Drug Discovery at Mannkind

Drug discovery at MannKind is focused on two key areas:

  1. Developing therapeutics to make cancer cells more sensitive to classical chemotherapy or novel immunotherapeutics.
  2. Developing therapeutics that block growth signals found inside cancer cells.

Oncology

Developing therapeutics to make cancer cells more sensitive to classical chemotherapy or novel immunotherapeutics. Over the last 15 years, using emerging technologies, scientists have confirmed that apoptosis – or cell death that has been genetically programmed -- plays a central role within developing organisms by shaping the neural and immune systems and molding tissue specificity. They also demonstrated that apoptosis helps to establish a natural balance between cell death and cell renewal in mature animals by destroying excess, damaged or abnormal cells. In fact, apoptosis plays a broad role in normal life processes, and its failure contributes to a variety of diseases, including cancer.

Researchers at MannKind are exploring how apoptosis is regulated, how it might be repaired through genetic therapies, and how it can be selectively triggered through tailored treatments to induce suicide in cancer cells while leaving healthy cells unharmed.

Cancer Kinases

Developing therapeutics that block growth signals found inside cancer cells. An emerging theme in cancer biology is that many, if not all cancers are caused, to some extent by the aberrant activation of a class of enzymes known as kinases. Kinases are produced by some of the most commonly mutated genes in cancer. The goal of significant research efforts is to develop effective therapies that can modulate or inhibit various kinase pathways as well as the ability to identify which patients would mostly benefit from specific anti-kinase drugs. To date, there have been significant advance in the ability to synthesize specific kinase inhibitors. However, a major need remains to better understand the structural basis of compound selectivity, prospectively identify patients likely to respond to a specific kinase inhibitor, design improved pharmacodynamic endpoints, and understand the molecular basis of resistance to kinase inhibitor therapy.
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