Lunit to Present Six AI Studies at AACR 2026 Highlighting Advances in Precision Oncology and Real-World Clinical Application

On April 17, 2026 Lunit (KRX:328130), a leading provider of AI for cancer diagnostics and precision oncology, reported six studies at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, taking place from April 17 to 22 in San Diego, California.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

The presentations highlighted Lunit’s continued advancements in AI-driven biomarker development, tumor microenvironment (TME) analysis, and real-world clinical applicability. Several studies were conducted in collaboration with global partners, including Agilent Technologies.

In a study conducted with Agilent Technologies and Ajou University Medical Center, researchers used Lunit SCOPE IO and uIHC to analyze over 25,000 non-small cell lung cancer (NSCLC) samples. The results showed that tumors with high c-MET expression exhibited a significant reduction in immune cell density within 30 μm of tumor cells (p<0.001), revealing a spatial immune exclusion pattern not captured by conventional analysis. These findings suggest a potential link between c-MET overexpression and immune evasion, supporting combination strategies involving MET-targeted therapy and immunotherapy.

Researchers also present findings from an exploratory analysis of the phase II MOUNTAINEER trial, demonstrating that AI- quantified HER2 expression is strongly associated with treatment response in patients with HER2-positive metastatic colorectal cancer treated with tucatinib plus trastuzumab. The overall objective response rate (ORR) was 43.4%, increasing to as high as 80% in patients with higher HER2 expression, indicating a clearer dose-dependent relationship. Tumor-Infiltrating Lymphocyte (TIL) density independently predicted progression-free survival. Notably, patients with low stromal TIL levels showed no response (ORR 0%) and a significantly higher risk of disease progression.

These findings highlight the increasing complexity of biomarker assessment, where both tumor characteristics and immune context need to be considered, underscoring the potential role of AI in supporting treatment decision-making.

In addition to these representative studies, Lunit presented additional research abstracts at AACR (Free AACR Whitepaper) 2026, further demonstrating the breadth of its AI-powered oncology research. These include studies on

AI-based analysis of tumor-infiltrating lymphocyte in NSCLC in collaboration with Dr. David Rimm’s lab at Yale University School of Medicine
AI-based target discovery for bi-specific antibodies
Biomarker research in CD47-targeted therapies
"Our AACR (Free AACR Whitepaper) presentations reflect how AI is increasingly translating into real-world clinical impact" said Brandon Suh, CEO of Lunit. "Across these studies, we demonstrate how AI-driven biomarkers can enhance precision, deepen our understanding of tumor biology and increasingly support treatment decision-making in clinical practice."

Visit Lunit at Booth #2248 during AACR (Free AACR Whitepaper) 2026 to learn more about its latest research and AI-powered solutions in cancer diagnostics and therapeutics.

Lunit’s featured presentations at AACR (Free AACR Whitepaper) 2026 include:

[Poster #0011/11] Artificial intelligence-based spatial analysis of the local tumor microenvironment in relation to c-MET expression in non-small cell lung cancer
April 19, 2:00 PM – 5:00 PM, Section 1

[Poster #7735/26] HER2 expression and tumor-infiltrating lymphocytes predict response to tucatinib plus trastuzumab in HER2-positive metastatic colorectal cancer (MOUNTAINEER): Exploratory analysis of a multicenter, Phase II trial
April 22, 9:00 AM – 12:00 PM, Section 41

[Poster #4415/23] AI-powered analysis of millions of IHC images identifies 19 spatially highly co-expressed protein pairs to enable bispecific antibody development
April 21, 9:00 AM – 12:00 PM, Section 11

[Poster #0080/11] Quantitative assessment of tumor-infiltrating lymphocytes using AI in non-small cell lung cancer and association with immunotherapy response
April 19, 2:00 PM – 5:00 PM, Section 4

[Poster #4355/26] Cryo EM-based structural characterization of IMC-002, a next-generation anti-CD47 antibody with a unique binding site and biomarker candidates, supporting evidence of enhanced safety and efficacy
April 21, 9:00 AM – 12:00 PM, Section 9

