The present invention relates to compositions and methods for cancer treatment comprising compounds of Formulae I, II, and III. In some aspects, the invention relates to the treatment of B-cell Lymphoma or other hematopoietic cancers. In other aspects, the invention provides methods for treating particular types of hematopoietic cancers, such as, for example, B-cell lymphoma, using a combination of one or more compounds of Formulae I, II, and III. Combination therapy with, for example, 26S proteasome inhibitors, such as, for example, Bortezomib, are also included. In another aspect the present invention relates to autoimmune treatment with compounds of Formulae I, II, and III. In another aspect, this invention relates to methods for identifying compounds, for example, compounds of the BH3 mimic class, that have in vitro properties that predict in vivo efficacy against B-cell lymphoma tumors and other cancers as well as autoimmune disease.

The present invention relates provides methods of predicting cell sensitivity to a test agent. In some embodiments, the cells are cultured in a culture medium having serum.

The invention relates to a method for determining the activity of a component of the electron transport chain or any associated protein thereof and for determining the effect of a compound on the activity of a component of the electron transport chain or any associated protein thereof. The invention also relates to a kit comprising a redox probe, at least one electron donor compound of a component of the electron transport chain or a protein associated thereof and optionally comprising a sample comprising mitochondrial membranes and to the use of said kit in the methods of the invention.

The present invention is directed to a method of quantifying intracellular metabolite effluxes in permeabilized cancer cells for selecting cancer patients responsive for a cancer treatment, the method comprising the steps of: a) providing a sample of cancer cells taken from a patient; b) permeabilizing said cancer cells; c) incubating said permeabilized cancer cells in a reaction medium for a period of time allowing biological activity of intracellular organelles and accumulation of metabolites produced by said activity into the reaction medium in the presence of a substrate or substrates relating to a metabolite efflux or effluxes of interest, wherein said substrates used are at least glutamine and pyruvate; d) determining the quantity of metabolites relating to said metabolite efflux or effluxes of interest accumulated in the reaction medium during step c); and e) comparing the amounts of metabolites determined in step d) to equal measurements performed on control samples of the same tissue type and assessing the aggressiveness of the cancer cells or the treatment response of the cancer cells to a drug affecting a metabolic pathway or pathways relating to said metabolite efflux or effluxes of interest.

Embodiments herein include methods for enhancing post-ischemic functional recovery through administration of mitochondria and related devices and methods. In an embodiment, a method for enhancing post-ischemic functional recovery is included. The method can include harvesting somatic cells from a patient or a donor, converting the somatic cells into induced pluripotent stem cells, extracting mitochondria from the induced pluripotent stem cells, and transplanting the mitochondria into the patient. Other embodiments are also included herein.

The present disclosure relates to methods of identifying patients that may be responsive to mitochondrial inhibitor therapies to target and eradicate cancer stem cells. Also described are diagnostic kits that may be used to identify patients responsive to mitochondrial inhibitor therapies.

In various aspects the invention provides methods of predicting sensitivity of a cancer cell to a therapeutic agent by contacting a test cell population BH3 domain peptide; measuring the amount of BH3 domain peptide induced mitochondrial outer membrane permeabilization in the test cell population; and comparing the amount of BH3 domain peptide induced mitochondrial outer membrane permeabilization in the test cell population to a control cell population that has not been contacted with the therapeutic agent. An increase in mitochondrial membrane permeabilization in the test cell population compared to the control cell population indicates the cell is sensitive to the therapeutic agent.

The present disclosure relates to compounds that bind to flavin-containing enzymes and inhibit mitochondrial function, referred to herein as mitoflavoscins. Methods of screening compounds for mitochondrial inhibition and anti-cancer properties are disclosed. Also described are methods of using mitoflavoscins to prevent or treat cancer, bacterial infections, and pathogenic yeast, as well as methods of using mitoflavoscins to provide anti-aging benefits. Specific mitoflavoscin compounds are also disclosed.

Mitochondria are central to the intrinsic apoptotic pathway of programmed cell death. Commitment to cell death occurs upon mitochondrial outer membrane permeabilization, and dysregulation of this vital apoptotic control point is implicated in various pathologies. Provided herein are novel sensors which can detect, in real time and with great sensitivity, the release of protons from intact mitochondria caused by mitochondrial outer membrane permeabilization. Embodiments include graphene based ion-sensitive field effect transistors.

The present invention is inter alia concerned with a method of diagnosing Alzheimer's disease in a patient, wherein said method is based on determining the amount of at least one premature mitochondrial protein. Further, the present invention relates to the use of such a protein as marker for Alzheimer's disease. Accordingly, antibodies binding to such a preprotein may be used for diagnosing Alzheimer's disease. The present invention is based on the finding that premature mitochondrial proteins accumulate in Alzheimer's disease.