Cambridge Innovation Capital, which earlier this week rolled out a second fund worth $300 million, is investing in two exciting global life science startups – Epitopea and Pretzel Therapeutics.

CIC has backed a $13.6m seed round by Cambridge’s Epitopea, a transatlantic cancer immunotherapeutics company and global leader in exploiting a new class of untapped tumour-specific antigens (TSAs).

And it has invested from its new Fund II in US and Swedish company Pretzel Therapeutics which is developing treatments to address the genetic roots of mitochondrial dysfunction. The University of Cambridge is listed as a fellow backer of the business.

As Business Weekly revealed earlier today, CIC now has a war chest of more than $642 million to invest in DeepTech and life science companies after raising the oversubscribed Fund II.

The Epitopea fundraising has been backed by a transatlantic syndicate of top-tier life sciences investors; besides CIC they include Advent Life Sciences, CTI Life Sciences and Fonds de solidarité FTQ.

The round was also supported by Novateur Ventures and the Harrington Discovery Institute/University Health Holdings.

Epitopea says the money will leverage its ground-breaking Cryptigen™ approach to create transformational immunotherapies that target broad cancer patient populations in both solid and haematological cancers.

The company’s proprietary technology provides an innovative approach to identifying shared, aberrantly expressed tumour specific antigens, known as Cryptigens™, that it has exclusively licensed from the Université de Montréal.

The seed round will be deployed to build the company’s executive team, advance further research on this new class of antigens and catalyse their translation into novel cancer immunotherapeutics, including therapeutic vaccines, cell therapies, and TCR-based biologics.

Dr Jon Moore, CEO of Epitopea and Operating Partner at Advent Life Sciences, said:

“The outstanding work of Epitopea’s co-founders, Université de Montréal scientists Drs. Claude Perreault, and Pierre Thibault, has opened a tremendous and potentially transformative opportunity for future cancer patients. With this significant seed financing by a syndicate of world-class investors from Canada and the UK, we can start translating these discoveries into novel therapeutics. We will be guided by science, deploying the best modalities available to help cancer patients achieve durable benefits.”

Pretzel is focused on developing groundbreaking therapies to reverse mitochondrial dysfunction by leveraging a deep mechanistic understanding of mitochondrial biology.

Mitochondria are essential energy-converting cellular organelles found in nearly every cell type throughout the body. Dysfunctional mitochondria are involved in more than 50 diseases.

The most severe of these are broadly termed mitochondrial diseases, a group of rare genetic conditions which affect individuals of all ages. Mitochondrial dysfunction also plays an important role in more common diseases, including ageing-related disorders.

Pretzel says it is attacking mitochondrial dysfunction at its roots.

“By taking aim at the genetic drivers of mitochondrial dysfunction, we believe our approach could be effective across a wide range of diseases which lack meaningful treatment options today,” the company says.

Pretzel was founded by some of the world’s foremost academics in mitochondrial biology and benefits from the leadership of accomplished experts in drug discovery, drug development, and company formation.

One of the co-founders, Michal Minczuk, is a programme leader and MRC investigator at the MRC Mitochondrial Biology Unit, University of Cambridge, with more than 20 years of experience in biotechnology.

At Cambridge, he leads the Mitochondrial Genetics programme. His work is focused on discovering the genetic links between mitochondrial dysfunction and human disease, with an emphasis on mitochondrial genome engineering.

His laboratory has made profound contributions to establishing the genetic basis and molecular mechanisms of disorders resulting from defects of mitochondrial gene expression.