Introduction

PARP inhibitor resistance is not a single biologic state. Patients enter clinical trials after different durations of PARP exposure, depths of prior response, platinum sensitivities, and molecular mechanisms of homologous recombination restoration or replication stress.[1,2,10] These distinctions matter because ATR- and WEE1-directed treatment has not produced uniform activity across apparently similar DNA damage response populations.[1,4-6,10]

Researchers study ATR and WEE1 because they regulate cellular responses to replication stress and DNA damage. Their inhibition can reduce tumor cells’ ability to delay cell-cycle progression while managing genomic injury.[4,9,11] Mechanistic rationale alone, however, does not establish a therapeutic class effect. Current clinical data support evaluating specific tumor-biomarker-drug hypotheses rather than broadly assuming that any DDR-abnormal tumor will respond to ATR or WEE1 inhibition.[4-6,11]

Why the Topic Matters

The post-PARP treatment question is particularly relevant in ovarian cancer, where PARP inhibitor exposure has created a growing population of patients whose tumors have progressed after prolonged pathway inhibition.[1-3] Small prospective studies show that clinically measurable responses can still occur when another checkpoint within the DNA damage response network is targeted.[1-3]

Evidence maturity remains the central limitation. CAPRI and EFFORT establish signals of clinical activity, but neither demonstrates superior survival compared with a contemporary active control in the post-PARP setting.[1,3] Objective response in a small selected cohort should therefore not be equated with evidence supporting routine clinical adoption.

WEE1 development has nevertheless advanced into confirmatory testing. Azenosertib is being evaluated in Cyclin E1-positive platinum-resistant ovarian cancer through the phase II DENALI program and the randomized phase III ASPENOVA trial.[7,8]

ATR Inhibition After PARP Resistance

Ceralasertib Plus Olaparib

The most directly relevant published ATR-PARP dataset is the acquired PARP inhibitor-resistant CAPRI cohort.[1] Eligible patients had recurrent, platinum-sensitive BRCA1/2-mutated or homologous recombination-deficient high-grade serous ovarian cancer. They had previously derived clinical benefit from PARP inhibition and subsequently progressed without intervening chemotherapy.[1]

Thirteen patients were treated, and 12 were evaluable for efficacy. Six achieved partial responses, corresponding to an objective response rate of 50% with a 95% confidence interval of 15% to 72%.[1] Median treatment duration was eight cycles, and grade 3 or 4 toxicity occurred in 38% of treated patients.[1]

These findings are hypothesis-generating rather than confirmatory. The cohort was very small, lacked a control group, and selected patients with platinum-sensitive disease and prior meaningful PARP inhibitor benefit.[1] The results support further study of ATR-PARP treatment in this phenotype but do not establish that ceralasertib broadly reverses PARP resistance.

An earlier basket study also included seven patients with BRCA-mutated, PARP inhibitor-resistant high-grade serous ovarian cancer treated with ceralasertib plus olaparib. One patient achieved a partial response and five had stable disease lasting 16 to 72 weeks, yielding a clinical benefit rate of 86% under the study definition.[2] These results provide additional evidence of biological and clinical activity but remain limited by the very small subgroup.[2]

Why the Population Matters

A separate CAPRI cohort provides an important counterpoint.[10] Fourteen PARP inhibitor-naive patients with platinum-resistant high-grade serous ovarian cancer were evaluable for toxicity, and 12 were evaluable for response. No objective responses occurred; nine patients had stable disease, and three had progressive disease.[10]

The difference between this platinum-resistant, PARP inhibitor-naive cohort and the later acquired-resistance cohort should not be interpreted as a randomized comparison.[1,10] It does show why disease setting, platinum sensitivity, prior PARP response, HRD status, and other biological factors must remain part of the interpretation of ATR-PARP data.

WEE1 Inhibition After PARP Resistance

EFFORT provides the most direct clinical evidence for WEE1 inhibition after PARP inhibitor resistance.[3] The study enrolled patients with recurrent ovarian, primary peritoneal, or fallopian tube cancer who had documented progression while receiving a licensed PARP inhibitor or within six months of completing PARP inhibitor therapy.

