Form 8-K

8-K — Zentalis Pharmaceuticals, Inc.

Accession: 0001725160-26-000020

Filed: 2026-04-17

Period: 2026-04-17

CIK: 0001725160

SIC: 2834 (PHARMACEUTICAL PREPARATIONS)

Item: Regulation FD Disclosure

Documents

8-K — zntl-20260417.htm (Primary)

EX-99.1 (ex991aacr2026datapressrele.htm)

EX-99.2 (ex992-leeetalazenointnbc.htm)

EX-99.3 (ex993-jeongetal_realworl.htm)

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8-K

8-K (Primary)

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0001725160FALSE00017251602026-04-172026-04-17

UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

Washington, D.C. 20549

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FORM 8-K

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CURRENT REPORT

Pursuant to Section 13 or 15(d)

of the Securities Exchange Act of 1934

Date of report (Date of earliest event reported): April 17, 2026

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ZENTALIS PHARMACEUTICALS, INC.

(Exact name of registrant as specified in its charter)

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Delaware 001-39263 82-3607803

(State or other jurisdiction

of incorporation or organization)

(Commission

File Number)

(IRS Employer

Identification No.)

10275 Science Center Drive, Suite 200

San Diego, California 92121

(Address of principal executive offices) (Zip Code)

(858) 263-4333

(Registrant’s telephone number, include area code)

N/A

(Former name or former address, if changed since last report)

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Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions:

☐ Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)

☐ Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)

☐ Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))

☐ Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))

Securities registered pursuant to Section 12(b) of the Act:

Title of each class Trading Symbol(s) Name of each exchange on which registered

Common Stock, $0.001 par value per share ZNTL The Nasdaq Global Market

Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (§230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§240.12b-2 of this chapter).

Emerging growth company ☐

If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act. ☐

Item 7.01 Regulation FD Disclosure.

On April 17, 2026, Zentalis Pharmaceuticals, Inc ("Zentalis" or the "Company") issued the press released furnished as Exhibit 99.1 to this Current Report on Form 8-K (the "Current Report") and incorporated herein by reference.

Additionally, the Company is presenting the posters furnished as Exhibits 99.2 and 99.3 to this Current Report and incorporated herein by reference at the 2026 American Association for Cancer Research ("AACR") Annual Meeting taking place April 17-22, 2026, in San Diego, CA.

The information contained in Item 7.01 of this Current Report (including Exhibits 99.1, 99.2 and 99.3 attached hereto) shall not be deemed “filed” for purposes of Section 18 of the Securities Exchange Act of 1934, as amended (the “Exchange Act”), or otherwise subject to the liabilities of that section, nor shall they be deemed incorporated by reference in any filing under the Securities Act of 1933, as amended, or the Exchange Act, whether made before or after the date hereof, except as expressly provided by specific reference in such a filing.

Item 9.01 Financial Statements and Exhibits.

(d) Exhibits

The following Exhibits 99.1, 99.2 and 99.3 relating to Item 7.01 shall be deemed to be furnished, and not filed:

Exhibit No.

Description

99.1

Press Release issued on April 17, 2026

99.2

AACR poster titled "WEE1 Inhibition as a Therapeutic Strategy in Triple-Negative Breast Cancer: Evaluating Single Agent and Combination Activity of Azenosertib in Preclinical Models"

99.3

AACR poster titled "Real-World Treatment Patterns and Outcomes Reveal Distinct Clinical Trajectories of Patients with Cyclin E1-Positive Ovarian Cancer"

104 Cover Page Interactive Data File (embedded within the inline XBRL document)

SIGNATURES

Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.

ZENTALIS PHARMACEUTICALS, INC.

Date: April 17, 2026 By: /s/ Julie Eastland

Julie Eastland

President and Chief Executive Officer

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Document

Exhibit 99.1

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

•Preclinical data show encouraging activity of azenosertib combinations in ADC-resistant TNBC, supporting the potential for pipeline expansion beyond ovarian cancer

•Real-world data demonstrate Cyclin E1-positive ovarian cancer patients have significantly worse outcomes, independent of CCNE1 gene amplification status, reinforcing the potential for azenosertib to address the unmet need for these patients

SAN DIEGO, 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, today announced data from two posters being presented at the 2026 American Association for Cancer Research (AACR) 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.

Compelling Preclinical Activity in Triple-Negative Breast Cancer with Azenosertib

"The preclinical data in triple-negative breast cancer being presented at AACR 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 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.

About Zentalis Pharmaceuticals

Zentalis is a clinical oncology innovator developing a treatment approach for ovarian cancer and multiple tumor types. Leveraging therapeutics development and biomarker expertise, Zentalis is advancing monotherapy and combination studies of its first-in-class WEE1 inhibitor, azenosertib. Focused on translating WEE1 science into clinical practice, we aim to equip physicians with a targeted, non-chemo, orally available medicine that enhances treatment experience, choice, and outcomes. Our mission: to unburden cancer patients with more convenience and care.

For more information, please visit www.zentalis.com. Follow Zentalis on LinkedIn at www.linkedin.com/company/zentalis-pharmaceuticals

Forward-Looking Statements

This press release contains forward-looking statements within the meaning of the U.S. Private Securities Litigation Reform Act of 1995, as amended. All statements contained in this press release that do not relate to matters of historical fact should be considered forward-looking statements, including, but not limited to, statements regarding the continued development of azenosertib; the clinical and therapeutic potential of azenosertib; the potential for azenosertib to be first-in-class; the potential benefits of azenosertib, including the potential for azenosertib to be an important treatment option for patients with ovarian cancer, triple negative breast cancer or other indications, the mechanisms through which azenosertib may fill unmet needs, and the ability of azenosertib combinations to induce complete tumor responses; the unmet need for treatments in ovarian cancer, triple negative breast cancer or other indications; the broad franchise potential of azenosertib; the Company’s biomarker-driven strategy for azenosertib; the future direction of our pipeline, including the potential for pipeline expansion; and our participation in poster presentations. The terms “anticipate,” “advance,” “believe,” “design,” “develop,” “encouraging” “expect,” “future,” “intent,” “look forward,” “may,” “on track,” “plan,” “position,” “potential,” “runway,” “strategy,” “target,” “upcoming,” and “will” and similar references are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. These statements are neither promises nor guarantees, but involve known and unknown risks, uncertainties and other important factors that may cause our actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements, including, but not limited to, the following: our limited operating history, which may make it difficult to evaluate our current business and predict our future success and viability; we have and expect to continue to incur significant losses; our need for additional funding, which may not be available; our substantial dependence on the success of azenosertib; our plans, including the costs thereof, of development of companion diagnostics; the outcome of preclinical testing and early trials may not be predictive of the success of later clinical trials; potential unforeseen events during clinical trials could cause delays or other adverse consequences; risks relating to the regulatory approval process or ongoing regulatory obligations; our product candidates

may cause serious adverse side effects; the interim, initial, “topline,” and preliminary data from our clinical trials may change as more patient data becomes available, and are subject to audit and verification procedures that could result in material changes in the final data; our reliance on third parties; effects of significant competition; the possibility of system failures or security breaches; risks relating to intellectual property; our ability to attract, retain and motivate qualified personnel, and risks relating to management transitions; significant costs as a result of operating as a public company; and the other important factors discussed under the caption “Risk Factors” in our most recently filed periodic report on Form 10-K or 10-Q and subsequent filings with the U.S. Securities and Exchange Commission (SEC) and our other filings with the SEC. Any such forward-looking statements represent management’s estimates as of the date of this press release. While we may elect to update such forward-looking statements at some point in the future, we disclaim any obligation to do so, even if subsequent events cause our views to change.

ZENTALIS® and its associated logo are trademarks of Zentalis and/or its affiliates. All website addresses and other links in this press release are for information only and are not intended to be an active link or to incorporate any website or other information into this press release.

