Abstract: 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): wherein: L represents a linker selected from —C?C—, (a tolan), —CH?CH— (a stilbene, preferably trans); or —CRa?CRb— a stilbene derivative; where Ra and Rb are independently H or phenyl optionally substituted with —(R3)p or —(R4)q; R1 to R4 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 R1 to R2 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.

Abstract: 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): wherein: L represents a linker selected from —C?C—, (a tolan), —CH?CH— (a stilbene, preferably tram); or —CRa?CRb— a stilbene derivative; where Ra and Rb are independently H or phenyl optionally substituted with —(R3)p or —(R4)q; R1 to R4 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 R1 to R2 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.

Abstract: 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): wherein: L represents a linker selected from —C?C—, (a tolan), —CH?CH— (a stilbene, preferably trans); or —CRa?CRb— a stilbene derivative; where Ra and Rb are independently H or phenyl optionally substituted with —(R3)p or —(R4)q; R1 to R4 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 R1 to R2 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.

Abstract: 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): wherein: L represents a linker selected from —C?C—, (a tolan), —CH?CH— (a stilbene, preferably trans); or —CRa?CRb— a stilbene derivative; where Ra and Rb are independently H or phenyl optionally substituted with —(R3)p or —(R4)q; R1 to R4 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 R1 to R2 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.

Abstract: 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): wherein: L represents a linker selected from —C?C—, (a tolan), —CH?CH— (a stilbene, preferably trans); or —CRa?CRb— a stilbene derivative; where Ra and Rb are independently H or phenyl optionally substituted with —(R3)p or —(R4)q; R1 to R4 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 R1 to R2 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.

Abstract: 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): wherein: L represents a linker selected from —C?C—, (a tolan), —CH?CH— (a stilbene, preferably trans); or —CRa?CRb— a stilbene derivative; where Ra and Rb are independently H or phenyl optionally substituted with —(R3)p or —(R4)q; R1 to R4 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 R1 to R2 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.

Abstract: 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): wherein: L represents a linker selected from —C?C—, (a tolan), —CH?CH— (a stilbene, preferably trans); or —CRa?CRb— a stilbene derivative; where Ra and Rb are independently H or phenyl optionally substituted with —(R3)p or —(R4)q; R1 to R4 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 R1 to R2 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.

Abstract: A combination of Vitamin C and a quinone used as a supplemental treatment for a cancer patient. The combination may be administered before, during and after the patient undergoes a conventional cancer treatment protocol. The combination may be administered orally, intravenously, or intraperitoneally. Oral administration may be in the form of capsules containing a predetermined ratio of Vitamin C to Vitamin K3. The supplemental treatment is effective to inhibit metastases of cancer cells and inhibit tumor growth. The ratio of Vitamin C to Vitamin K3 is in the range of about 50 to 1 to about 250 to 1. A method for evaluating the effectiveness of the supplemental treatment includes monitoring the patient's serum DNase activity throughout the course of treatment.

Abstract: A combination of Vitamin C and a quinone used as a supplemental treatment for a cancer patient. The combination may be administered before, during and after the patient undergoes a conventional cancer treatment protocol. The combination may be administered orally, intravenously, or intraperitoneally. Oral administration may be in the form of capsules containing a predetermined ratio of Vitamin C to Vitamin K3. The supplemental treatment is effective to inhibit metastases of cancer cells and inhibit tumor growth. The ratio of Vitamin C to Vitamin K3 is in the range of about 50 to 1 to about 250 to 1. A method for evaluating the effectiveness of the supplemental treatment includes monitoring the patient's serum DNase activity throughout the course of treatment.