Among 35 response-evaluable patients in each reported arm, objective response rates were 23% with adavosertib alone and 29% with adavosertib plus olaparib.[3] Median progression-free survival was 5.5 months and 6.8 months, respectively.[3]

The numerical difference between treatment arms should not be interpreted as evidence of superiority. EFFORT was designed as a randomized, two-arm, non-comparative phase II study.[3] As of the August 7, 2026 verification, its principal efficacy findings remain represented by the 2021 ASCO meeting abstract rather than a full peer-reviewed efficacy publication.[3]

The trial nevertheless supports an important clinical hypothesis: WEE1 inhibition may retain activity after PARP inhibitor resistance, and continuation or reintroduction of PARP inhibition may not be required for every subsequent DDR-directed strategy.[3]

WEE1 Activity Outside a Specifically Post-PARP Population

Randomized evidence supports WEE1 as an active therapeutic target in platinum-resistant or platinum-refractory high-grade serous ovarian cancer, although not specifically after PARP inhibitor progression.[12]

In the randomized double-anonymized phase II study by Lheureux and colleagues, median progression-free survival was 4.6 months with adavosertib plus gemcitabine versus 3.0 months with gemcitabine plus placebo, with a hazard ratio of 0.55 (95% CI, 0.35-0.90; P=.015).[12] Grade 3 or higher hematologic toxicity was more frequent with the WEE1-containing combination, including neutropenia in 62% versus 30% and thrombocytopenia in 31% versus 6%.[12]

The trial validates clinical activity of WEE1 inhibition in ovarian cancer but does not establish efficacy specifically after PARP inhibitor resistance.[12]

Key Clinical Studies at a Glance

Strategy	Population	Interpretation
Ceralasertib + olaparib	Acquired PARPi-resistant, platinum-sensitive BRCA1/2-mutated or HRD HGSOC	6/12 partial responses; highly selected, very small, nonrandomized cohort.[1]
Ceralasertib + olaparib	BRCA-mutated PARPi-resistant HGSOC within a DDR basket trial	1/7 partial response and 5/7 stable disease; exploratory subgroup.[2]
Adavosertib ± olaparib	PARPi-resistant ovarian cancer	ORR 23% and 29%; randomized allocation but non-comparative statistical design and abstract-level efficacy report.[3]
Camonsertib	DDR-selected advanced solid tumors	13% response rate at biologically effective doses; phase I, heterogeneous biomarker population.[4]
Ceralasertib	ATM-altered advanced cancers	Limited responses in PLANETTE; argues against treating ATM alteration alone as a highly discriminating biomarker.[5]
Olaparib + ceralasertib	PARPi-naive mCRPC	Limited activity in HR-proficient disease; HRR-mutated response rate did not exceed historical PARPi results.[6]
Adavosertib	CCNE1-amplified refractory solid tumors	ORR 27% overall and 36% in epithelial ovarian cancer subgroup; not specifically a post-PARP trial.[11]

Abbreviations: ATR, ataxia telangiectasia and Rad3-related; DDR, DNA damage response; HGSOC, high-grade serous ovarian cancer; HRD, homologous recombination deficiency; HRR, homologous recombination repair; mCRPC, metastatic castration-resistant prostate cancer; ORR, objective response rate; PARPi, PARP inhibitor.

Biomarker Selection: Moving Beyond a Generic DDR Label

Prior PARP Response and HRD

The acquired-resistance CAPRI cohort raises the possibility that clinical history may contribute to biological selection.[1] Patients were required to have derived meaningful prior benefit from PARP inhibition, and all had platinum-sensitive BRCA1/2-mutated or HRD disease.[1]

These findings should not be converted into a validated selection rule. The study cannot determine whether the observed responses were driven by prior PARP sensitivity, HRD, platinum sensitivity, a specific resistance mechanism, or another feature of this highly selected population.[1]

CCNE1 Amplification and Cyclin E1 Protein Expression

CCNE1 amplification has become an important developmental biomarker for WEE1-directed therapy.[11] In a phase II study of 30 patients with CCNE1-amplified refractory solid tumors, eight achieved partial responses, producing an overall ORR of 27%.[11] Among 14 patients with epithelial ovarian cancer, the ORR was 36%.[11]

