The current document is directed to digital-image-normalization methods and systems that generate accurate intensity mappings between the intensities in two digital images. The intensity mapping generated from two digital images is used to normalize or adjust the intensities in one image in order to produce a pair of normalized digital images to which various types of change-detection methodologies can be applied in order to extract differential data. Accurate intensity mappings facilitate accurate and robust normalization of sets of multiple digital images which, in turn, facilitates many additional types of operations carried out on sets of multiple normalized digital images, including change detection, quantitative enhancement, synthetic enhancement, and additional types of digital-image processing, including processing to remove artifacts and noise from digital images.

Compounds, compositions, and methods for use in inhibiting the E3 enzyme Cbl-b in the ubiquitin proteasome pathway are disclosed. The compounds, compositions, and methods can be used to modulate the immune system, to treat diseases amenable to immune system modulation, and for treatment of cells in vivo, in vitro, or ex vivo.

Compounds, compositions, and methods for use in inhibiting the E3 enzyme Cbl-b in the ubiquitin proteasome pathway are disclosed. The compounds, compositions, and methods can be used to modulate the immune system, to treat diseases amenable to immune system modulation, and for treatment of cells in vivo, in vitro, or ex vivo.

The present invention provides compounds, compositions thereof, and methods of using the same. The compounds include an IRAK binding moiety capable of binding to IRAK4 and a degradation inducing moiety (DIM). The DIM could be DTM a ligase binding moiety (LBM) or lysine mimetic. The compounds could be useful as IRAK protein kinase inhibitors and applied to IRAK mediated disorders.

The present invention provides compounds, compositions thereof, and methods of using the same for the inhibition of HPK1, and the treatment of HPK1-mediated disorders.

The present invention provides compounds, compositions thereof, and methods of using the same for the inhibition of HPK1, and the treatment of HPK1-mediated disorders.

The present disclosure provides substituted indole compounds of Formula I: (I) and the pharmaceutically acceptable salts and solvates thereof, wherein R.sup.1a, R.sup.1e, G1, G2, Q.sup.1, Q.sup.2, Q.sup.3, and (II) are defined as set forth in the specification. The present disclosure is also directed to the use of compounds of Formula I to treat a disease, disorder, or condition such as cancer in a subject.

##STR00001##

The present disclosure provides substituted indole compounds of Formula I: (I) and the pharmaceutically acceptable salts and solvates thereof, wherein R.sup.1a, R.sup.1e, G1, G2, Q.sup.1, Q.sup.2, Q.sup.3, and (II) are defined as set forth in the specification. The present disclosure is also directed to the use of compounds of Formula I to treat a disease, disorder, or condition such as cancer in a subject.

##STR00001##

Isoquinoline compounds for treating various diseases and pathologies are disclosed. More particularly, the present disclosure concerns the use of an isoquinoline compound or analogs thereof, in the treatment of disorders characterized by the activation of Wnt pathway signaling (e.g., cancer, abnormal cellular proliferation, angiogenesis, Alzheimer's disease, lung disease, inflammation, auto-immune diseases and osteoarthritis), the modulation of cellular events mediated by Wnt pathway signaling, as well as neurological conditions/disorders/diseases linked to overexpression of DYRK1A.

Isoquinoline compounds for treating various diseases and pathologies are disclosed. More particularly, the present disclosure concerns the use of an isoquinoline compound or analogs thereof, in the treatment of disorders characterized by the activation of Wnt pathway signaling (e.g., cancer, abnormal cellular proliferation, angiogenesis, Alzheimer's disease, lung disease, inflammation, auto-immune diseases and osteoarthritis), the modulation of cellular events mediated by Wnt pathway signaling, as well as neurological conditions/disorders/diseases linked to overexpression of DYRK1A.