(Press release, Lunit, APR 17, 2026, View Source [SID1234664482])

New Clinical and Preclinical Data for Investigational Candidate Zidesamtinib Presented at AACR Annual Meeting 2026

On April 17, 2026 Nuvalent, Inc. (Nasdaq: NUVL), a clinical-stage biopharmaceutical company focused on creating precisely targeted therapies for clinically proven kinase targets in cancer, reported new clinical and preclinical data for zidesamtinib, an investigational ROS1-selective inhibitor, to be presented during poster sessions at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026 being held April 17-22 in San Diego.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

"The strong patient enrollment in our ARROS-1 trial has reflected meaningful investigator enthusiasm for zidesamtinib’s profile and generated a robust data set that enables deep characterization of its activity for patients with ROS1-positive NSCLC beyond our initial pivotal data presentation," said James Porter, Ph.D., Chief Executive Officer at Nuvalent. "We’re highly encouraged by these clinical data for patients previously treated with repotrectinib or taletrectinib in our ARROS-1 trial, which we believe further reinforce the medical needs that remain for patients with ROS1-positive NSCLC despite the availability of new treatment options."

"Zidesamtinib demonstrated clinically meaningful activity in this heavily pre-treated subgroup, including activity in tumors with the ROS1 G2032R resistance mutation and intracranial complete responses for patients with CNS disease. Importantly, this indicates that ROS1-positive NSCLC tumors may remain ROS1-dependent beyond treatment with repotrectinib or taletrectinib and we believe supports the potential for zidesamtinib, if approved, to provide a clinically meaningful treatment option for patients who have exhausted available therapies," said Christopher Turner, M.D., Chief Medical Officer at Nuvalent. "Furthermore, these clinical findings are consistent with the improved preclinical brain penetrance and intracranial ROS1 G2032R antitumor activity of zidesamtinib compared to repotrectinib and taletrectinib, and continue to support the potential for a differentiated clinical profile in earlier lines of therapy."

The U.S. Food and Drug Administration (FDA) has accepted the New Drug Application (NDA) for zidesamtinib for the treatment of adult patients with locally advanced or metastatic ROS1-positive NSCLC who received at least 1 prior ROS1 TKI, and assigned a Prescription Drug User Fee Act (PDUFA) target action date of September 18, 2026. Pending FDA review, Nuvalent anticipates U.S. commercial launch of zidesamtinib in 2026. Additionally, the company plans to submit data to the FDA to support a potential label expansion of zidesamtinib in TKI-naïve patients with advanced ROS1-positive NSCLC in the second half of 2026.

New Clinical Data for Zidesamtinib in Subset of TKI Pre-treated Patients in ARROS-1 Trial

Title: Zidesamtinib in Patients with ROS1+ NSCLC Previously Treated with Repotrectinib or Taletrectinib
Presenting Author: Geoffrey Liu, M.Sc., M.D.1
Abstract Number: CT248
Session Title: Phase II Clinical Trials
Session Date and Time: Tuesday, April 21, 2026, 2:00-5:00 p.m. PT
Location: Poster Section 50
Poster Board Number: 13

Zidesamtinib is being evaluated in ARROS-1, a first-in-human, single-arm Phase 1/2 clinical trial in patients with advanced ROS1-positive NSCLC and other solid tumors. Clinical data presented are from a subgroup of patients with advanced ROS1-positive NSCLC in ARROS-1 who had been previously treated with the dual TRK/ROS1 TKIs repotrectinib and/or taletrectinib. No available ROS1 TKIs have demonstrated activity in this heavily pre-treated population.