Current azenosertib development uses Cyclin E1 protein expression rather than simply requiring CCNE1 amplification.[7,8] DENALI Part 2 prospectively enrolls patients whose tumors are Cyclin E1-positive using the sponsor’s investigational immunohistochemistry assay, and ASPENOVA uses Cyclin E1 positivity for phase III enrollment.[7,8]

CCNE1 amplification and Cyclin E1 protein overexpression are related biological concepts but should not be presented as interchangeable clinical tests. Their assays, thresholds, and validation strategies differ.[7,8,11]

ATM Alterations

ATM deficiency remains a biologically plausible setting for ATR inhibition, but PLANETTE illustrates the difficulty of converting that rationale into a robust clinical biomarker.[5]

Among patients with centrally confirmed ATM-altered advanced solid tumors, the objective response rate was 7.1%. In metastatic castration-resistant prostate cancer, the composite response rate was 7.7%.[5] Median progression-free survival was 3.7 months in both cohorts.[5]

In patients with centrally confirmed ATM protein loss, the solid-tumor ORR was higher at 18.2%, but the subgroup was small.[5] These findings support refining ATM selection rather than using any ATM alteration as a sufficient predictor of ATR inhibitor sensitivity.

Broader DDR Alterations

The phase I camonsertib study enrolled 120 patients with advanced solid tumors harboring prespecified loss-of-function alterations predicted to confer ATR inhibitor sensitivity.[4] Among patients receiving biologically effective doses, the clinical response rate was 13%, the clinical benefit rate was 43%, and the molecular response rate was 43%.[4] Clinical benefit was greater in ovarian cancer and in tumors with biallelic loss-of-function alterations.[4]

These findings support attention to functional and allelic context rather than treating all DDR gene alterations as equivalent.[4]

Why Cross-Tumor Extrapolation Is Risky

DDR abnormalities and replication stress occur across many malignancies, but current evidence does not establish tumor-agnostic efficacy for ATR or WEE1 inhibition.[4-6,11]

In the TRAP study, four of 35 homologous-recombination-proficient patients with metastatic castration-resistant prostate cancer met the disease-response definition after treatment with olaparib plus ceralasertib.[6] Four of 12 patients in the HRR-mutated cohort also responded.[6] Investigators concluded that activity was limited in homologous-recombination-proficient disease and that the HRR-mutated response rate was not greater than that reported in previous single-agent PARP inhibitor trials.[6]

PLANETTE similarly showed limited ceralasertib monotherapy responses despite molecular selection for ATM alterations.[5]

The available evidence therefore supports interpreting each development program by tumor lineage, biomarker definition, prior treatment exposure, and regimen, rather than treating ATR or WEE1 inhibition as a single clinically validated DDR strategy.

Safety and Treatment Feasibility

Hematologic toxicity is a recurring feature of ATR- and WEE1-directed therapy.[1-5,12]

In the post-PARP CAPRI cohort, grade 3 or 4 toxicity occurred in five of 13 treated patients. Grade 3 anemia occurred in two patients, grade 3 thrombocytopenia in three, and grade 4 neutropenia in one.[1] Four patients required dose reductions, although no patient discontinued treatment because of toxicity.[1]

Camonsertib monotherapy produced grade 3 anemia in 32% of patients in the phase I study.[4] In PLANETTE, grade 3 or higher adverse events occurred in 50% of the advanced solid-tumor cohort and 53.3% of the prostate cohort; common adverse events observed in the study included fatigue or asthenia, nausea, and anemia.[5]

EFFORT also reported grade 3 and 4 toxicity in both treatment arms and required supportive care, treatment interruption, and dose reduction in some patients.[3]

The randomized adavosertib-gemcitabine study further demonstrates the potential for clinically important marrow toxicity when WEE1 inhibition is combined with cytotoxic therapy.[12]

Azenosertib Safety and Regulatory History

Azenosertib requires additional regulatory context because FDA placed the ZN-c3-001, DENALI, and TETON monotherapy studies on partial clinical hold in June 2024 after two deaths due to presumed sepsis in DENALI.[15] FDA lifted the partial clinical hold in September 2024 and cleared enrollment to resume without requiring changes to the clinical development plan.[14]

This history does not establish that the current azenosertib program is unsafe. It remains clinically relevant, however, when interpreting an investigational WEE1 inhibitor whose ongoing development depends on continued characterization of efficacy, marrow tolerance, infectious complications, dose intensity, and patient selection.

