A61K31/50

METHODS OF SYNTHESIZING THYROID HORMONE ANALOGS AND POLYMORPHS THEREOF

The disclosure describes methods of synthesis of pyridazinone compounds as thyroid hormone analogs and their prodrugs. Preferred methods according to the disclosure allow for large-scale preparation of pyridazinone compounds having high purity. In some embodiments, preferred methods according to the disclosure also allow for the preparation of pyridazinone compounds in better yield than previously used methods for preparing such compounds. Also disclosed are morphic forms of a pyridazinone compound. Further disclosed is a method for treating resistance to thyroid hormone in a subject having at least one TRβ mutation.

Inhibitors of receptor interacting protein kinase I for the treatment of disease

Disclosed herein are compounds which inhibit RIPK1, pharmaceutical compositions, and methods of treatment of RIPK1-mediated diseases, such as neurodegenerative disorders, inflammatory disorders, and cancer.

Inhibitors of receptor interacting protein kinase I for the treatment of disease

Disclosed herein are compounds which inhibit RIPK1, pharmaceutical compositions, and methods of treatment of RIPK1-mediated diseases, such as neurodegenerative disorders, inflammatory disorders, and cancer.

Pyrimidine cyclohexenyl glucocorticoid receptor modulators

The present invention provides a class of pyrimidinedione cyclohexenyl compounds and methods of using these compounds as glucocorticoid receptor modulators.

TREATMENT OF NEURODEGENERATION VIA REPROGRAMMING METABOLISM BY INHIBITING PHD
20220409606 · 2022-12-29 ·

The present disclosure relates to methods and compounds for promoting anabolic pathways in neuronal cells leading to improved neuronal survival. In particular, the present disclosure relates to inhibiting PHD to promote glycolysis and neuronal survival in a variety of neurodegenerative conditions such as retinitis pigmentosa.

TREATMENT OF NEURODEGENERATION VIA REPROGRAMMING METABOLISM BY INHIBITING PHD
20220409606 · 2022-12-29 ·

The present disclosure relates to methods and compounds for promoting anabolic pathways in neuronal cells leading to improved neuronal survival. In particular, the present disclosure relates to inhibiting PHD to promote glycolysis and neuronal survival in a variety of neurodegenerative conditions such as retinitis pigmentosa.

CHEMOKINE RECEPTOR BINDING HETEROCYCLIC COMPOUNDS WITH ENHANCED EFFICACY

The invention relates to heterocyclic compounds consisting of a core nitrogen atom surrounded by three pendant groups, wherein two of the three pendant groups are preferably benzimidazolyl methyl and tetrahydroquinolyl, and the third pendant group contains N and optionally contains additional rings. The compounds bind to chemokine receptors, including CXCR4 and CCR5, and demonstrate protective effects against infection of target cells by a human immunodeficiency virus (HIV).

CHEMOKINE RECEPTOR BINDING HETEROCYCLIC COMPOUNDS WITH ENHANCED EFFICACY

The invention relates to heterocyclic compounds consisting of a core nitrogen atom surrounded by three pendant groups, wherein two of the three pendant groups are preferably benzimidazolyl methyl and tetrahydroquinolyl, and the third pendant group contains N and optionally contains additional rings. The compounds bind to chemokine receptors, including CXCR4 and CCR5, and demonstrate protective effects against infection of target cells by a human immunodeficiency virus (HIV).

ALK INHIBITORS FOR TREATMENT OF ALK-NEGATIVE CANCER AND PLASMA CELL-MEDIATED DISEASES

The present invention provides a method of treating ALK-negative/LTK-positive cancer in a subject, comprising administering to the subject a pharmaceutically-effective dose of a linear inhibitor of ALK. The invention is of particular utility in treating multiple myeloma, including proteasome inhibitor-resistant multiple myeloma.

Benzocarbonyl compounds

Provided herein are compounds and pharmaceutical compositions comprising said compounds that are useful for treating cancers. Specific cancers include those that are mediated by YAP/TAZ or those that are modulated by the interaction between YAP/TAZ and TEAD.