Akshat Jain: Daraxonrasib and a New Chapter in Pancreatic Ductal Adenocarcinoma
Akshat Jain/lluh.org

Akshat Jain: Daraxonrasib and a New Chapter in Pancreatic Ductal Adenocarcinoma

Akshat Jain, Medical Director of Pediatric and Young Adult Program for Hemostasis/Thrombosis and Sickle Cell Disease at Loma Linda University Children’s Health, shared a post on LinkedIn:

Godzilla of cancer news !

The fight of metastatic pancreatic cancer patients has for decades been one sided, with odds against them.

With this announcement at American Society of Clinical Oncology (ASCO) history has been made and hope restored.

Disease: Pancreatic Ductal Adeno Carcinoma (most prevalent panceratic maligancy) – a death sentence with limited hope and life expectancy despite conventional chemotherapy.

Drug: Why this Pan-RAS inhibitor Works in PDAC?

1. >90% of PDAC has KRAS mutations (predominantly G12D, G12V, G12R) — daraxonrasib targets all of them.
2. Overcomes resistance mechanisms:

  • Secondary KRAS mutations.
  • Wild-type RAS allele amplification.
  • Compensatory NRAS/HRAS activation via RTKs.

3. Exploits oncogene addiction: RAS-driven tumors are highly dependent on RAS signaling, making them vulnerable to direct RAS inhibition.
4. Tumor Microenvironment (TME) Remodeling.
5. RAS(ON) inhibitors also reverse immunosuppression in PDAC.

Clincial Trial : presented to standing ovation- RASolute 302, a phase 3 trial Data presented at American Society of Clinical Oncology (ASCO) 2026 and published in NEJM Group

Median Overall Survival : 13.2 mo with Daraxonrasib vs 6.7 mo chemotherapy

This is the “First time” PDAC patients lived >1 year median in second-line therapy.

What Makes RAS(ON) Inhibition novel : For decades, KRAS was ‘undruggable’ in 90%+ of PDAC cases. Daraxonrasib breaks through with a ‘tri-complex mechanism’.

Its not a slam dunk or a cure , which is the final goal, but this is a step in direction!”

Akshat Jain: Daraxonrasib and a New Chapter in Pancreatic Ductal Adenocarcinoma

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