The 2026 Development Landscape

Development across the ATR and WEE1 field has been uneven.

Camonsertib-PARP Development

ATTACC evaluated camonsertib with niraparib or olaparib in molecularly selected advanced solid tumors.[13] The study enrolled 156 patients, but the sponsor terminated it early, and the planned phase II portion was not conducted.[13]

The registry does not establish that the biological strategy lacks efficacy. It does establish that the planned confirmatory development within ATTACC did not proceed.[13]

DENALI

DENALI is a multi-part phase II study of azenosertib in platinum-resistant high-grade serous ovarian, fallopian tube, or primary peritoneal cancer.[7] Part 2 prospectively selects patients with Cyclin E1-positive tumors using the sponsor’s investigational assay.[7]

As of the current 2026 development program, 400 mg once daily on an intermittent five-days-on, two-days-off schedule was selected as the pivotal monotherapy dose for the registration-intent DENALI Part 2 program.[14] This is a clinical-trial development dose, not a recommended clinical dose outside a trial.

The sponsor expects a DENALI Part 2 topline readout by the end of 2026.[14] Azenosertib has FDA Fast Track designation for Cyclin E1-positive platinum-resistant epithelial ovarian, fallopian tube, or primary peritoneal cancer.[14] Fast Track designation facilitates development and regulatory interaction but does not constitute FDA approval or increase the certainty that approval will ultimately occur.[14]

ASPENOVA

ASPENOVA is a recruiting randomized phase III trial in Cyclin E1-positive platinum-resistant high-grade serous ovarian, primary peritoneal, or fallopian tube cancer.[8] The study is expected to enroll approximately 420 patients and compares azenosertib with investigator’s choice single-agent chemotherapy.[8,14]

The first patient was dosed in May 2026.[14] ASPENOVA is designed as a confirmatory study that may support full regulatory approval if efficacy and safety results are favorable.[14] No phase III efficacy results were available at the August 7, 2026 cutoff.

Dual WEE1-PKMYT1 Inhibition

The phase I MYTHIC study is evaluating zedoresertib, a WEE1 inhibitor, with lunresertib, a PKMYT1 inhibitor, in molecularly selected advanced solid tumors.[9] The AACR 2026 abstract reported preliminary antitumor activity in tumors with CCNE1 amplification or deleterious FBXW7 or PPP2R1A alterations, with ovarian cancer representing the largest tumor subgroup.[9]

The findings remain preliminary. The study is phase I, includes multiple dose levels but lacks an active comparator, and uses small molecularly defined subgroups.[9]

The lunresertib-zedoresertib combination subsequently received FDA Fast Track designation for adults with platinum-resistant or refractory ovarian cancer characterized by CCNE1 amplification or a deleterious FBXW7 or PPP2R1A mutation.[16] The designation does not constitute FDA approval.

Patient Selection

Current evidence does not support selecting patients for ATR or WEE1 therapy merely because they previously progressed during PARP inhibitor treatment.[1,3-8,10,11]

The strongest clinical signals have generally involved additional clinical or molecular selection. These include prior PARP benefit and HRD in CAPRI, CCNE1 amplification in the adavosertib phase II study, prespecified DDR loss-of-function alterations in camonsertib development, and Cyclin E1 protein expression in current azenosertib trials.[1,4,7,8,11]

For clinical-trial evaluation, potentially relevant information includes tumor histology, platinum sensitivity when applicable, previous PARP exposure and duration of benefit, germline and somatic BRCA1/2 status, broader HRR findings, CCNE1 or Cyclin E1 status when required by a protocol, ATM protein loss or allelic context, and other trial-specific genomic eligibility criteria.[1,4,5,7-9,11]

A commercial sequencing report showing a DDR-associated variant should not automatically be interpreted as evidence of sensitivity to an ATR or WEE1 inhibitor.[4,5]

Practical Clinical Approach

The available evidence does not establish ATR- or WEE1-directed treatment as a routine standard strategy after PARP inhibitor progression.