Contact:

Aron Feingold

VP, Investor Relations & Corporate Communications

ir@zentalis.com

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METHODS Analysis of pharmacogenomic and proteomic datasets • Comparison of Cyclin E1 protein levels in serous ovarian cancer (SOC) and basal‑like breast cancer was determined from TCGA pan‑cancer analysis.5 Although not all basal‑like breast cancers are TNBC, they demonstrate substantial molecular and histological overlap6 and are consequently enriched for TNBC. For simplicity, we refer to this population as ~TNBC • Breast cancer cell lines were classified as TNBC or non‑TNBC, based on molecular and histological features and literature sources6‑8 • In vitro sensitivity of breast cancer cell lines to WEE1i was evaluated using a cell‑based screen of the OncoPanel cancer cell lines (Eurofins). Cells were incubated with 9 serial dilutions of azenosertib for 5 days. Comparative screening data for adavosertib was obtained from the Genomics of Drug Sensitivity in Cancer (GDSC) database9 • Cyclin E1 protein levels in breast cancer cell lines were determined using proteomic data available from the Cancer Cell Line Encyclopedia (CCLE)10 In vivo animal studies • Monotherapy efficacy of azenosertib was evaluated in a panel of 12 TNBC CDX and PDX models • Combinations of azenosertib with ADCs carrying TOP1i payloads (SG, Dato‑DXd, and T‑DXd were tested in two ADC‑naïve models, MDA‑MB‑231 (CDX) and CTG‑3103 (PDX) • Combinations of azenosertib with chemotherapy (paclitaxel) and, separately, azenosertib with a microtubule inhibitor (MTI) payload ADC (EV) were tested in a TOP1i payload ADC‑resistant PDX model of TNBC • All tumor models were implanted subcutaneously in immunocompromised mice. Azenosertib was delivered orally, paclitaxel was delivered intraperitoneally, and all ADCs were delivered intravenously Table 1. ADCs used in this study ADC Abbreviation Target Payload Payload Class Sacituzumab govitecan SG TROP2 SN38 Topoisomerase 1 inhibitor Datopotamab deruxtecan Dato‑DXd TROP2 DXd Topoisomerase 1 inhibitor Trastuzumab deruxtecan T‑DXd HER2 DXd Topoisomerase 1 inhibitor Enfortumab vedotin EV Nectin‑4 MMAE Microtubule inhibitor RESULTS Figure 3. Basal‑like breast cancers (~TNBC) exhibit molecular features consistent with impaired G1‑S cell cycle checkpoint regulation CCNE1 amplification, Cyclin E1 expression, TP53 mutation in TCGA pan‑cancer dataset5 Cancer Type Total N Prevalence CCNE1 Amplified (%) Prevalence Cyclin E1 Positive (%) Prevalence TP53 Mutated (%) Serous ovarian cancer (SOC) 405 76/405 (19%) 253/405 (62%) 277/405 (68%) Basal‑like Breast cancer (~TNBC) 129 19/129 (15%) 123/129 (95%) 113/129 (88%) −5 0 5 10 ~TNBC Amplified (N=19) ~TNBC Non−Amplified (N=110) Other BC All (N=503) SOC Amplified (N=76) SOC Non−Amplified (N=329) Cy cl in E 1 ex pr es si on (R PP A Z −s co re ) • High level of Cyclin E1 expression: Positive Cyclin E1 expression observed in most CCNE1 non‑amplified tumors and in 95% and 62% of ~TNBC and SOC cases, respectively • Frequent loss of TP53 observed in 88% and 68% of ~TNBC and SOC cases, respectively • Weakened G1‑S cell cycle checkpoint may result in high replication stress and vulnerability to WEE1 inhibition Distribution of Cyclin E1 protein expression levels (Z‑score) from analysis of RPPA data in SOC and ~TNBC patients from TCGA pan‑cancer analysis. CCNE1 amplified and non‑amplified are separated, and red segments denote the indication‑specific expression level of the 10th percentile of CCNE1 amplified sample (“TPA cutoff”). Expression levels above TPA cutoff are considered positive. Figure 4. TNBC cell lines are more sensitive to WEE1 inhibition and exhibit higher Cyclin E1 protein expression compared with non‑TNBC cell lines 0.06 0.07 0.08 0.09 TNBC N=23 A U C (a da vo se rti b do se r es po ns e) Cy cl in E 1 ex pr es si on (R PP A Z -s co re ) Non-TNBC N=27 −1 0 1 2 3 TNBC N=19 Non-TNBC N=21 Wilcox P-value = 2.74e-06 Wilcox P-value = 0.065 A U C (a ze no se rti b do se r es po ns e) TNBC N=7 Non-TNBC N=10 Wilcox P-value = 0.0046 0.6 0.7 0.8 0.9 A CBAdavosertib sensitivity across breast cancer cell lines (GDSC9) Cyclin E1 expression across breast cancer cell lines (CCLE10) Azenosertib sensitivity across breast cancer cell lines (Eurofins) A. Distribution of area under the curve (AUC) values for breast cancer cell lines treated with adavosertib in the GDSC dataset, where lower AUC indicates increased drug sensitivity. B. Distribution of AUC values for breast cancer cell lines treated with azenosertib in the Eurofins dataset, where lower AUC indicates increased drug sensitivity. C. Distribution of Cyclin E1 protein expression levels (Z‑score) from analysis of RPPA data in TNBC and non‑TNBC breast cancer cell lines from the CCLE dataset. Figure 5. Clinically relevant doses of azenosertib demonstrate monotherapy antitumor activity across a diverse panel of TNBC xenograft models in vivo 100 75 50 25 0 Model Molecular Characteristics SUM149PT TP53 mut; BRCA1 mut (∆11q) HCC1937 TP53 mut; BRCA1 mut; FAM35A del; RB1 mut MDA-MB-468 TP53 mut; RB1 mut HBCx-17 TP53 mut; BRCA2 mut; AKT1 mut; CDKN2A mut; KDM6A del MDA-MB-436 BRCA1 mut; RB1 mut HCC1806 TP53 mut MDA-MB-231 TP53 mut; KRAS G13D HBCx-10 TP53 mut; BRCA2 mut; RB1 del; PTEN del HBCx-9 TP53 mut CTG-3103 TP53 mut; CCNE1 amp; MYC amp MDA-M B-436 Nir-R * % T G I SUM149PT HCC1937 MDA-M B-468* HBCx-17 MDA-M B-436 Ola-R* MDA-M B-436* HCC1806* MDA-M B-231* HBCx-10 HBCx-9 CTG-3103 60 mg/kg 80 mg/kg A B Azenosertib monotherapy efficacy in TNBC TNBC xenograft models harboring diverse mutations and copy number alterations were treated in vivo with 60 or 80 mg/kg of azenosertib. A. Key molecular characteristics of each model. B. Antitumor efficacy of azenosertib across models, expressed as percent tumor growth inhibition (TGI), calculated using the formula (1 ‑ [Td ‑ T0] / [Cd ‑ C0]) × 100%. HBCx-17, HBCx-10, HBCx-9, and CTG-3103 are PDX models; all other models are CDX. Models labeled “Nir‑R” and “Ola‑R” have derived resistance to niraparib and olaparib, respectively. Models labeled with * were dosed once daily (QD) continuously; all other models were dosed QD using a 5:2 schedule. Figure 6. Combinations of azenosertib with TOP1i‑payload ADCs enhance tumor growth inhibition and duration of response in TNBC xenograft models 0 10 20 30 40 50 -20 -10 0 10 20 M ea n ΔB W (% ) M ea n ΔB W (% ) 0 10 20 30 40 50 -20 -10 0 10 20 M ea n ΔB W (% ) 0 20 40 60 -20 -10 0 10 20 0 10 20 30 40 50 0 500 1000 1500 2000 Days M ea n TV ± S EM (m m 3 ) M ea n TV ± S EM (m m 3 ) M ea n TV ± S EM (m m 3 ) 0 10 20 30 40 50 0 500 1000 1500 2000 Days 0 10 20 30 40 50 60 70 80 90 0 250 500 750 1000 Days no Tx Day 59 Day 86 Day 59 Day 86 0 200 400 600 800 TV (m m 3 ) T-DXd Azenosertib + T-DXd * ns 28% TGI 71% TGI 91% TGI 28% TGI 98% TGI 103% TGI Vehicle Azenosertib 60 mg/kg QD 5:2 SG 0.5 mg D0, 7, 21, 28, 42 Azenosertib 60 mg/kg QD 5:2 + SG 0.5 mg D0, 7, 21, 28, 42 Vehicle Azenosertib 60 mg/kg QD 5:2 Dato-DXd 10 mg/kg Q3W Azenosertib 60 mg/kg QD 5:2 + Dato-DXd 10 mg/kg Q3W Vehicle Azenosertib 60 mg/kg QD 5:2 T-DXd 3 mg/kg Q3W Azenosertib 60 mg/kg QD 5:2 + T-DXd 3 mg/kg Q3W A B MDA-MB-231 (TROP2+ TNBC) C D CTG-3103 (HER2-low TNBC) TNBC xenograft models treated with azenosertib in combination with ADCs carrying TOP1i payloads (n=8/group). (A,B.) Mean TV ± SEM of MDA‑MB‑231 CDX treated with the indicated doses of azenosertib and (A) SG or (B) Dato‑DXd for 46 days. Antitumor efficacy is expressed as percent TGI, calculated using the formula (1 ‑ [Td ‑ T0] / [Cd ‑ C0]) × 100%. Inset graphs depict mean percent change in body weight from day 0 (∆BW), where the black