Described are polymerizable high energy light absorbing compounds of formula I:

##STR00001##

wherein R.sup.1, R.sup.2, R.sup.3, R.sup.4, R.sup.5, R.sup.6, R.sup.7, R.sup.8, R.sup.9, and X are as described herein. The compounds absorb various wavelengths of ultraviolet and/or high energy visible light and are suitable for incorporation in various products, such as biomedical devices and ophthalmic devices.

The present invention relates to novel lignin-derived compounds and compositions comprising the same and their use as redox flow battery electrolytes. The invention further provides a method for preparing said compounds and compositions as well as a redox flow battery comprising said compounds and compositions. Additionally, an assembly for carrying out the inventive method is provided.

The present disclosure relates to heterocyclic compounds, pharmaceutically acceptable salts thereof, and pharmaceutical preparations thereof. Also described herein are compositions and the use of such compounds in methods of treating diseases and conditions mediated by deficient CFTR activity, in particular cystic fibrosis.

A cosmetic composition is provided, which comprises a carrier and a Vetiver root extract, in particular an extract from exhausted Vetiver root. This composition provides a stimulation of sebum production, stimulation of sebum antimicrobial, lipids production, activation of adipocytes volume increase, skin hydration, skin tonicity booster, skin fatigue reduction, perilabial wrinkles reduction, skin replumping, and fragrance long-lastingness enhancement.

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.

Provided are compounds of Formula I, or pharmaceutically acceptable salts thereof, and methods for their use as Nrf2 activators and for their production. ##STR00001##

The invention relates to substituted ureas, and compositions comprising the same, which in certain embodiments are useful for treating and/or preventing pain in a subject in need thereof.

A TRPM8 antagonist is provided that comprises the following the formula (I) described herein. In the formula (I), R.sub.1 is selected from a cycloalkyl, a bicycloalkyl, or a tricycloalkyl group. Each R.sub.1 group has 5 to 12 carbon atoms. Further, each R.sub.1 group is optionally substituted with an alkyl group having 1 to 5 carbons atoms or with a cycloalkyl group having 4 to 12 carbon atoms, and each R.sub.1 group is optionally saturated or partially unsaturated. Methods for treating pain are further provided and comprise administering to a subject in need thereof an effective amount of a TRPM8 antagonist comprising the formula (I).

Cryptosporidium parvum is a highly prevalent zoonotic and anthroponotic protozoan parasite that causes a diarrheal syndrome in children and neonatal livestock, culminating in growth retardation and mortalities. Disclosed herein are inhibitors against the enzymatic activity of recombinant CpLDH protein that were identified. The inhibitors were tested for anti-Cryptosporidium effect using in vitro infection assays of HCT-8 cells monolayers. Compounds NSC158011 and NSC10447 were identified to inhibit the proliferation of intracellular C. parvum in vitro, with IC50 values of 14.88 and 72.65 μM, respectively. At doses tolerable in mice, both NSC158011 and NSC10447 significantly reduced the shedding of C. parvum oocysts in infected immunocompromised mice's feces and prevented intestinal villous atrophy as well as mucosal erosion due to C. parvum. These findings have unveiled anti-Cryptosporidium drug candidates that can be explored further for the development of therapeutic agents against C. parvum infections.

The present invention provides compounds, compositions thereof, and methods of using the same for the inhibition of USP30, and the treatment of USP30-mediated disorders.