The Protein Kinase C Beta Type pipeline drugs market research report outlays comprehensive information on the Protein Kinase C Beta Type targeted therapeutics, complete with analysis by indications, stage of development, mechanism of action (MoA), route of administration (RoA), and molecule type. GlobalData’s report assesses the drugs in the Protein Kinase C Beta Type pipeline by therapy areas, indications, stages, MoA, RoA, molecule type and the key players in the development pipeline. Buy the report here.
The report also covers products from therapy areas such as Oncology, Ophthalmology, Dermatology, and Undisclosed which include the indications Breast Cancer, Ovarian Cancer, Diabetic Retinopathy, Hyperpigmentation, Melasma (Chlosma), and Unspecified. It also reviews key players involved in Protein Kinase C Beta Type targeted therapeutics development with respective active and dormant or discontinued products.
The Protein Kinase C Beta Type pipeline targets constitutes close to five molecules. Out of which, approximately five molecules are developed by companies and the remaining by the universities/institutes. The molecules developed by companies in Phase III, Phase II, and Discovery stages are 1, 3, and 1 respectively.
Protein Kinase C Beta Type overview
Protein kinase C beta type is a serine/threonine-protein kinase that requires calcium, phospholipids, and diacylglycerol (DAG) for activation. It participates in a range of cellular processes, including the regulation of the B-cell receptor (BCR) signalosome, apoptosis induced by oxidative stress, transcriptional regulation dependent on the androgen receptor, insulin signaling, and the proliferation of endothelial cells. It plays a crucial role in B-cell activation by modulating BCR-induced NF-kappa-B activation. Additionally, it facilitates the activation of the canonical NF-kappa-B pathway (NFKB1) by directly phosphorylating CARD11/CARMA1 at specific serine residues (‘Ser-559,’ ‘Ser-644,’ and ‘Ser-652’). This phosphorylation prompts the association of CARD11/CARMA1 with lipid rafts and the recruitment of the BCL10-MALT1 complex, as well as MAP3K7/TAK1. Subsequently, this cascade activates the IKK complex, leading to the translocation of NFKB1 to the nucleus and its activation. Furthermore, it directly participates in the negative feedback regulation of BCR signaling by diminishing the function of BTK through direct phosphorylation at ‘Ser-180.’ This modification alters BTK’s plasma membrane localization, thereby inhibiting BTK activity. Lastly, PKC beta type is involved in apoptosis triggered by oxidative damage
For a complete picture of Protein Kinase C Beta Type’s drug pipeline, buy the report here.
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