PAQ Therapeutics Targets 'Undruggable' Cancer with New Pan-KRAS Drug and $77M Financing

BURLINGTON, Mass. – January 22, 2026 – Clinical-stage oncology firm PAQ Therapeutics today announced two major milestones in its campaign against some of the most formidable cancers, securing a total of $77 million in Series B financing and dosing the first patient in a Phase 1 clinical trial for its novel pan-KRAS degrader, PT0511.

The dual announcement signals significant momentum for the company, which is focused on developing therapies for KRAS-driven cancers—a group of malignancies long considered notoriously difficult to treat. The fresh capital infusion, an extension of its previously announced Series B round, strengthens PAQ’s financial position to advance a multi-program pipeline aimed at a protein once deemed “undruggable.”

"Completing this Series B extension and dosing the first patient in our PT0511 Phase 1 study represent important milestones for PAQ," said Nan Ji, PhD, Chief Executive Officer of PAQ Therapeutics. "Together, these achievements highlight our continued execution against a multi-program clinical strategy and our focus on addressing significant unmet need across KRAS-driven cancers."

The KRAS Challenge: A Notoriously Difficult Target

For decades, the KRAS protein has been a frustrating target for cancer researchers. As a key regulator of cell growth and division, mutated KRAS acts like a stuck gas pedal, driving uncontrolled proliferation in approximately one in seven of all human cancers. These mutations are especially prevalent in some of the deadliest forms of the disease, found in over 90% of pancreatic cancers, about 40% of colorectal cancers, and a significant portion of non-small cell lung cancers (NSCLC).

The protein’s smooth, spherical structure lacks the obvious pockets that drugs typically bind to, earning it the “undruggable” moniker. This changed recently with the landmark approval of KRAS G12C-specific inhibitors like Amgen's sotorasib and Bristol Myers Squibb's adagrasib. While revolutionary, these drugs only work for patients with the specific G12C mutation, which accounts for only a fraction of all KRAS-driven tumors. More than 85% of patients with KRAS-mutated cancers, such as those with the common G12D or G12V variants, have been left without a targeted therapy.

Furthermore, even patients who initially respond to G12C inhibitors often develop resistance, as the cancer finds new ways to reactivate the KRAS pathway. This has created an urgent need for new therapeutic strategies that can offer broader coverage and more durable responses.

A New Strategy: Degrading the Problem Protein

PAQ Therapeutics is tackling this challenge with a fundamentally different approach: targeted protein degradation. Instead of merely blocking the KRAS protein's function, PAQ's drugs are designed to eliminate it entirely. Their candidate, PT0511, is a pan-KRAS degrader that acts like a molecular matchmaker, tagging multiple variants of the oncogenic KRAS protein for destruction by the cell's own waste disposal machinery, the proteasome.

This method offers several potential advantages over traditional inhibitors. By removing the protein, it disrupts both its catalytic and non-catalytic functions, which could lead to a deeper and more sustained suppression of cancer-driving signals. Critically, PT0511’s pan-KRAS design means it is intended to work against a wide spectrum of KRAS mutations, not just a single variant. This could dramatically expand the number of patients who might benefit and potentially overcome some of the resistance mechanisms that plague mutation-specific drugs.

"The initiation of clinical dosing with PT0511 expands our clinical portfolio beyond single-mutation KRAS targeting," said Andrew Krivoshik, MD, PhD, Chief Medical Officer of PAQ Therapeutics. "A pan-KRAS degradation approach has the potential to address key limitations for patients observed with existing KRAS- or pan-RAS inhibitor therapies."

The Phase 1 trial for PT0511 is a first-in-human, open-label study designed to evaluate the drug's safety, tolerability, and preliminary anti-tumor activity in patients with advanced solid tumors that harbor KRAS alterations.

Fueling the Pipeline: Investor Confidence and Clinical Momentum

The successful Series B extension, which brought the round’s total to $77 million with participation from new and existing investors, provides PAQ with a robust financial runway to execute its ambitious clinical plans. The proceeds are earmarked not only for the advancement of the pan-KRAS degrader PT0511 but also for the continued development of PT0253, the company's other clinical-stage asset.

PT0253 is a degrader specifically targeting the KRAS G12D mutation, which is particularly common in pancreatic, colorectal, and lung cancers and represents a patient population more than twice as large as that for G12C. By pursuing both a mutation-specific and a pan-variant strategy, PAQ is building a differentiated pipeline that attacks the KRAS challenge from multiple angles, increasing its chances of delivering a meaningful clinical impact.

Navigating a Crowded and Competitive Field

PAQ Therapeutics enters the clinical arena at a time of intense activity and competition in the KRAS space. The initial success of G12C inhibitors has ignited a global race to develop the next generation of KRAS-targeted therapies. Major pharmaceutical companies and agile biotech firms are all vying to create drugs that are more potent, more durable, and more broadly applicable.

Competitors are exploring various innovative modalities. Companies like Revolution Medicines and Erasca are developing pan-RAS “molecular glues,” which work differently than degraders but also aim for broader activity. Others, including Astellas and Neomorph, are also advancing their own protein degrader candidates. Meanwhile, companies like Mirati and Novartis are working on inhibitors for other specific mutations beyond G12C.

In this dynamic landscape, PAQ's strategy of leveraging targeted protein degradation to achieve what it calls “deep and selective suppression of oncogenic signaling” is a key differentiator. The initiation of the PT0511 trial marks a critical step in validating this approach in humans. The data from this study will be closely watched by the oncology community, as it could provide the first clinical proof-of-concept for a pan-KRAS degrader and potentially shift the paradigm for treating one of modern medicine's most challenging cancer targets.