Patients received at least 1 dose of zidesamtinib at 100 mg QD as of a data cut-off date of September 22, 2025. The population for this analysis was unique and heavily pre-treated:

46 efficacy-evaluable patients had received prior repotrectinib, 19 had received prior taletrectinib, and 3 had previously received both;
85% (39/46) of repotrectinib-treated patients and 89% (17/19) of taletrectinib-treated patients had received ≥2 prior ROS1 TKIs;
63% (29/46) of repotrectinib-treated patients and 53% (10/53) of taletrectinib-treated patients had received prior chemotherapy;
Active CNS disease was assessed by BICR in 46% (21/46) of repotrectinib-treated patients and 53% (10/19) of taletrectinib-treated patients at baseline; and
Secondary ROS1 resistance mutations were reported in 35% (16/46) of repotrectinib-treated patients and 42% (8/19) of taletrectinib-treated patients, with a ROS1 G2032R mutation identified in 26% (12/46) and 21% (4/19), respectively.
Treatment with zidesamtinib resulted in clinically meaningful activity in this population, including in patients with the ROS1 G2032R resistance mutation and those with CNS disease. As of the data cut-off date:

Efficacy Parameter
(RECIST v1.1, BICR)

Prior repotrectiniba

Prior taletrectinibb

ORR, % (n/n)

[95% CI]

41% (19/46)

[27, 57]

47% (9/19)

[24, 71]

CR, n (%)

7% (3/46) c

5% (1/19)

mDOR, months d

[95% CI]

15.7

[5.6, NE]

NR

[5.2, NE]

ROS1 G2032R resistance mutation

ORR, % (n/n)

[95% CI]

67% (8/12)

[35, 90]

50% (2/4) e

[7, 93]

CR, n (%)

8% (1/12)

0 %

mDOR, months d

[95% CI]

15.7

[3.5, NE]

NR

[NE, NE]

Intracranial Activity f

IC-ORR, % (n/n)

[95% CI]

44% (8/18)

[22, 69]

71% (5/7)

[29, 96]

IC-CR, n (%)

11% (2/18)

43% (3/7)

mIC-DOR, months d

[95% CI]

NR

[5.2, NE]

NR

[5.2, NE]

IC-DOR ≥6 months d

86%

[33, 98]

80%

[20, 97]

BICR, blinded independent central review; CI, confidence interval; CR, complete response; IC, intracranial;
IC-DOR, intracranial duration of response; mDOR, median duration of response; NE, not estimable; NR, not
reached; ORR, objective response rate.

a Prior repotrectinib ± other ROS1 TKIs and/or chemotherapy.

b Prior taletrectinib ± other ROS1 TKIs and/or chemotherapy.

c Includes one single time-point CR pending confirmation in an ongoing patient who previously experienced
confirmed PR.

d Kaplan-Meier estimates.

e Responses also observed in pts with ROS1 D2033N (n=1) and L2086F (n=1).

f Includes patients with measurable (≥5mm) CNS lesions by BICR at baseline.

The safety profile of zidesamtinib in this population was consistent with the previously reported safety results from ARROS-1 for patients with advanced ROS1-positive NSCLC, including low rates of dose reductions and treatment discontinuations, and the avoidance of TRK-related neurologic adverse events.

New Preclinical Data for Zidesamtinib

Title: Zidesamtinib Has Differentiated Preclinical Brain Penetrance and Intracranial Activity Compared to Other ROS1 Inhibitors
Presenting Author: Anupong Tangpeerachaikul, Ph.D.2
Abstract Number: LB366
Session Title: Late-Breaking Research: Experimental and Molecular Therapeutics 3
Session Date and Time: Tuesday, April 21, 2026, 2:00-5:00 p.m. PT
Location: Poster Section 53
Poster Board Number: 23

Data presented are from preclinical analyses of the brain penetrance and intracranial ROS1 G2032R antitumor activity of zidesamtinib compared to the dual TRK/ROS1 inhibitors repotrectinib and taletrectinib.3

Among the three ROS1 TKIs, all of which have reported activity against the ROS1 G2032R mutation, zidesamtinib demonstrated:

Highest cell permeability in MDCK-MDR1 cell lines and highest brain-to-plasma partitioning in rats, supporting zidesamtinib’s potential for high brain penetrance;
Most sustained intracranial efficacy in a mouse ROS1 G2032R brain tumor model, with all mice surviving to study end; and,
Efficacy after progressive disease on earlier-line taletrectinib treatment in a mouse ROS1 G2032R brain tumor model. Data demonstrating that switching from repotrectinib to zidesamtinib resulted in more sustained tumor suppression in the same preclinical model have been previously reported.4
1 Princess Margaret Hospital, Toronto, Ontario, Canada;
2 Nuvalent, Inc., Cambridge, MA, USA;
3 Head-to-head clinical studies comparing zidesamtinib with other treatments have not been conducted. Data presented are from preclinical studies, and no clinical conclusions can be drawn.
4Tangpeerachaikul et al. Annals of Oncology 2024; 35(2):S217.

