A61K31/45

SMALL MOLECULE RPN13 INHIBITORS WITH ANTITUMOR PROPERTIES

Compounds of formula (I), (II), and (III) having the structure shown below are presented: wherein R-R.sub.6 are defined herein. These molecules work as proteasome inhibitors and bind to the RPN13 subunit of the 19S regulatory particle, and can be used in methods of treating a condition or a disease, such as cancer, in a mammal

SMALL MOLECULE RPN13 INHIBITORS WITH ANTITUMOR PROPERTIES

Compounds of formula (I), (II), and (III) having the structure shown below are presented: wherein R-R.sub.6 are defined herein. These molecules work as proteasome inhibitors and bind to the RPN13 subunit of the 19S regulatory particle, and can be used in methods of treating a condition or a disease, such as cancer, in a mammal

Small molecule stimulators of steroid receptor coactivator-3 and methods of their use as cardioprotective and/or vascular regenerative agents

Small molecule stimulators of steroid receptor coactivator-3 (SRC-3) and methods of their use as cardioprotective agents are provided. The small molecule stimulators are useful for promoting cardiac protection and repair and vascular regeneration after myocardial infarction. The compounds are also useful in preventing cardiac hypertrophy and collagen deposition and improving cardiac post-infarction function.

COVALENT INHIBITORS OF CDK-7
20180008604 · 2018-01-11 ·

The disclosure includes compounds of Formula (I)

##STR00001## wherein R.sub.0, R.sub.1, R.sub.2, R.sub.3, R.sub.4, R.sub.5, and L are defined herein. Also disclosed is a method for treating a neoplastic disease, autoimmune disease, and inflammatory disorder with these compounds.

SMALL MOLECULES AGAINST CEREBLON TO ENHANCE EFFECTOR T CELL FUNCTION

Disclosed are small molecules against cereblon to enhance effector T cell function. Methodos of making thes molecules and methods of using them to treat various disease states are also disclosed.

SMALL MOLECULES AGAINST CEREBLON TO ENHANCE EFFECTOR T CELL FUNCTION

Disclosed are small molecules against cereblon to enhance effector T cell function. Methodos of making thes molecules and methods of using them to treat various disease states are also disclosed.

COMBINATION THERAPY OF A TYPE II ANTI-CD20 ANTIBODY WITH A SELECTIVE BCL-2 INHIBITOR

The present invention is directed to a combination therapy involving a type II anti-CD20 antibody and a selective Bcl-2 inhibitor for the treatment of a patient suffering from cancer, particularly, a CD20-expressing cancer.

COMBINATION THERAPY OF A TYPE II ANTI-CD20 ANTIBODY WITH A SELECTIVE BCL-2 INHIBITOR

The present invention is directed to a combination therapy involving a type II anti-CD20 antibody and a selective Bcl-2 inhibitor for the treatment of a patient suffering from cancer, particularly, a CD20-expressing cancer.

REGENERATING FUNCTIONS AND PHENOTYPES OF CONNECTIVE TISSUE THROUGH NPAS2 SUPPRESSION

The present invention provides methods for improving or accelerating wound healing in a subject comprising administering to a wound of the subject in need thereof an agent that suppresses expression of a clock gene, wherein the clock gene is neuronal PAS domain protein 2 (Npas2). This invention also relates to methods for regenerating alveolar bone, regenerating connective tissue at a wound site, and for decreasing wound area size comprising administering to a bone loss site or a wound site, in particular, an open wound site, of a subject an agent that suppresses expression of Npas2.

REGENERATING FUNCTIONS AND PHENOTYPES OF CONNECTIVE TISSUE THROUGH NPAS2 SUPPRESSION

The present invention provides methods for improving or accelerating wound healing in a subject comprising administering to a wound of the subject in need thereof an agent that suppresses expression of a clock gene, wherein the clock gene is neuronal PAS domain protein 2 (Npas2). This invention also relates to methods for regenerating alveolar bone, regenerating connective tissue at a wound site, and for decreasing wound area size comprising administering to a bone loss site or a wound site, in particular, an open wound site, of a subject an agent that suppresses expression of Npas2.