass transition temperature of >120° C. This compound improves luminous efficiency in the OLED display panel and the electronic device.