The present disclosure relates to amoebae (slime molds) and uses thereof. In particular, the present disclosure relates to the use of amoebae or their environmentally stable spores to control agricultural infections and other uses.

The present disclosure relates to amoebae (slime molds) and uses thereof. In particular, the present disclosure relates to the use of amoebae or their environmentally stable spores to control agricultural infections and other uses.

The present invention includes a method of inhibiting or reducing deregulated JAK tyrosine kinase activity or JAK/ STAT signaling in a subject with a disease by administering Moxidectin or derivatives thereof in an amount sufficient to treat the disease in a subject, a therapeutically or prophylactically effective amount of the compound of Formula I or pharmaceutically acceptable salt thereof.

The present disclosure relates to a method of treating a glioblastoma by conjointly administering to a subject a BCL-xL inhibitor and a second therapy such as an alkylating agent, irradiation, or an MCL-1 inhibitor.

Embodiments of the disclosure encompass improvements on cell therapies by allowing the cells to be more effective for cancer treatment, including in a solid tumor microenvironment. In specific cases, the cells are modified to have reduced or inhibited levels of expression of T-Cell Death Associated Gene 8 (TDAG8), such as by CRISPR gene editing. In specific cases, the cells are further modified to express, for example, one or more engineered receptors, one or more cytokines, and optionally a suicide gene.

Embodiments of the disclosure encompass improvements on cell therapies by allowing the cells to be more effective for cancer treatment, including in a solid tumor microenvironment. In specific cases, the cells are modified to have reduced or inhibited levels of expression of T-Cell Death Associated Gene 8 (TDAG8), such as by CRISPR gene editing. In specific cases, the cells are further modified to express, for example, one or more engineered receptors, one or more cytokines, and optionally a suicide gene.

Provided is an improved cell-permeable nuclear import inhibitor (iCP-NI) for inhibition of cytokine storm or an inflammatory disease, in which solubility and stability are improved by introducing an advanced macromolecule transduction domain (aMTD)-based therapeuticmolecule systemic delivery technology (TSDT) into a cell-permeable nuclear import inhibitor (CP-NI, cSN50.1 peptide). The improved cell-permeable nuclear import inhibitor synthetic peptide according to the present disclosure more efficiently blocks signal transduction mediated by stress-responsive transcription factors (SRTFs) including NF-κB, based on remarkable cell permeability, and thus it may be used as an excellent prophylactic or therapeutic agent for cytokine storm or inflammatory diseases.

The present disclosure provides methods for predicting and thereby treating cancer or increasing the efficacy of an anti-cancer medication, in part by measuring checkpoint proteins on extracellular vesicles released from non-cancer cells. These checkpoint proteins promote cancer progression and/or compensate for the loss of signal from the checkpoint proteins being inhibited by the checkpoint inhibitory therapy. Compositions and methods of treatment are also provided.

The present disclosure relates generally to certain compounds, pharmaceutical compositions comprising said compounds, and methods of making and using said compounds and pharmaceutical compositions. The compounds and compositions disclosed herein may be used for the treatment or prevention of a Retroviridae viral infection, including an infection caused by the HIV virus.

The present disclosure relates generally to certain compounds, pharmaceutical compositions comprising said compounds, and methods of making and using said compounds and pharmaceutical compositions. The compounds and compositions disclosed herein may be used for the treatment or prevention of a Retroviridae viral infection, including an infection caused by the HIV virus.