dashed line indicates 0% change and the red dashed line indicates ‑15% change. C. Mean TV ± SEM of CTG‑3103 PDX treated with the indicated doses of azenosertib and T‑DXd. Treatment was discontinued on day 59, and tumor regrowth was monitored thereafter, indicated by the shaded gray box labeled “no Tx.” Inset graph depicts mean percent change in body weight from day 0 (∆BW), where the black dashed line indicates 0% change and the red dashed line indicates ‑15% change. D. Distribution of individual mouse tumor volumes on last day of treatment (day 59) compared to last day of monitoring for tumor regrowth (day 86). Significant tumor regrowth was detected in T‑DXd group after treatment discontinuation, P value <0.016 by Wilcoxon matched‑pairs test. Azenosertib enhances the antitumor activity of ADCs in ADC‑sensitive models • Combination of azenosertib and SG (Panel A) or Dato‑DXd (Panel B) was well‑tolerated and increased TGI in MDA‑MB‑231 tumors • Combination of azenosertib and T‑DXd (Panels C, D) was well‑tolerated and increased both TGI and durability of response in CTG‑3103 tumors Table 2. Patient treatment history of a TNBC PDX model with clinically derived resistance to SG Line Treatment Treatment Duration and Response 1 Doxorubicin + cyclophosphamide 4 cycles 2 Paclitaxel + carboplatin 4 cycles, mastectomy with residual disease 3 Capecitabine 8 cycles, local recurrence 4 Multi‑kinase inhibitor + nivolumab 1 cycle, disease progression 5 Bispecific anti‑MUC1 x EGFR ADC 6 cycles, disease progression 6 Sacituzumab govitecan 2 cycles, disease progression Figure 7. Combination of azenosertib with paclitaxel enhances TGI in a PDX model of SG‑resistant TNBC 0 5 10 15 20 25 -20 -10 0 10 20 M ea n ΔB W (% ) 0 5 10 15 20 25 0 500 1000 1500 2000 Days 16% TGI 17% TGI 51% TGI M ea n TV ± S EM (m m 3 ) Vehicle Azenosertib 60 mg/kg QD 5:2 SG 3 mg/kg D1, 8 T-DXd 3 mg/kg D1 Paclitaxel 15 mg/kg QW Azenosertib 60 mg/kg QD 5:2 + paclitaxel 15 mg/kg QW SG-Resistant TNBC • Control treatments with SG and T‑DXd confirmed resistance to both SG and T‑DXd, suggesting TOP1i payload cross‑resistance • In addition to prior SG, the patient received 4 cycles of paclitaxel treatment in 2L, which may explain the model’s resistance to paclitaxel • Although the model demonstrated resistance to monotherapy paclitaxel, combination treatment with azenosertib demonstrated potential to resensitize tumors to paclitaxel • As TOP1i payload ADCs advance into 1L, combination of azenosertib and paclitaxel may be a promising therapeutic strategy post‑ADC treatment Mean TV ± SEM of an SG‑resistant PDX model treated with azenosertib +/‑ paclitaxel (n=8/group). Antitumor efficacy is expressed as percent TGI, calculated using the formula (1 ‑ [Td ‑ T0] / [Cd ‑ C0]) × 100%. Inset graph depicts mean percent change in body weight from day 0 (∆BW), where the black dashed line indicates 0% change and the red dashed line indicates ‑15% change. Figure 8. Combination of azenosertib with an MTI‑payload ADC (EV) induces tumor regressions and complete responses in a TNBC PDX model resistant to a TOP1i‑payload ADC (SG) 0 10 20 30 -20 -10 0 10 20 M ea n ΔB W (% ) M ea n TV ± S EM (m m 3 ) 0 10 20 17% TGI 101% TGI 112% TGI 30 0 500 1000 1500 2000 Days -100 Treatment Group PR at Day 25 CR at Day 25 EV 2/8 (25%) 0/8 (0%) Azenosertib + EV 1/8 (12.5%) 7/8 (87.5%) -50 0 50 100 150 200 % Change in Tumor Volume Δ T V a t da y 25 (% ) -30% -100% EV Azenosertib + EV Vehicle Azenosertib 60 mg/kg QD 5:2 SG 3 mg/kg D1, 8 T-DXd 3 mg/kg D1 EV 3 mg/kg D1, 8, 15 (28d cycle) Azenosertib 60 mg/kg QD 5:2 + EV 3 mg/kg D1, 8, 15 BA SG-Resistant TNBC A. Mean TV ± SEM of an SG‑resistant PDX model treated with azenosertib +/‑ EV (n=8/group). Antitumor efficacy is expressed as percent TGI relative to the vehicle group on day 22, calculated using the formula (1 ‑ [Td ‑ T0] / [Cd ‑ C0]) × 100%. Inset graph depicts mean percent change in body weight from day 0 (∆BW), where the black dashed line indicates 0% change and the red dashed line indicates ‑15% change. B. Waterfall plot showing percent change in TV (∆TV) for individual mice on the last day of treatment (day 25), calculated using the formula ([TVd – TV0] / TV0) × 100%. Orange dashed line denotes a change of ‑30%, corresponding to the threshold for partial response (PR). Blue dashed line denotes a change of ‑100%, corresponding to complete response (CR). Table summarizes the frequency of PRs and CRs observed on day 25; any PRs or CRs occurring before or after day 25 are not reflected here but can be seen in Fig 9B. Figure 9. Combination of azenosertib with EV drives durable tumor responses and extends PFS in a PDX model of SG‑resistant TNBC M ea n TV ± S EM (m m 3 ) Treatment Group Median DoR Median PFS EV 12 days 22 days Azenosertib + EV >56 days Not reached 0 10 20 30 40 50 60 70 0 500 1000 1500 2000 Days no Tx 0 10 20 30 40 50 60 70 0 25 50 75 100 Time to Progression Day Pr og re ss io n- Fr ee S ur vi va l ( % ) 0 10 20 30 40 50 60 70 1 2 3 4 5 6 7 8 1 2 3 4 5 6 7 8 Days M ic e Vehicle Azenosertib 60 mg/kg QD 5:2 SG 3 mg/kg D1, 8 T-DXd 3 mg/kg D1 EV 3 mg/kg D1, 8, 15 (28d cycle) Azenosertib 60 mg/kg QD 5:2 + EV 3 mg/kg D1, 8, 15 EV Azenosertib + EV Azenosertib + EV EV PD SD PR CR Ongoing Response EOT A CB A. Mean TV ± SEM of an SG‑resistant PDX model treated with azenosertib +/‑ EV (n=8/group). Treatment was discontinued after day 25, and tumor regrowth was monitored thereafter, indicated by the shaded gray box labeled “no Tx.” Observation of tumor regrowth in the azenosertib + EV group occurred in only 3 mice on days 52, 56, and 59, and mean TV on day 63 remained small at 17mm3. B. Swimmer plot depicting treatment response for individual mice. Dashed line indicates end of treatment (EOT) on day 25. C. Kaplan‑Meier plot of PFS, defined as time from treatment initiation to documented disease progression, where progression is defined as >20% increase from the smallest recorded tumor volume: P value<0.0001 by log‑rank (Mantel‑Cox) test, HR: 0.14, 95% CI: 0.036‑0.52. The table summarizes median duration of response (DoR) and median PFS. DoR was defined as the time from first PR to PD. Median DoR for combination group includes 5 ongoing responders at final measurement. Figure 10. Sequential treatment of SG‑ or T‑DXd‑progressed tumors with azenosertib + EV provides robust antitumor activity compared to monotherapy EV TV (m m 3 ) TV (m m 3 ) 0 10 20 30 40 50 60 70 0 500 1000 1500 2000 Rechallenge with EV Days 0 10 20 30 40 50 60 70 0 500 1000 1500 2000 Rechallenge with Azenosertib + EV Days SG 3 mg/kg D1, 8 T-DXd 3 mg/kg D1 EV 3 mg/kg D15, 22, 29, 43, 50, 57 Azenosertib 60 mg/kg QD 5:2 + EV 3 mg/kg D15, 22, 29, 43, 50, 57 A B Spider plots displaying TVs of individual mice bearing SG‑resistant PDX tumors that were first treated with SG or T‑DXd for 14 days, rerandomized into new groups to minimize the impact of prior treatment, then rechallenged on day 15 with (A) monotherapy EV (n=7), or (B) combination of azenosertib + EV (n=8). Average TV on day 15 at the start of rechallenge was 850‑950mm3. Treatment and tumor measurements continued until day 63. RESULTSBACKGROUND • WEE1 kinase maintains genomic integrity by regulating the G1‑S and G2‑M cell cycle checkpoints to prevent cells with damaged DNA from progressing to the next phase • Azenosertib is a potent and selective oral WEE1 inhibitor currently in clinical development • Treating tumor cells with azenosertib promotes premature cell cycle progression, leading to increased replication stress, accumulation of DNA damage, and ultimately mitotic catastrophe and cell death1 • Mechanisms such as TP53 inactivation and Cyclin E1 