Backdrop to the Type6 Approach:
Hallmarks of Cancer, Kinases and Tumor Escape


Hallmarks of cancer continue to drive the emergence of resistance to therapy,
severely blunting the impact of marketed drugs and limiting the prospects for clinical candidates

We address hallmarks of cancer that drive resistance to therapy


Kinases are vital components within the circuitry of all cells and their action is carefully orchestrated in healthy tissues. Cancers reprogram these mechanics to enable sustained growth signaling and to resist cell death - even (and especially) when challenged by therapy.

Over the past three decades, and in recognition of the need to overcome these and other hallmarks of cancer, kinase drug discovery has generated an incredible wealth of chemical, structural, and biological information, dozens of marketed drugs, and >60b USD in annual revenue - yet progress has been usually underwhelming when measured in patient outcome.

While the field has come a long way and while our knowledge has never been more detailed, dose-limiting toxicities and incomplete inhibition have continued to allow for evasive tumor responses to kinase drugs - severely restricting their reach and utility.

At Type6 Tx, we have pioneered a class of kinase inhibitors that solve for these long-standing challenges, and that unlock opportunities for researchers, drug developers, and patients alike.

Central to the development of drug resistance: The hijacking of kinase signaling

  • Adaptive and compensatory tumor response - and ultimately the development of resistance to treatment - is a hallmark of cancers that severely blunts the therapeutic impact of marketed kinase drugs (and of those in the pipeline)

  • Due to their central role within tumor mechanics, kinases offer cancerous cells a range of levers with which to mount their escape

  • At its core, kinase-dependent tumor escape relies on two foundational pillars:

Adaptive: Tumors exploit the step-wise activation of kinases for growth and adaptive response upstream of blockades

Protective: Upon catalytic inhibition, kinases can compensate and relay anti-apoptotic signaling (pseudo-kinase activity)