About Zidesamtinib
Zidesamtinib is an investigational, brain-penetrant, ROS1-selective inhibitor created with the aim to overcome limitations observed with currently available ROS1 inhibitors. Zidesamtinib is designed to remain active in tumors that have developed resistance to currently available ROS1 inhibitors, including tumors with treatment-emergent ROS1 mutations such as G2032R. In addition, zidesamtinib is designed for central nervous system (CNS) penetrance to improve treatment options for patients with brain metastases, and to avoid inhibition of the structurally related tropomyosin receptor kinase (TRK) family. Together, these characteristics have the potential to avoid TRK-related CNS adverse events seen with dual TRK/ROS1 inhibitors and to drive deep, durable responses for patients across all lines of therapy.

Based on results for tyrosine kinase inhibitor (TKI) pre-treated patients with advanced ROS1-positive non-small cell lung cancer (NSCLC) enrolled in the global registrational ARROS-1 Phase 1/2 clinical trial, the U.S. Food and Drug Administration (FDA) has accepted for filing Nuvalent’s NDA submission for zidesamtinib for the treatment of adult patients with locally advanced or metastatic ROS1-positive NSCLC who received at least 1 prior ROS1 TKI. The application has been assigned a Prescription Drug User Fee Act (PDUFA) target action date of September 18, 2026. Zidesamtinib has received breakthrough therapy designation for the treatment of patients with ROS1-positive metastatic NSCLC who have been previously treated with 2 or more ROS1 TKIs and orphan drug designation for ROS1-positive NSCLC.

(Press release, Nuvalent, APR 17, 2026, View Source [SID1234664481])

SK Life Science Labs to Present New Preclinical Data on Targeted Protein Degradation at AACR Annual Meeting 2026

On April 17, 2026 SK Life Science Labs, a subsidiary of SK Biopharmaceuticals Co., Ltd., a global biotech focused on the research, development, and commercialization of treatments for disorders of the central nervous system (CNS) and cancer, reported the presentation of three posters at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, taking place April 17–22 in San Diego, California.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

The presentations highlight SK Life Science Labs’ continued progress in advancing targeted protein degradation approaches against key oncology targets, including p300 and PRMT5, with the potential to address unmet needs across multiple cancer types.

"Our latest findings further demonstrate the power of targeted protein degradation to selectively eliminate key cancer vulnerabilities with depth and precision that may not be achievable with traditional inhibition," said Ryan Kruger, Ph.D., Chief Scientific Officer at SK Life Science Labs. "We are particularly encouraged by the breadth of anti-tumor activity and improved safety profiles observed in our p300 and PRMT5 degrader programs, which underscore their potential to deliver meaningful therapeutic advances for patients."

Data to be presented include:

Selective p300 degraders in CBP mutant cancers, demonstrating deep anti-tumor activity with robust tumor regression across multiple preclinical models.
Selective p300 degraders in p300-dependent cancers, showing broad efficacy in prostate cancer and multiple myeloma models, with strong suppression of oncogenic transcriptional programs and improved tolerability versus dual inhibition approaches.
Next-generation PRMT5 activity modulation through rapid, potent, and selective degradation of PRMT5, enabling comprehensive suppression of its catalytic and non-catalytic functions and overcoming limitations associated with first- and second-generation inhibitors.
Poster Presentation Details (All times are PDT):