overexpression often disrupt the G1‑S checkpoint in tumors, increasing intrinsic replication stress and reliance on the G2‑M checkpoint, thereby rendering tumor cells more vulnerable to WEE1 inhibition • While clinically meaningful activity of azenosertib has been observed in Cyclin E1‑positive platinum‑resistant ovarian cancer (PROC)2, other indications may have similarly high levels of replication stress and could benefit from WEE1 inhibition • Triple‑negative breast cancer (TNBC) represents 15%‑20% of breast cancers diagnosed in the United States each year and is a particularly aggressive subtype with limited availability of targeted therapies for patients • Although recent approvals of immune checkpoint inhibitors and antibody‑drug conjugates (ADCs) have improved outcomes in some patients with TNBC, disease progression remains frequent, highlighting limitations such as ADC payload cross‑resistance3,4, and underscoring the need for new therapeutic strategies Figure 1. Mechanism of action of azenosertib DNA damagePhosphorylation, causing inactivation of CDK1/2 Cyclin E1 CDK2 G2 M G1 S G1-S checkpoint G2-M checkpoint Cyclin CDK WEE1 CDK2 Inactive CDK1 Inactive WEE1 Cell Proliferation DNA Damage Repaired G2 M G1 S G1-S checkpoint G2-M checkpoint Cyclin E1 CDK2 Cyclin CDK Azenosertib Azenosertib WEE1 CDK2 Active CDK1 Active WEE1 Mitotic Catastrophe and Death DNA Damage Accumulates Normal Cell Cycle Regulation The Effect of Azenosertib on Cancer Cells Figure 2. ADCs have the potential to reshape the treatment landscape of TNBC Disease progression and cross‑resistance to similar payloads are becoming relevant unmet needs in the clinic 1L Pembrolizumab + chemotherapy (if PD-L1+) Chemotherapy, often taxane/platinum (if PD-L1-) PARPi (if gBRCA+) Ph3 ASCENT-04: Sacituzumab govitecan + pembrolizumab (if PD-L1+) Ph3 TROPION-Breast05: Datopotamab deruxtecan + durvalumab (if PD-L1+) Ph3 ASCENT-03: Sacituzumab govitecan (if PD-L1-) Ph3 TROPION-Breast02: Datopotamab deruxtecan (if PD-L1-) 2L Sacituzumab govitecan Trastuzumab deruxtecan (if HER2-low) PARPi (if gBRCA+ and not used previously) Other biomarker-directed, targeted therapies 3L Chemotherapy Trastuzumab deruxtecan (if HER2-low and not used previously) PARPi (if gBRCA+ and not used previously) Other biomarker-directed, targeted therapies • Topoisomerase 1 inhibitor (TOP1i) payload ADCs are currently approved for treatment of TNBC in the ≥2L setting and are rapidly advancing toward 1L use • Sequential treatment with ADCs bearing the same payload class has demonstrated limited clinical benefit3,4, highlighting the need for alternative post‑ADC treatment strategies CONCLUSIONS • TNBCs likely have high replication stress and are sensitive to WEE1 inhibition in vitro and in vivo – Most ~TNBC exhibited high Cyclin E1 protein expression and TP53 mutation, suggesting dysregulated G1‑S checkpoint control and high levels of replication stress in this patient population – Compared to non‑TNBC breast cancer cell lines, TNBC cell lines expressed higher levels of Cyclin E1 and showed increased sensitivity to pharmacologic inhibition of WEE1 in vitro – Azenosertib demonstrated meaningful in vivo monotherapy activity (range, 42%‑99% TGI) across a molecularly diverse panel of 12 TNBC xenograft models – In ADC‑naïve models, combination treatment with azenosertib and TOP1i‑payload ADCs (SG, Dato‑DXd, or T‑DXd) further enhanced antitumor efficacy, improving both depth and duration of response over the monotherapy treatments • Azenosertib combinations may be promising therapeutic strategies for TOP1i‑ADC–resistant TNBC – Azenosertib restored sensitivity to paclitaxel when combined in a PDX from a heavily pretreated TNBC patient (including prior paclitaxel and a TOP1i‑ADC) – Azenosertib + EV combination led to a majority of complete responses in a TOP1i‑ADC–resistant TNBC model – Azenosertib + EV combination substantially delayed relapse, while single‑agent EV treatment led to relapse at least twice as quickly and more frequently in a TOP1i‑ADC–resistant model – Combination of azenosertib with EV has potential to improve the clinical efficacy observed with EV alone in patients with breast cancer11 (NCT04225117), especially in patients with TNBC previously treated with SG References 1. Kim D, et al. NPJ Precis Oncol. 2025;9(1):3. 2. Simpkins F, et al. Presented at the SGO Annual Meeting 2025. Abstract 814654. 3. Tarantino P, et al. J Natl Cancer Inst. 2025;117(11):2327‑2335. 4. Huppert LA, et al. NPJ Breast Cancer. 2025;11(1):34. 5. Akbani R, et al. Nat Commun. 2014;5:3887. 6. Dai X, et al. J Cancer. 2017;8(16):3131‑3141. 7. Chavez KJ, et al. Breast Dis. 2010;32(1‑2):35‑48. 8. American Type Culture Collection 2022. Triple negative breast cancer panels. 2022. Accessed March 6, 2026. https://www.atcc.org/‑/media/ product‑assets/documents/panels/cell‑biology/ triple‑negative‑breast‑cancer‑panels. pdf?rev=67ddbf2f83dd415d88f367b4b3ab9fc3 . 9. Garnett MJ, et al. Nature. 2012;483(7391):570‑575. 10. Chen MM, et al. JCO Clin Cancer Inform. 2030;4:357‑366. 11. Giordano A, et al. J Clin Oncol. 2024;42:16_ suppl:1005‑1005. Acknowledgments This study was sponsored by Zentalis Pharmaceuticals, Inc. Animal studies were conducted at Pharmaron (Ningbo/Beijing), Champions Oncology, and Crown Bioscience (Beijing). Editorial support for this poster was provided by Second City Science, LLC. Additional Information For more information on this study, visit www.zentalis.com or contact publications@zentalis.com. Abbreviations 1L, first line; 2L, second line; 3L, third line; 5:2, 5 days on, 2 days off; ADC, antibody‑drug conjugate; Amp, amplified; AUC, area under the curve; BC, breast cancer; ∆BW, change in body weight; BRCA, breast cancer gene; CCLE, Cancer Cell Line Encyclopedia; CCNE1, Cyclin E1; CDK, cyclin‑dependent kinase; CDX, cell line‑derived xenograft; CI, confidence interval; CR, complete response; D, day; Dato‑DXd, datopotamab deruxtecan; del, deletion; DoR, duration of response; EGFR, epidermal growth factor receptor; EOT, end of treatment; EV, enfortumab vedotin; gBRCA, germline BRCA; G1‑S, GAP1‑Synthesis; G2‑M, GAP2‑Mitosis; GDSC, Genomics of Drug Sensitivity in Cancer; HBCx, Human breast cancer xenograft; HER2, human epidermal growth factor receptor 2; HR, hormone receptor; KRAS, Kirsten rat sarcoma viral oncogene homolog; MMAE, monomethyl auristatin E; MTI, microtubule inhibitor; mut, mutation; Nectin‑4, nectin cell adhesion molecule 4; ns, not significant; PARPi, poly (ADP‑ribose) polymerase inhibitor; PD, progressive disease; PD‑L1, programmed death‑ligand 1; PDX, patient‑derived xenograft; PFS; progression‑free survival; Ph, phase; PR, partial response; QD, once daily; QW, once weekly; Q3W, once every 3 weeks; RB1, retinoblastoma 1; RPPA, reverse phase protein array; SD, stable disease; SEM, standard error of the mean; SG, sacituzumab govitecan; SOC, serous ovarian cancer; TCGA, The Cancer Genome Atlas; T‑DXd, trastuzumab deruxtecan; TGI, tumor growth inhibition; TNBC, triple‑negative breast cancer; TOP1i, topoisomerase 1 inhibitor; TP53, tumor protein 53; TPA, tenth percentile of amplification; TROP2, trophoblast cell surface antigen 2; ∆TV, change in tumor volume; TV, tumor volume; Tx, treatment. PRESENTED AT: American Association for Cancer Research (AACR), April 17‑22, 2026, San Diego, California, USA Poster #3902 WEE1 Inhibition as a Therapeutic Strategy in Triple‑Negative Breast Cancer: Evaluating Single Agent and Combination Activity of Azenosertib in Preclinical Models Catherine Lee, Alexandra Levy, Mona Abed, Heekyung Chung, Olivier Harismendy, Doris Kim Zentalis Pharmaceuticals, Inc. San Diego, CA, USA Exhibit 99.2

