CFT8919 exhibits potent and selective activity against EGFR L858R in patients with non-small cell lung cancer. Credit: Helena Nechaeva via Shutterstock.com.

C4 Therapeutics has entered an exclusive licensing agreement with Betta Pharmaceuticals to develop and commercialise CFT8919 across the greater China region.

The agreement will cover the Hong Kong special administrative region (SAR), the Macau SAR and Taiwan.

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It is expected to accelerate the development of CFT8919 in important international markets.

CFT8919 is an orally bioavailable BiDAC degrader designed to exhibit potent and selective activity against EGFR L858R in patients with non-small cell lung cancer (NSCLC).

In vivo and in vitro pre-clinical studies demonstrated that CFT8919 provides wider coverage of on-target resistant mutations and intracranial activity, indicating its potential to be effective against brain metastases.

Betta chairman and CEO Lieming Ding stated: “The collaboration will further expand Betta’s product pipeline and improve the productivity of the company’s research and development from discovery to clinical development and to commercialisation.”

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C4T will receive $35m, including a $25m one-time equity investment and an upfront cash component of $10m.

C4T can also earn up to $357m in milestone payments and receive low to mid-double-digit percentage royalties on net sales of the product in greater China.

Betta will be responsible for the development, manufacture and commercialisation of CFT8919 in the licensed territories. The company will also secure low single-digit percentage royalties on net sales outside these territories.

C4T will hold the exclusive rights to develop and commercialise the product in all regions except greater China.

C4 Therapeutics president and CEO Andrew Hirsch stated: “With their strong track record of developing and commercialising NSCLC therapies in China, we believe Betta is the ideal partner to advance CFT8919 clinical development in a region where there is a high prevalence of lung cancer patients with the EGFR L858R mutation.”