Kishan Kumar

In oncology, targeted therapies work by targeting the tumor’s specific genes, proteins, or tissue environment that may have been responsible for the cancer’s growth. As these are targeted narrowly, they can limit the damage to normal cells. Targeted therapies have generated great interest amongst pharmaceutical manufacturers and several products are currently being commercialized. The existing cancer therapies are targeted to patients whose tumors have a particular mutation such as EGFR, HER2… Show more

In oncology, targeted therapies work by targeting the tumor’s specific genes, proteins, or tissue environment that may have been responsible for the cancer’s growth. As these are targeted narrowly, they can limit the damage to normal cells. Targeted therapies have generated great interest amongst pharmaceutical manufacturers and several products are currently being commercialized. The existing cancer therapies are targeted to patients whose tumors have a particular mutation such as EGFR, HER2, BCR-ABL, ALK or BRAF inhibitors, which has proven to take a front seat in many research and development activities.For pharmaceutical companies, it is important to understand the potential value of purchasing this data and building capabilities around it. This presentation evaluates the possibilities of leveraging diagnostic test data, based on an engagement that we explored by building capabilities around these data-sets and using it to enhance understanding of diagnosis, testing, and treatment behavior. In this presentation, we will demonstrate how to effectively use diagnostic testing data, as well as share our findings on its capabilities in forecasting and other commercial and clinical applications. Show less

Fabry disease, due to the deficiency of α-galactosidase A (α-Gal), causes lysosomal accumulation of globotriaosylceramide (Gb3) in multiple tissues and prominently in the vascular endothelium. Although enzyme replacement therapy (ERT) by injection of recombinant α-Gal improves the disease outcome, the effects on the vasculopathy associated with life-threatening cerebrovascular, cardiac and renal complications are still limited. We designed a strategy to enhance the delivery of α-Gal to organs… Show more

Fabry disease, due to the deficiency of α-galactosidase A (α-Gal), causes lysosomal accumulation of globotriaosylceramide (Gb3) in multiple tissues and prominently in the vascular endothelium. Although enzyme replacement therapy (ERT) by injection of recombinant α-Gal improves the disease outcome, the effects on the vasculopathy associated with life-threatening cerebrovascular, cardiac and renal complications are still limited. We designed a strategy to enhance the delivery of α-Gal to organs and endothelial cells (ECs). We targeted α-Gal to intercellular adhesion molecule 1 (ICAM-1), a protein expressed on ECs throughout the vasculature, by loading this enzyme on nanocarriers coated with anti-ICAM (anti-ICAM/α-Gal NCs). In vitro radioisotope tracing showed efficient loading of α-Gal on anti-ICAM NCs, stability of this formulation under storage and in model physiological fluids, and enzyme release in response to lysosome environmental conditions. In mice, the delivery of 125I-α-Gal was markedly enhanced by anti-ICAM/125I-α-Gal NCs in brain, kidney, heart, liver, lung, and spleen, and transmission electron microscopy showed anti-ICAM/α-Gal NCs attached to and internalized into the vascular endothelium. Fluorescence microscopy proved targeting, endocytosis and lysosomal transport of anti-ICAM/α-Gal NCs in macro- and micro-vascular ECs and a marked enhancement of Gb3 degradation. Therefore, this ICAM-1-targeting strategy may help improve the efficacy of therapeutic enzymes for Fabry disease. Show less