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Filename: ex993-jeongetal_realworl.htm · Sequence: 4

ex993-jeongetal_realworl

METHODS (cont'd) BOX1: Cyclin E1 status determination The definition of Cyclin E1 positivity depends on purpose (predictive, prognostic), available measurement (RNA, proteomics, IHC) and study design (observation, investigation, retrospective, etc). Since the predictive definition (referred to as clinical status) is still under development for azenosertib and other investigational drugs, this study uses alternate Cyclin E1 status definitions explained below: • Using RNA (application to TLOv) – TLOv patients' tumors were profiled via RNA‑seq only, but a subset of ReSET patients (n=92) have both RNA‑seq and clinical IHC‑based status – TLOv and ReSET expression of CCNE1 RNA follow a similar distribution, suggesting the classifier can be applied to TLOv data (Figure B1) – A logistic regression model was fitted to predict IHC status from CCNE1 RNA Z‑score, and the classification threshold was optimized using ROC curve analysis – CCNE1 RNA‑based classifier predicted Cyclin E1 clinical status with 72% accuracy (Table B1) Table B1. Concordance between RNA‑based and clinical IHC‑based Cyclin E1 status in a subset of ReSET (n=92) Clinical IHC‑based Cyclin E1 (IHC‑clinical CycE1) status served as the reference standard. P=2.3e‑5 (n=92) IHC‑clinical CycE1+ IHC‑clinical CycE1+ Predictive metric CCNE1 RNA High 32 9 PPV 78% (62‑89) CCNE1 RNA Low 17 34 NPV 67% (52‑79) RNA‑high rate = 45% (41‌/‌92) Sensitivity = 65% Accuracy = 72% • Using research cutoff (application to ReSET) – Research classification of Cyclin E1 positivity was defined as a level of H‑score greater than or equal to the level of expression of 90% of tumors with CCNE1 amplification from central lab testing resulting in H ≥145 – Cyclin E1 research status predicted Cyclin E1 clinical status (the proprietary, clinically defined cutoff being developed for azenosertib) with 92% accuracy and 100% positive predictive value (Table B2) Table B2. Concordance between clinical and research IHC‑based Cyclin E1 status in ReSET (n=398) Clinical IHC‑based Cyclin E1 status served as the reference standard P=1.1e‑80 (n=398) IHC‑clinical CycE1+ IHC‑clinical CycE1‑ Predictive metric IHC‑Research CycE1+ 200 0 PPV 100% (98‑100) IHC‑Research CycE1‑ 31 167 NPV 84% (79‑89) IHC Research‑positive rate = 50% (200‌/‌398) Sensitivity = 87% Accuracy = 92% PPV, NPV, sensitivity, specificity, and overall accuracy are shown. Statistical significance was assessed using a two‑sided Fisher's exact test. Analysis subset description • Patient Subsets: Within each cohort, different subsets of patients were used for analysis depending on their treatment lines or regimen evaluated (Table 1). For biomarker and prognostic analyses, the subsets were further selected using the timing of their tissue collection and the availability of outcome data as follows: – Biomarker subset: includes patients whose tissues were collected up to 42 days after the end of the 1L treatment (for 1L cohort) or before the start of the specific line treatment (for other cohorts) considered – Outcome subset: within biomarker subset, includes patients evaluable for rwPFS (TLOv), TTNT (ReSET) or ORR‌/‌DCR (both cohorts). For ReSET cohort, restricted to patients enrolled in high‑quality clinical sites defined as those with a low proportion of patients with incomplete or ambiguous prior systemic therapy information below a sample‑size‑adaptive threshold (adapted from Spiegelhalter DJ3) Table 1. Patient subset definitions Line or Regimen Considered Definition 1L All patients 1L‑PSOC Patients with more than 6 mo PFI following end of 1L 1L‑PSOC+ Patients with more than 12 mo PFI following end of 1L 1L‑PROC Patients with less than 6 mo PFI following end of 1L 2L Patients who received 2L treatment 2L‑PROC Patients from 1L‑PROC who received 2L treatment Taxane‑PROC Patients treated with regimen including taxane and excluding platinum compound Mirv Patients treated with Mirv regimen Analysis subset description (cont'd) Dataset TLOv ReSET Source Tempus Lens HGSOC RWD Azenosertib HGSOC studies Inclusion criteria HGSOC first treated in 2022 with tissue transcriptome profile HGSOC treated with MIRV with tissue transcriptome profile PROC enrolled in azenosertib studies with central Cyclin E1 IHC N 220 70 320 Biomarker Subset 1L 1L PSOC 1L PSOC+ 1L PROC 2L Taxane PROC Mirv 1L 1L PSOC 1L PSOC+ 1L PROC 2L Taxane Mirv N 203 123 76 30 98 13 70 273 162 81 109 309 43 24 Cyclin E1 status definition RNA‑seq expression classifier (Box1) Protein expression IHC H‑score cutoff (Box1) Prognosis Subset 1L 2L‑PROC Mirv 1L 2L‑PROC N 197 (rwPFS) 159 (ORR‌/‌DCR) 31 (rwPFS) 20 (ORR‌/‌DCR) 65 (rwPFS) 63 (ORR‌/‌DCR) 187 (TTNT) 194 (ORR‌/‌DCR) 31 (TTNT) 43 (ORR‌/‌DCR) Outcome metric rwPFS, ORR, DCR TTNT, ORR, DCR Early treatment landscape reflects the expected SOC • Nearly all patients received platinum+taxane doublet as 1L therapy • 60%‑62% patients received 1Lm therapy, including 33%‑50% PARPi – Use of PARPi in ReSET is lower likely due to inclusion of non‑US patients or patients diagnosed prior to PARPi approval • 61%‑63% of patients received a platinum regimen as 2L therapy consistent with expected rate of PSOC after 1L treatment • Doxorubicin was the preferred chemotherapy regimen in 2L treatment of patients with PROC Figure 1. Distribution of regimens by treatment line for all 2L patients 1% 99% 11% 38% 1% 41% 9% 20% 1% 4% 8% 1% 26% 18% 18% 3% 18% 23% 11% <1% 1%41% 4% 6% 23% 10% 2% <1% <1% <1% 30% 14% 99% 15% 3% 0.00 0.25 0.50 0.75 1.00 0.00 0.25 0.50 0.75 1.00 1L 1Lm 2L Treatment Line Treatment Line Fr ac ti on o f P ati en ts Fr ac ti on o f P ati en ts 1L 1Lm 2L None Other Bevacizumab alone PARPi+Bevacizumab PARPi Azenosertib Mirvetuximab Taxane Gemcitabine Doxorubicin Platinum+Gemcitabine Platinum+Doxorubicin Platinum+Taxane Platinum TLOv-2L (N=98) ReSET-2L (N=309)A B Stacked bars show the proportion of patients receiving each base regimen during 1L, 1Lm, and 2L therapy in TLOv‑2L (A) and ReSET‑2L (B). Figure 2. Comparison of platinum responses at 1L in TLOv and ReSET 