Session: PO.CH01.01 – Targeted Protein Degradation and Induced Proximity
Abstract 5178 / 28: Discovery and characterization of a selective p300 degrader reveals deep anti-tumor activity in CBP mutant cancers
Lead Author: Harshil D. Dhruv
Date/Time: April 21, 2026, 9:00 AM – 12:00 PM; Section 39
Session: PO.CH01.01 – Targeted Protein Degradation and Induced Proximity
Abstract 5179 / 29: Discovery and characterization of a selective p300 degrader reveals broad anti-tumor activity in p300-dependent cancers
Lead Author: Harshil D. Dhruv
Date/Time: April 21, 2026, 9:00 AM – 12:00 PM; Section 39
Session: PO.ET09.04 – Proximity-Induced Drug Discovery 2
Abstract 5790 / 17: Next-generation PRMT5 activity modulation through directed degradation
Lead Author: Jose C. Clemente
Date/Time: April 21, 2026, 2:00 PM – 5:00 PM; Section 15
For more information about SK Life Science Labs, visit www.sklslabs.com.

Frequently Asked Questions (FAQ)

What is SK Life Science Labs announcing at AACR (Free AACR Whitepaper) 2026?
SK Life Science Labs is presenting three posters showcasing new preclinical data from its targeted protein degradation pipeline, including programs focused on p300 and PRMT5.

What are the key programs being highlighted?
The company is presenting data on selective p300 degraders in both CBP mutant and p300-dependent cancers, as well as PRMT5 degraders designed to achieve deeper and more durable target modulation.

Why is p300 an important target in cancer?
p300 is a transcriptional co-activator involved in regulating gene expression in multiple cancers. Selective degradation of p300 enables precise targeting of tumor-driving pathways, particularly in cancers with CBP mutations or p300 dependency.

What differentiates SK Life Science Labs’ p300 degraders?
The company’s p300 degraders are designed to be highly selective, avoiding degradation of the closely related CBP protein. This selectivity may enable strong anti-tumor activity while reducing hematologic toxicity seen with dual p300/CBP inhibition.

What is the significance of targeting PRMT5 through degradation?
PRMT5 is an epigenetic regulator implicated in multiple cancers. Targeted degradation has the potential to eliminate both catalytic and non-catalytic functions of PRMT5, potentially overcoming limitations of traditional inhibitors and enabling more complete target suppression.

What stage of development are these programs in?
The p300 degrader program is currently progressing through IND-enabling studies and the PRMT5 program data are in support of ongoing research efforts to advance it toward potential clinical development.

What is targeted protein degradation?
Targeted protein degradation is a therapeutic approach that harnesses the body’s natural ubiquitin-proteasome system (UPS) to selectively identify and eliminate disease-causing proteins, including those that have historically been difficult to drug.

Where and when will the data be presented?
All three posters will be presented on April 21, 2026, during AACR (Free AACR Whitepaper) Annual Meeting poster sessions in San Diego, California.

(Press release, SK biopharmaceuticals, APR 17, 2026, View Source [SID1234664480])

Gilead Receives All Required Regulatory Approvals for the Acquisition of Arcellx and Extends Tender Offer

On April 17, 2026 Gilead Sciences, Inc. (Nasdaq: GILD) reported that all required regulatory approvals have been obtained for its previously announced acquisition of Arcellx and that Gilead has extended the expiration of the tender offer to purchase all outstanding shares of common stock of Arcellx.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

On April 13, 2026, the Australian Competition and Consumer Commission (ACCC) published its decision that the acquisition of Arcellx may be put into effect, subject to expiration of a 14-calendar day waiting period. Assuming that the ACCC’s determination remains unchallenged during this waiting period, the waiting period expires at 10:00 a.m., Eastern Time, on April 27, 2026. Additionally, the relevant review period for the Austrian competition authorities has expired. Accordingly, all required regulatory approvals for the transaction have been obtained, and the "Regulatory Approvals Condition" (as defined in the Offer to Purchase, dated March 6, 2026, relating to the offer) will be satisfied upon expiration of the 14-calendar day review period pursuant to Australian competition law.

