Monoethanolamine (Etn) displays strong in vitro and in vivo efficacy in prostate cancer cell lines and xenograft models, respectively, as well as in cell lines from diverse cancer types. Etn is a pro-drug, which upon entry into tumor cells, is converted into cytotoxic phosphoethanolamine (PhosE). Etn treatment potently down-regulates HIF-1α and drives a catastrophic uncoupling of multiple pathways to induce metabolic crisis and cell death, selectively in tumor cells, while sparing normal cells. Importantly, the ovarian cancer cell line OVCAR3 was more sensitive to Etn than all the prostate, breast, colon, and pancreatic cancer cell lines tested. An Etn-based formulation with favorable pharmacokinetics/pharmacodynamics (PK/PD) can therefore in some embodiments be used as single therapeutic for EOC or OCCC.

Monoethanolamine (Etn) displays strong in vitro and in vivo efficacy in prostate cancer cell lines and xenograft models, respectively, as well as in cell lines from diverse cancer types. Etn is a pro-drug, which upon entry into tumor cells, is converted into cytotoxic phosphoethanolamine (PhosE). Etn treatment potently down-regulates HIF-1α and drives a catastrophic uncoupling of multiple pathways to induce metabolic crisis and cell death, selectively in tumor cells, while sparing normal cells. Importantly, the ovarian cancer cell line OVCAR3 was more sensitive to Etn than all the prostate, breast, colon, and pancreatic cancer cell lines tested. An Etn-based formulation with favorable pharmacokinetics/pharmacodynamics (PK/PD) can therefore in some embodiments be used as single therapeutic for EOC or OCCC.

The present invention describes methods and compositions for improving the therapeutic efficacy of therapeutic agents previously limited by suboptimal therapeutic performance by either improving efficacy as monotherapy or reducing side effects. Such methods and compositions are particularly applicable to mustard-based alkylating agents such as uracil mustard and analogs, derivatives, or prodrugs thereof, including 6-methyluracil mustard and 6-ethyluracil mustard.

The present invention describes methods and compositions for improving the therapeutic efficacy of therapeutic agents previously limited by suboptimal therapeutic performance by either improving efficacy as monotherapy or reducing side effects. Such methods and compositions are particularly applicable to mustard-based alkylating agents such as uracil mustard and analogs, derivatives, or prodrugs thereof, including 6-methyluracil mustard and 6-ethyluracil mustard.

The present invention describes methods and compositions for improving the therapeutic efficacy of therapeutic agents previously limited by suboptimal therapeutic performance by either improving efficacy as monotherapy or reducing side effects. Such methods and compositions are particularly applicable to mustard-based alkylating agents such as uracil mustard and analogs, derivatives, or prodrugs thereof, including 6-methyluracil mustard and 6-ethyluracil mustard.

Provided herein are formulations for topical and/or transdermal administration, and methods of using these formulations for increasing resistance to viral infections and improving immune system activity. Also provided are formulations for topical and/or transdermal administration, and methods of using these formulations for modulating the pH (e.g., raising) of a tissue or microenvironment for the prevention of and treatment of a viral infection and improving the immune response by activating immune cells (e.g., neutrophils, monocytes and macrophages, natural killer cells, dendritic cells, and platelets and endothelial cells).

Provided herein are formulations for topical and/or transdermal administration, and methods of using these formulations for increasing resistance to viral infections and improving immune system activity. Also provided are formulations for topical and/or transdermal administration, and methods of using these formulations for modulating the pH (e.g., raising) of a tissue or microenvironment for the prevention of and treatment of a viral infection and improving the immune response by activating immune cells (e.g., neutrophils, monocytes and macrophages, natural killer cells, dendritic cells, and platelets and endothelial cells).

The present invention relates to methods for treating, preventing, or reducing the risk of microbial infections while minimizing adverse gastrointestinal effects using a two-stage dosing regimen comprising about 1 to about 7 days of intravenous administration followed by about 1 to about 14 days of oral administration of an antimicrobial agent.

The present invention relates to methods for treating, preventing, or reducing the risk of microbial infections while minimizing adverse gastrointestinal effects using a two-stage dosing regimen comprising about 1 to about 7 days of intravenous administration followed by about 1 to about 14 days of oral administration of an antimicrobial agent.

The present disclosure provides methods method for alleviating liver injury using a Farnesoid X receptor (FXR) activator.