20% 50% 31% 40% 30% 30% 0.00 0.25 0.50 0.75 1.00 Fr ac ti on o f P ati en ts ReSET−1L (N=271) TLOv−1L (N=153) PFI <6mo 6mo−12mo >12mo • From 1L patients with sufficient follow‑up time, ReSET includes more 1L‑PROC patients (40% vs 20%) The percentage of patients within each PFI range (less than 6 mo, between 6‑12 mo, or more than 12 mo) is shown for each cohort. Biomarker prevalence varies between subsets of patients • Differences in Cyclin E1 positive prevalence between TLOv and ReSET are likely attributable to differences in inclusion criteria and survivor bias in ReSET. Trends across subsets remain consistent – Compared to 1L‑PSOC, 1L‑PROC is more likely to be CCNE1 amplified, Cyclin E1 positive or BRCAwt – Patients in 2L are more likely CCNE1 amplified or Cyclin E1 positive compared to 1L‑PSOC+ patients Figure 3: Biomarker prevalence across cohort and patient subsets 37% 38% 33%40% 46% 38% 41% 58% 53% 51%66% 58% 49% 79% 20% 22% 18%28% 23% 15% 17% 31% 26% 20%44% 32% 25% 26% 16% 19% 26%0% 9% 8% 17% 14% 17% 18%9% 15% 16% 26% 0 25 50 75 100 Pr ev al en ce (% ) 203N= 123 7630 98 13 70 0 25 50 75 100 Pr ev al en ce (% ) N= 0 20 40 60 Pr ev al en ce (% ) N= Pr ev al en ce (% ) N= 0 10 20 30 40 50 Pr ev al en ce (% ) N= Pr ev al en ce (% ) N= 0 20 40 60 0 10 20 30 40 50 273 162 81109 309 43 24 199 122 7629 96 13 70 140 106 5432 161 36 23 199 122 7629 96 13 70 227 140 6685 258 38 23 1L 1L PROC 1L PSOC 1L PSOC+ 2L Taxane Mirv A B C D E F CycE1+ (TLOv) CycE1+ (ReSET) CCNE1−amp (TLOv) CCNE1−amp (ReSET) BRCAm (TLOv) BRCAm (ReSET) The prevalence of Cyclin E1 positive (A,B), CCNE1 amplification (C,D), and BRCA1‌/‌2 mutation (E,F) in different subsets of patients from the TLOv (A,C,E) and ReSET (B,D,F) cohort. Cyclin E1 positive definition is cohort specific (see Box1). Error bars represent the 95% confidence interval. Clinical outcome characteristics TLOv ReSET 1L 2L PROC Mirv 1L 2L PROC Censoring rate 49% (96‌/‌197) 42% (13‌/‌31) 31% (20‌/‌65) 0% (0‌/‌187) 0% (0‌/‌31) Median observation 11.7m 2.8m 4.6m 12.5m 5.1m Median follow‑up 23.3m 11.8m 11.2m ‑ ‑ Median rwPFS‌/‌TTNT 16.7m 3.7m 6.6m 12.5m 5.1m ORR 90% (143‌/‌159) 20% (4‌/‌20) 38% (24‌/‌63) 66% (124‌/‌188) 14% (6‌/‌43) DCR 94% (150‌/‌159) 55% (11‌/‌20) 57% (36‌/‌63) 88% (166‌/‌188) 42% (18‌/‌43) Median observation is the median duration from the start of treatment to the date of last known follow‑up, including both events and censored observations. Median follow‑up and median rwPFS (TLOv)‌/‌TTNT (ReSET) are calculated by reverse KM and KM method, respectively. ORR is the proportion of patients achieving CR or PR. DCR is the proportion achieving CR, PR, or SD. Responses were not adjudicated per RECIST criteria. Cyclin E1 positive patients have worse outcomes after 1L Figure 4. Survival analysis after 1L treatment stratified by Cyclin E1 status 75 72 66 49 35 24 22 15 11 8 8 8 2 1 1 122 115 99 73 61 46 42 30 25 15 10 8 5 3 1 110 108 103 84 55 31 19 17 12 8 5 3 2 0 0 77 75 71 67 47 32 27 23 17 15 15 13 8 6 5CycE1- CycE1+ Number at risk CycE1- CycE1+ Number at risk p = 0.10 0 25 50 75 100 0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 Months % P ro gr es si on −f re e p = 0.00083 0 25 50 75 100 0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 Months % N ex t T re at m en t- fr ee TLOv-1L ReSET-1L mPFS (95% CI) HR (95% CI) CycE1+ 13.5 (11.7-19.1) 1.4 (0.93-2.1) CycE1- 18.9 (14.4-25.1) Ref mTTNT (95% CI) HR (95% CI) CycE1+ 12.0 (10.8-12.9) 1.7 (1.2-2.3) CycE1- 13.3 (12.0-15.6) Ref A B rwPFS or TTNT are compared according to Cyclin E1 status in TLOv‑1L (A; n=197) and in ReSET‑1L (B; n=187). mPFS, mTTNT, and HR with 95% CI are shown in inset tables. P values are from log‑ranked test. Ref indicates a reference group for cox proportional HR calculation. Cyclin E1 positive patients regardless of CCNE1 amplification have worse outcomes after 1L Figure 5. Survival analysis after 1L treatment, stratified by Cyclin E1 and CCNE1 status CycE1+/ Nonamp CycE1- CycE1+/ Amp CycE1+/ Nonamp CycE1- CycE1+/ Amp Number at risk Number at risk 32 31 31 25 16 12 9 6 2 2 2 2 1 0 0 41 40 33 24 19 13 13 9 9 6 4 2 2 1 1 120 113 97 71 60 45 41 30 25 15 10 8 5 3 1 22 22 22 21 13 7 2 2 2 0 0 0 0 0 0 26 26 26 24 19 13 9 8 6 4 3 3 2 0 0 31 30 29 29 26 19 16 13 10 9 9 8 5 4 4 0 25 50 75 100 0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 Months 0 25 50 75 100 0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 Months p = 0.18 p = 0.0021 TLOv-1L ReSET-1L % P ro gr es si on −f re e % N ex t T re at m en t- fr ee mPFS (95% CI) HR (95% CI) CycE1+/ Amp 13.6 (11.4-20.0) 1.6 (0.97-2.6) CycE1+/ Nonamp 13.5 (10.5-25.5) 1.2 (0.72-1.99) mTTNT (95% CI) HR (95% CI) CycE1+/ Amp 13.2 (10.2-16.0) 2.9 (1.6-5.2) CycE1+/ Nonamp 14.9 (12.5-20.7) 1.6 (0.94-2.8) CycE1- 18.9 (14.4-25.1) Ref CycE1- 19.5 (13.3-23.7) Ref A B rwPFS or TTNT are compared according to Cyclin E1 and CCNE1 status in TLOv‑1L (A; n=193) and in ReSET‑1L (B; n=79). mPFS, mTTNT, and HR with 95% CI are shown in inset tables. P values are from log‑ranked test. Ref indicates a reference group for cox proportional HR calculation. Summary of first‑line prognostic stratifications in TLOv and ReSET Figure 6. Hazard ratios for first‑line survival stratified by Cyclin E1, CCNE1, and BRCA‌ /‌first‑line maintenance status Hazard ratio Hazard ratio 1/16 1/8 1/4 1/2 1 2 4 1/8 1/4 1/2 1 2 4 8 Ref 1.39 (0.93−2.07) Ref 1.59 (0.97−2.60) 1.20 (0.72−1.99) Ref 0.26 (0.11−0.62) 1.13 (0.34−3.74) 1.13 (0.72−1.78) 1.32 (0.66−2.63) 0.105 0.068 0.487 0.003 0.843 0.596 0.427 18.9 (14.4−25.1) 13.5 (11.7−19.1) 18.9 (14.4−25.1) 13.6 (11.4−20.0) 13.5 (10.5−25.5) 16.1 (11.7−23.2) NA (25.5−NA) 14.8 (13.1−NA) 14.2 (12.9−20.0) 13.9 (8.71−16.7) Cyclin E1 expression status (Figure 4A) Cyclin E1 expression and CCNE1 amplification status (Figure 5A) Cyclin E1 expression status (Figure 4B) Cyclin E1 expression and CCNE1 amplification status (Figure 5B) BRCA mutation status and first-line maintenance regimen type BRCA mutation status and first-line maintenance regimen type CycE1− CycE1+ CycE1− CycE1+/CCNE1−amp CycE1+/CCNE1−nonamp BRCAwt/No 1Lm BRCAm/PARPi BRCAm/No 1Lm BRCAwt/PARPi BRCAwt/Other 1Lm CycE1− CycE1+ CycE1− CycE1+/CCNE1−amp CycE1+/CCNE1−nonamp BRCAwt/No 1Lm BRCAm/PARPi BRCAm/No 1Lm BRCAwt/PARPi BRCAwt/Other 1Lm 122/197 (62%) 75/197 (38%) 120/193 (62%) 32/193 (17%) 41/193 (21%) 86/193 (45%) 20/193 (10%) 11/193 (6%) 59/193 (31%) 17/193 (9%) 77/187 (41%) 110/187 (59%) 31/79 (39%) 22/79 (28%) 26/79 (33%) 59/151 (39%) 11/151 (7%) 8/151 (5%) 36/151 (24%) 37/151 (25%) Ref 1.68 (1.23−2.29) Ref 2.86 (1.55−5.29) 1.63 (0.93−2.85) Ref 0.45 (0.23−0.87) 0.71 (0.33−1.51) 0.67 (0.44−1.03) 0.64 (0.42−0.97) 0.001 0.001 0.084 0.017 0.369 0.067 0.038 13.3 (12.0−15.6) 12.0 (10.8−12.9) 19.5 (13.3−23.7) 13.2 (10.2−16.0) 14.9 (12.5−20.7) 10.7 (8.54−12.0) 18.0 (13.3−27.7) 9.87 (3.78−31.9) 14.0 (11.6−17.0) 13.5 (12.5−16.3) Stratification of TLOv-1L n/N (%) HR (95% CI) p mPFS (95% CI) Stratification of ReSET-1L n/N (%) HR (95% CI) p mTTNT (95% CI) TLOv 1L ReSET 1L A B (A) rwPFS hazard ratios across stratifications in TLOv‑1L. (B) TTNT hazard ratios across stratifications in ReSET‑1L. HRs with 95% CIs are shown. Ref indicates the reference group (HR=1.0) for each variable. Median PFS or TTNT (mPFS‌/‌mTTNT) with 95% CI is reported in months. n‌/‌N indicates the number of events over the total number of patients in each subgroup. P values were derived from Cox proportional hazards regression. Stratifications correspond to Figures 4 and 5. Prognosis of PROC patients treated with 2L non‑platinum chemotherapy is poor • PROC patients treated in 2L have poor prognosis irrespective of Cyclin E1 status. • The rapid disease progression, combined with a limited sample size (N), limits the statistical sensitivity of the analysis • Nevertheless, a trend toward shorter progression‑free survival (TLOv) or time to next treatment (ReSET) was observed in Cyclin E1-positive groups Figure 7. Survival analysis of 1L‑PROC patients after 2L treatment stratified by Cyclin E1 status CycE1- CycE1+ Number at risk CycE1- CycE1+ Number at risk 12 8 1 1 1 1 1 19 13 9 8 7 5 4 20 20 13 10 3 3 2 11 11 7 5 5 4 3 0 25 50 75 100 0 2 4 6 8 12 Months % P ro gr es si on −f re e 0 25 50 75 100 0 2 4 6 8 10 10 12 Months % N ex t T re at m en t- fr ee p = 0.35 p = 0.40 TLOv-2L PROC ReSET-2L PROC mPFS (95% CI) RMST (95% CI) HR (95% CI) CycE1+ 3.7 (1.8-NA) 5.7 (1.0-10.3) 1.6 (0.55-4.5) CycE1- 5.3 (1.9-NA) 8.6 (5.2-12.1) Ref mTTNT (95% CI) RMST (95% CI) HR (95% CI) CycE1+ 5.6 (3.8-7.1) 6.5 (4.8-8.1) 1.4 (0.65-3.1) CycE1- 4.5 (3.2-13.3) 7.9 (4.8-10.9) Ref A B rwPFS or TTNT are compared according to Cyclin E1 status in TLOv‑2L‑PROC (A; n=31) and in ReSET‑2L‑PROC (B; n=31). RMST metric (tau = 18) is used since proportional hazards assumption is violated in both TLOv and ReSET. mPFS, mTTNT, RMST, and HR with 95% CI are shown in inset tables. P values are from log‑ranked test. Ref indicates a reference group for cox proportional HR calculation. Cyclin E1 positivity is associated with a trend toward reduced clinical benefit from Mirv • TLOv Cyclin E1 positive patients exhibited a higher progression rate on Mirv (52% vs 36%; NS) • Note: Prognosis of ReSET‑Mirv cohort was not included due to a limited cohort size and imbalanced Cyclin E1 status Figure 8. Prognostic evaluation after treatment with Mirv in TLOv patients stratified by Cyclin E1 status 11% 26% 11% 52% 6% 33% 25% 36% 0% 25% 50% 75% 100% CycE1- (N=36) CycE1+ (N=27) Pe rc en ta ge o f P ati en ts BOR CR PR SD PD CycE1- CycE1+ Number at risk 27 20 16 12 7 2 2 2 1 38 35 22 15 11 7 6 1 1 0 25 50 75 100 0 2 4 6 8 10 161412 Months % P ro gr es si on -f re e p = 0.30 TLOv-Mirv mPFS (95% CI) HR (95% CI) CycE1+ 5.7 (3.0-7.4) 1.4 (0.74-2.5) CycE1- 6.8 (4.0-8.5) Ref A B BOR (A) and rwPFS (B) are compared according to Cyclin E1 status in TLOv‑Mirv (n=65). mPFS and HR with 95% CI are shown in inset tables. P values are from log‑ranked test. Ref indicates a reference group for cox proportional HR calculation. BACKGROUND • The success of novel therapies as they progress in later phases of clinical development requires accurate benchmarking of the benefit provided by the standard of care (SOC) at the time of clinical study completion • Information collected from published investigational studies or retrospective registries may be outdated or not reflect the most current SOC • Furthermore, the development of novel agents ‑ such as the WEE1 inhibitor azenosertib ‑ may be restricted to select populations, not previously characterized in the literature, perhaps defined by criteria such as a novel biomarker (eg, Cyclin E1 positive tumors) or indication subtypes (eg, platinum‑resistant ovarian cancer [PROC] with less than N prior therapy lines) • To build an up to date and realistic picture of the treatment landscape in high‑grade serous ovarian cancer (HGSOC), including biomarker prevalence and outcome stratification, we leveraged RWD and screening datasets from recent early‑phase clinical studies METHODS Cohorts description • Tempus Lens Ovarian cancer (TLOv) – Inclusion Criteria: Patients with HGSOC from Tempus Lens (data cutoff: 05Sep2025) who initiated first line of treatment in 2022 or received Mirv at any time and had their tumor tissue (purity ≥20%) profiled by RNA‑seq (Tempus xR assay) and DNA‑seq (Tempus xT assay) – Treatment Lines and Drug Regimen were curated according to Tempus Lens procedure.1 Additional scrutiny and manual review clarified the use and duration of maintenance regimens as well as the sequence of treatment lines – Outcomes: • rwPFS was established according to Tempus Lens procedure.1 In brief, rwPFS is defined as the time from the start of the investigated line to the date of first progression or death from any cause • Objective response was determined based on the overall disease burden as documented by the primary treating oncologist. When assessments were provided by non‑primary physicians, outcomes were captured only if the visit was for cancer symptom review. Responses were curated with association to the corresponding line of treatment. Responses were not adjudicated per RECIST criteria – Biomarker Status: • Genomic alterations (CCNE1 amplification and BRCA1‌/‌2 mutations) were obtained from the tumor DNA sequencing assay (Tempus xT) • Cyclin E1 expression