The tender offer, which was previously scheduled to expire at 5:00 p.m., Eastern Time, on April 24, 2026, has been extended to expire at 5:00 p.m., Eastern Time, on April 27, 2026, and remains subject to the satisfaction or waiver of customary closing conditions, including the tender of a number of shares of Arcellx common stock that, together with shares already owned by Gilead, equals at least a majority of the then-outstanding Arcellx shares and other customary offer conditions.

The offer remains at a purchase price of (1) $115.00 per share, net to the seller in cash, without interest, subject to any withholding tax, plus (2) one contractual contingent value right (CVR), which represents the right to receive one contingent payment of $5.00 per CVR in cash, without interest, and subject to any withholding tax, payable on March 31, 2030, subject to cumulative worldwide sales of Arcellx’s anitocabtagene autoleucel (anito-cel) product exceeding $6.0 billion on or prior to December 31, 2029.

Computershare Trust Company, N.A., the depositary and paying agent for the tender offer, has advised Gilead that, as of 4:00 p.m., Eastern Time, on April 16, 2026, approximately 10,271,823 shares have been validly tendered and not validly withdrawn in the tender offer, representing approximately 17.5% of the outstanding shares as of such date and time. Holders that have previously tendered their shares do not need to re-tender their shares or take any other action in response to the extension of the tender offer. Questions or requests for assistance may be directed to Innisfree M&A Incorporated, the information agent for the tender offer, by calling toll free (877) 800-5182.

(Press release, Gilead Sciences, APR 17, 2026, View Source [SID1234664478])

Zentalis Pharmaceuticals To Present Azenosertib Preclinical Data in Triple-Negative Breast Cancer and Real-World Analysis of Unmet Need in Cyclin E1-Positive Ovarian Cancer at AACR 2026

On April 17, 2026 Zentalis Pharmaceuticals, Inc. (Nasdaq: ZNTL), a clinical oncology innovator advancing late-stage development of investigational first-in-class WEE1 inhibitor azenosertib as a biomarker-driven treatment approach for ovarian cancer, reported data from two posters being presented at the 2026 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, taking place April 17-22, 2026, in San Diego, CA. The data show encouraging preclinical activity of azenosertib in triple-negative breast cancer (TNBC) and highlight the poor prognosis of Cyclin E1-positive ovarian cancer patients with currently available treatments in a real-world data analysis.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

Compelling Preclinical Activity in Triple-Negative Breast Cancer with Azenosertib

"The preclinical data in triple-negative breast cancer being presented at AACR (Free AACR Whitepaper) showed that azenosertib combinations can induce complete tumor responses in a model resistant to emerging ADC therapies, supporting the potential to broaden the impact of azenosertib beyond ovarian cancer," said Julie Eastland, Chief Executive Officer of Zentalis. "This includes potential development of azenosertib through differentiated combination strategies with antibody-drug conjugates (ADCs) and chemotherapy. As ADCs advance toward first-line use in TNBC, effective post-ADC treatment strategies represent a growing unmet need that azenosertib combinations may be uniquely positioned to fill. Our data suggest azenosertib may achieve this through multiple mechanisms – possibly resensitizing tumors to chemotherapy, enhancing the responses to ADC, and extending the duration of response – which is an exciting potential future direction for our pipeline."

Preclinical evidence supports azenosertib as a therapeutic strategy in TNBC:
•TNBC cell lines showed higher Cyclin E1 expression and greater sensitivity to WEE1 inhibition compared to other breast cancer cell lines
oAzenosertib monotherapy demonstrated meaningful antitumor activity across a diverse panel of 12 TNBC in vivo xenograft models (42-99% tumor growth inhibition)
•In a patient-derived xenograft model of TNBC with clinical resistance to sacituzumab govitecan, an approved topoisomerase 1 inhibitor (TOPO1i) ADC, azenosertib + enfortumab vedotin (EV):
oInduced complete responses in 7 of 8 mice (87.5%); 5 mice did not progress after treatment discontinuation
oPrevented tumor progression in 8 of 8 mice for more than 52 days compared to 100% progression observed within 30 days with EV alone
oDrove deep tumor regression in mice models refractory to sacituzumab govitecan or trastuzumab deruxtecan with large tumor volumes (average ~900mm3)

