The invention provides methods of decreasing immune response by inhibiting iron-dependent cellular disassembly. The decrease in immune response may be used, for example, for treatment of a disorder associated with iron-dependent cellular disassembly, including an autoimmune disorder, allergy, or an inflammatory disorder. The invention also provides screening assays for identification of compounds that inhibit iron-dependent cellular disassembly and are also immunoinhibitory agents.

The invention provides methods of decreasing immune response by inhibiting iron-dependent cellular disassembly. The decrease in immune response may be used, for example, for treatment of a disorder associated with iron-dependent cellular disassembly, including an autoimmune disorder, allergy, or an inflammatory disorder. The invention also provides screening assays for identification of compounds that inhibit iron-dependent cellular disassembly and are also immunoinhibitory agents.

Methods and compounds are disclosed for wound healing by modulating autophagy. A formulation for modulating autophagy comprises a first modulating compound (FAM) selected from compounds having the general structure (I):

##STR00001## wherein: L represents a linker selected from —C≡C—, (a tolan), —CH═CH— (a stilbene, preferably tram); or —CR.sub.a═CR.sub.b— a stilbene derivative; where R.sub.a and R.sub.b are independently H or phenyl optionally substituted with —(R.sup.3).sub.p or —(R.sup.4).sub.q; R.sup.1 to R.sup.4 are independent substituents at any available position of the phenyl rings, preferably at 3, 3′, 4, 4′, and/or 5, 5′; and m, n, p, and q are independently 0, 1, 2, or 3 representing the number of substituents of the rings, respectively, but at least one of m or n must be ≥1. Each R.sup.1 to R.sup.2 is independently selected from substituents described herein, including but not limited to hydroxyl, alkoxy, halo, halomethyl and glycosides. The formulation may also include an auxiliary autophagy modulating compound (AAM) as described herein. The formulation may include a hydrogel formed by the compounds themselves or otherwise and may include salts and/or complexes.

Methods and compounds are disclosed for wound healing by modulating autophagy. A formulation for modulating autophagy comprises a first modulating compound (FAM) selected from compounds having the general structure (I):

##STR00001## wherein: L represents a linker selected from —C≡C—, (a tolan), —CH═CH— (a stilbene, preferably tram); or —CR.sub.a═CR.sub.b— a stilbene derivative; where R.sub.a and R.sub.b are independently H or phenyl optionally substituted with —(R.sup.3).sub.p or —(R.sup.4).sub.q; R.sup.1 to R.sup.4 are independent substituents at any available position of the phenyl rings, preferably at 3, 3′, 4, 4′, and/or 5, 5′; and m, n, p, and q are independently 0, 1, 2, or 3 representing the number of substituents of the rings, respectively, but at least one of m or n must be ≥1. Each R.sup.1 to R.sup.2 is independently selected from substituents described herein, including but not limited to hydroxyl, alkoxy, halo, halomethyl and glycosides. The formulation may also include an auxiliary autophagy modulating compound (AAM) as described herein. The formulation may include a hydrogel formed by the compounds themselves or otherwise and may include salts and/or complexes.

Methods and compounds are disclosed for wound healing by modulating autophagy. A formulation for modulating autophagy comprises a first modulating compound (FAM) selected from compounds having the general structure (I):

##STR00001## wherein: L represents a linker selected from —C≡C—, (a tolan), —CH═CH— (a stilbene, preferably tram); or —CR.sub.a═CR.sub.b— a stilbene derivative; where R.sub.a and R.sub.b are independently H or phenyl optionally substituted with —(R.sup.3).sub.p or —(R.sup.4).sub.q; R.sup.1 to R.sup.4 are independent substituents at any available position of the phenyl rings, preferably at 3, 3′, 4, 4′, and/or 5, 5′; and m, n, p, and q are independently 0, 1, 2, or 3 representing the number of substituents of the rings, respectively, but at least one of m or n must be ≥1. Each R.sup.1 to R.sup.2 is independently selected from substituents described herein, including but not limited to hydroxyl, alkoxy, halo, halomethyl and glycosides. The formulation may also include an auxiliary autophagy modulating compound (AAM) as described herein. The formulation may include a hydrogel formed by the compounds themselves or otherwise and may include salts and/or complexes.

This application relates generally to certain substituted pyrrolizine compounds, and pharmaceutical compositions which inhibit HBV replication, and methods of making and using them.

This application relates generally to certain substituted pyrrolizine compounds, and pharmaceutical compositions which inhibit HBV replication, and methods of making and using them.

This disclosure describes the characteristics of the “energetic” cancer stem cell (e-CSC) phenotype. This distinct sub-population of cancer stem cells (CSCs) has a unique energetic profile compared to bulk CSCs, being more glycolytic, having higher mitochondrial mass and elevated oxidative metabolism. e-CSCs also show an increased capacity to undergo cell cycle progression, enhanced anchorage-independent growth, and ALDH-positivity. The e-CSC phenotype presents new targets for cancer therapeutics, and in particular the anti-oxidant response, mitochondrial energy production, and mitochondrial biogenesis of e-CSCs makes them highly susceptible to mitochondrial inhibitors that target e-CSC anti-oxidant response, mitochondrial energy production, and mitochondrial biogenesis. Gene products for e-CSCs are disclosed, as well as classes of mitochondrial inhibiting therapeutic agents. Also disclosed are methods for identifying and separating e-CSCs from bulk cell populations.

This disclosure describes the characteristics of the “energetic” cancer stem cell (e-CSC) phenotype. This distinct sub-population of cancer stem cells (CSCs) has a unique energetic profile compared to bulk CSCs, being more glycolytic, having higher mitochondrial mass and elevated oxidative metabolism. e-CSCs also show an increased capacity to undergo cell cycle progression, enhanced anchorage-independent growth, and ALDH-positivity. The e-CSC phenotype presents new targets for cancer therapeutics, and in particular the anti-oxidant response, mitochondrial energy production, and mitochondrial biogenesis of e-CSCs makes them highly susceptible to mitochondrial inhibitors that target e-CSC anti-oxidant response, mitochondrial energy production, and mitochondrial biogenesis. Gene products for e-CSCs are disclosed, as well as classes of mitochondrial inhibiting therapeutic agents. Also disclosed are methods for identifying and separating e-CSCs from bulk cell populations.

Field of application: The invention relates to combinatorial chemistry, pharmacy and cosmetology, allows to synthesize new combinatorial libraries of derivatives of antibiotics for use in pharmacy, cosmetology and pharmacy.

Technical result: modified combinatorial derivatives of antibiotics with antimicrobial and antifungal activity against multiresistant and pan drug resistance strains of microorganisms and fungi. Means have a wide spectrum of action, and the supramolecular and combinatorial structure of their tens and hundreds of derivatives eliminates the resistance of microorganisms.