status was derived from CCNE1 RNA expression level and tumor purity (see Box1) • Zentalis Retrospective Study of Early Treatment (ReSET) – Inclusion Criteria: • Platinum‑Resistant Ovarian Cancer patients who have been enrolled in one of the following azenosertib studies: ZN‑c3‑001 (NCT04158336), MUIR‌/‌ZN‑c3‑002 (NCT04516447), DENALI (ZN‑c3‑005, Part1b; NCT05128825), MAMMOTH (ZN‑c3‑006; NCT05198804), irrespective of regimen and dose • Tumor tissue profiled for Cyclin E1 IHC using central laboratory test2 – Treatment Lines and Drug Regimen were collected from the study sites via eCRF. Drugs, regimen, lines of treatment, intent of treatment, start and end date were harmonized across studies and curated – Outcomes: • Time‑to‑next treatment (TTNT) is defined as the time from the start of the investigated line to the start of the next line of treatment • Objective response was collected through eCRF for each line of treatment – Biomarker status • Nuclear expression of Cyclin E1 expression was summarized using H‑score (weighted sum of fraction of cells at 0, 1+, 2+ and 3+ DAB staining level). Cyclin E1 positive status was defined as a level of expression equal or higher to the level of expression of 90% of tumors with CCNE1 amplification from central laboratory testing. Note: this status is similar, but not identical to the one investigated for its predictive value in an ongoing trial (Box1) • Genomic alterations were obtained from Foundation Medicine F1CDx assay on the same tissue specimen that was profiled for IHC or a prioritized set of central and local reports (CCNE1 amplification and BRCA1/2 mutations) CONCLUSIONS • Cyclin E1‑positive patients had consistently worse prognosis in early treatment in both TLOv and ReSET. The effect appears independent of CCNE1 amplification status and consistent between cohorts • The use of maintenance therapy, highly effective in BRCAm patients treated with PARPi is changing the characteristics of traditional PSOC‌/‌PROC populations after 1L, extending PFI • Prognosis in recurrent PROC disease (2L‑PROC, Mirv) is poor. While the small size of cohorts limited statistical sensitivity, Cyclin E1 positive PROC patients may be less likely to benefit from currently available treatments • Limitations: – RWD (ie, TLOv) and retrospective data (ie, ReSET) have unique specificities that can impact the results or their interpretation • Biomarker definitions: Both Cyclin E1 positive definitions are only proxies for Cyclin E1 positivity currently being investigated for predictive value in the clinic. Differences can contribute to discrepancies. Similarly, genetic alterations in TLOv and ReSET are relying on different sources • Outcome accuracy and reliability: – rwPFS is impacted by RW monitoring of patients and follow‑up quality – ReSET relied on site‑reported objective response or treatment interval duration (TTNT) • Design and inclusion: – Limited follow‑up time in TLOv quickly reduced the N of late‑stage patients evaluable – Survivorship bias in ReSET enriched for 1L‑PROC patients and PROC patients who survived up to trial enrollment References 1. https:‌/‌/‌www.tempus.com‌/‌life‑sciences‌/‌lens‌/‌. 2. Abed M, et al. Poster presented at: AACR‑NCI‑EORTC International Conference on Molecular Targets and Cancer Therapeutics; October 22–26, 2025; Boston, MA. Poster A011. 3. Spiegelhalter DJ. Stat Med. 2005 Apr 30;24(8):1185‑202. Acknowledgments This study is sponsored by Zentalis Pharmaceuticals, Inc. We thank to Christian Anderson, Ben Barnhart, Ayano Kondo, Karson Lychuk and Livia Nguyen from Tempus AI Inc for their support with Tempus Lens datasets. We are grateful to the Zentalis clinical development and operations teams for the design and conduct of azenosertib trials; The authors thank all patients participating in the azenosertib trials and their families’ support. Editorial support was provided by Second City Science, LLC. Abbreviations 1L, first line; 1Lm, first‑line maintenance; 2L, second line; amp, (copy number) amplified; BRCAm, BRCA1‌/‌2 mutated; BRCAwt, BRCA1‌/‌2 wild‑type; CCNE1, Cyclin E1 gene; CI, confidence interval; CR, complete response; CycE1, Cyclin E1; DAB, 3,3′‑diaminobenzidine; DCR, disease control rate; eCRF, electronic case report form; HGSOC, high‑grade serous ovarian cancer; HR, hazard ratio; H‑score, histologic score; IHC, immunohistochemistry; Mirv, mirvetuximab soravtansine; mPFS, median progression‑free survival; NPV, negative predictive value; NS, not significant; ORR, objective response rate; PARPi, poly(ADP‑ribose) polymerase inhibitor; PD, progressive disease; PFI, platinum‑free interval; PPV, positive predictive value; PR, partial response; PROC, platinum‑resistant ovarian cancer; PSOC, platinum‑sensitive ovarian cancer; Ref, reference; ReSET, Retrospective Study of Early Treatment; RMST, restricted mean survival time; ROC, receiver operating characteristic; RWD, real‑world data; rwPFS, real‑world progression‑free survival; SD, stable disease; SOC, standard of care; TLOv, Tempus Lens ovarian cancer cohort; TTNT, time to next treatment. PRESENTED AT: American Association for Cancer Research (AACR), April 17‑22, 2026, San Diego, California, USA Poster #1052 Real‑World Treatment Patterns and Outcomes Reveal Distinct Clinical Trajectories of Patients With Cyclin E1‑Positive Ovarian Cancer Jinkil Jeong1, Mona Abed1, Catherine Lee1, Heekyung Chung1, Alexandra Levy1, Nandini Molden1, Divya Rajendran1, Joyce F. Liu2, Leslie M. Randall3, Fiona Simpkins4, Funda Meric‑Bernstam5, Danielle D. Jandial1, Doris Kim1, Olivier Harismendy1 1Zentalis Pharmaceuticals, Inc. San Diego, CA, USA; 2Dana‑Farber Cancer Institute, Boston MA, USA; 3Gynecologic Oncology Clinical Research and Gynecologic Cancer Service Line, Inova Schar Cancer Institute, Inova Health System, Fairfax, VA, USA.; 4Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, Penn Ovarian Cancer Research Center, University of Pennsylvania, Philadelphia, PA, USA; 5Department of Investigational Cancer Therapeutics, University of Texas MD Anderson Cancer Center, Houston, TX, USA RESULTS Exhibit 99.3

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