•Combinations of azenosertib with TOPO1i-payload ADCs (sacituzumab govitecan, datopotamab deruxtecan, or trastuzumab deruxtecan) enhanced both depth and duration of response compared to ADC monotherapy in ADC-naïve models
•Azenosertib + paclitaxel restored substantial sensitivity to paclitaxel in a model resistant to both paclitaxel and TOPO1i ADCs (51% tumor growth inhibition vs. 16% with paclitaxel alone)

Cyclin E1 Protein Overexpression Characterizes Ovarian Cancer Patients with Poor Prognosis

"The real-world data being presented at AACR (Free AACR Whitepaper) provide important validation that Cyclin E1-positive ovarian cancer patients face a particularly challenging disease trajectory with standard-of-care therapies," said Ingmar Bruns, M.D., Chief Medical Officer of Zentalis. "The consistency of worse outcomes across independent cohorts and multiple treatment settings underscores the significant unmet need in this population. These findings provide important context for Zentalis’ registration-intended DENALI and ASPENOVA studies, which are evaluating WEE1 inhibition with azenosertib monotherapy as a targeted approach for the Cyclin E1-positive population that currently has limited effective treatment options."

Real-world data from two independent cohorts (Tempus Lens Ovarian cancer dataset and Zentalis’ historical clinical trials) consistently demonstrated that Cyclin E1-positive ovarian cancer patients experience worse clinical outcomes:
•After first-line treatment, Cyclin E1-positive patients, with or without CCNE1 gene amplification, had shorter time to next treatment compared to Cyclin E1-negative patients (13.2 months and 14.9 months, respectively, compared to 19.5 months, p=0.002)
•Cyclin E1-positivity is associated with a trend toward reduced clinical benefit from standard-of-care PROC treatments

AACR Poster Details

Title: "WEE1 Inhibition as a Therapeutic Strategy in Triple-Negative Breast Cancer: Evaluating Single Agent and Combination Activity of Azenosertib in Preclinical Models"
Abstract Number: 2012
Date/Time: Monday, April 20, 2026, 2:00 p.m. – 5:00 p.m. PDT
Presenting Author: Alexandra Levy, MS

Title: "Real-World Treatment Patterns and Outcomes Reveal Distinct Clinical Trajectories of Patients with Cyclin E1-Positive Ovarian Cancer"
Abstract Number: 1708
Date/Time: Sunday, April 19, 2026, 2:00 p.m. – 5:00 p.m. PDT
Presenting Author: Jinkil Jeong, PhD

The posters can be accessed on the Supporting Publications page of the Zentalis website.

About Azenosertib
Azenosertib is an investigational, potentially first-in-class, selective, and orally bioavailable inhibitor of WEE1 currently being evaluated in clinical studies in ovarian cancer and additional tumor types. WEE1 acts as a master regulator of the G1-S and G2-M cell cycle checkpoints, through negative regulation of both CDK1 and CDK2, to prevent replication of cells with damaged DNA. By inhibiting WEE1, azenosertib enables cell cycle progression, despite high levels of DNA damage, thereby resulting in the accumulation of DNA damage and leading to mitotic catastrophe and cancer cell death.

Azenosertib is in late-stage development as a potential treatment for Cyclin E1-positive platinum-resistant ovarian cancer (PROC). There is currently no approved treatment option specifically for this biomarker-selected population which comprises approximately 50% of PROC patients. Cyclin E1 protein overexpression has been established as a sensitive and specific predictive biomarker for identifying patients who could potentially derive benefit from azenosertib treatment, based on retrospective analysis of azenosertib studies in PROC. Validation of the Cyclin E1 companion diagnostic assay is ongoing in the DENALI and ASPENOVA trials.

Azenosertib has been granted Fast Track Designation by the U.S. FDA for the treatment of patients with Cyclin E1-positive platinum-resistant ovarian cancer. Fast Track Designation is intended to facilitate the development and expedite the review of therapies that have the potential to treat serious conditions and address unmet medical needs.

(Press release, Zentalis Pharmaceuticals, APR 17, 2026, View Source [SID1234664477])