Whitehawk Therapeutics Presents Comprehensive Preclinical Data Highlighting its Next-Generation ADC Portfolio at the AACR 2026

Data demonstrate preclinical proof-of-concept for HWK-007, HWK-016 and HWK-206, underpinned by Whitehawk's proprietary Carbon Bridge Cysteine Re-pairing platform

Tumor regressions observed across various cancer models at low single‑digit mg/kg doses, with favorable tolerability (HNSTD 60 mg/kg) and low systemic levels of free payload (≤0.01% AUC)

Phase 1 trials for HWK-007 and HWK-016 are ongoing; an IND submission for HWK-206 is on track for mid-2026

MORRISTOWN, N.J., April 19, 2026 /PRNewswire/ -- Whitehawk Therapeutics, Inc. (Nasdaq: WHWK), a clinical-stage oncology therapeutics company applying advanced technologies to established tumor biology to efficiently deliver improved antibody drug conjugate (ADC) cancer treatments, today announced the presentation of new preclinical data across its ADC portfolio at the American Association for Cancer Research (AACR) Annual Meeting 2026, taking place April 17-22, 2026, in San Diego, CA.

"Across our three ADC programs, we have a consistent preclinical profile characterized by potent tumor regressions, high plasma stability and favorable tolerability in non‑human primates, coupled with low systemic levels of free payload," said David Dornan, PhD, Chief Scientific Officer of Whitehawk Therapeutics. "These data support the potential for our next‑generation bioconjugation and proprietary Carbon Bridge Cysteine Re-pairing linker-payload to deliver a differentiated, potentially best-in-class therapeutic index among TOP1i-based ADCs, which is fundamental to realizing the promise of ADCs for patients."

Overview of Preclinical Presentations

"Preclinical assessment of HWK-007, a next-generation, PTK7-targeting ADC with novel bioconjugation and linker-payload technology" (Poster #4439)

HWK-007 targets PTK7, the third most highly expressed tumor marker among clinically validated and emerging ADC targets, present in ~70% of tumors. HWK‑007 is being evaluated in an ongoing Phase 1 clinical trial in patients with non-squamous, EGFR wild-type non-small cell lung cancer; platinum-resistant ovarian cancer; and endometrial cancer (NCT07444814). Key preclinical findings include:

• High‑affinity binding and efficient internalization across a range of PTK7 expression levels
• Demonstrates potent binding, internalization and tumor cell-killing in a range of solid cancer cell lines
• Exhibits bystander activity and produces tumor regressions at doses as low as 1 mg/kg in small cell lung cancer and ovarian cancer models
• Demonstrates favorable pharmacokinetics and is well tolerated in non‑human primates with an HNSTD of 60 mg/kg (the maximal dose tested)
• Demonstrates high stability with free payload of 0.0067% AUC detected in circulation

"Preclinical assessment of HWK-016, a next-generation, MUC16-targeting ADC with novel bioconjugation and linker-payload technology" (Minisymposium Oral Presentation #1324)

HWK‑016 targets the non‑shed extracellular domain of MUC16 to avoid binding to circulating CA125 and associated antigen sink effects observed with earlier MUC16‑directed ADCs. HWK‑016 is being evaluated in an ongoing Phase 1 clinical trial in patients with advanced ovarian and endometrial cancers (NCT07470853). Key preclinical findings include:

• Selectively binds membrane‑bound MUC16 to ensure delivery to the tumor instead of circulating CA125
• Demonstrates potent binding, internalization and tumor cell-killing, and is minimally impacted by exogenous CA125
• Exhibits bystander activity, and produces tumor regressions at doses as low as 1 mg/kg in ovarian cancer xenograft models that shed high levels of CA125
• Demonstrates favorable pharmacokinetics and is well tolerated in non‑human primates with an HNSTD of 60 mg/kg (the maximal dose tested)
• Demonstrates high stability with free payload of

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