Standard treatment selection should remain based on tumor type, disease setting, previous therapies, platinum sensitivity where relevant, validated biomarkers, approved treatment options, patient fitness, and contemporary disease-specific guidance.

For patients being considered for an investigational DDR strategy, match trial eligibility to the precise phenotype under study rather than the broad descriptor “PARP resistant.”[1,3-9,11]

A patient with platinum-sensitive, HRD-positive ovarian cancer who previously derived prolonged PARP benefit is not equivalent to a patient with platinum-resistant PARP inhibitor-naive disease, an ATM-altered prostate cancer, or a CCNE1-amplified refractory solid tumor.[1,5,6,10,11]

Baseline marrow reserve and cumulative treatment burden also warrant consideration because anemia, thrombocytopenia, neutropenia, gastrointestinal toxicity, fatigue, treatment interruptions, and dose reductions recur across these development programs.[1,3-5,12]

Clinical Implications

Current evidence supports three conclusions.

First, progression during PARP inhibition does not necessarily eliminate the therapeutic relevance of DNA damage response targeting. Objective responses have been observed with both ATR- and WEE1-directed strategies in selected PARP inhibitor-resistant ovarian cancer populations.[1-3]

Second, “post-PARP” is not itself a validated predictive biomarker. Contrasting results across CAPRI, TRAP, PLANETTE, and other studies show that tumor type, platinum sensitivity, prior PARP benefit, HRD status, and more specific molecular features can materially affect observed activity.[1,5,6,10]

Third, WEE1 development has entered a more definitive testing phase in ovarian cancer. DENALI is a registration-intent phase II program, while ASPENOVA is a randomized phase III confirmatory program in Cyclin E1-positive disease.[7,8,14]

Limitations of the Evidence

Sample size remains the most important limitation. Several influential post-PARP observations come from cohorts containing fewer than 20 efficacy-evaluable patients.[1,2]

Clinical heterogeneity is another major limitation. Studies differ in tumor lineage, platinum sensitivity, prior PARP exposure, duration of prior response, biomarker definition, treatment schedule, combination partner, and endpoint.[1-13]

Publication maturity also varies. EFFORT remains represented by an ASCO meeting abstract for its principal efficacy results, and the MYTHIC WEE1-PKMYT1 data remain phase I conference evidence.[3,9]

Development trajectories also differ substantially. ATTACC was terminated before its planned phase II portion, while azenosertib has advanced into phase III testing and the MYTHIC combination has received Fast Track designation.[8,13,14,16] These divergent programs argue against treating DDR inhibitor development as a single class-wide trajectory.

Future Directions

Future development will require more precise characterization of replication-stress dependency and treatment resistance.[4,5,7-9,11]

Cyclin E1-directed WEE1 studies, assessment of ATM protein loss and allelic status, and selection for specific biallelic DDR loss-of-function alterations are examples of efforts to move beyond broad genomic labels.[4,5,7,8,11]

Randomized evidence will be decisive. ASPENOVA is designed to compare azenosertib directly with active single-agent chemotherapy rather than relying on historical controls.[8,14]

The field is also moving beyond PARP rechallenge. MYTHIC tests simultaneous inhibition of WEE1 and PKMYT1, reflecting a strategy of exploiting complementary cell-cycle checkpoint dependencies rather than simply combining a new DDR inhibitor with continued PARP inhibition.[9]

The central challenge is therefore not to identify a universal treatment after PARP failure, but to define which resistant tumor state remains dependent on which checkpoint and then demonstrate that targeting that dependency improves outcomes against an appropriate comparator.

References

1. Wethington SL, Shah PD, Martin LP, et al. Combination ATR (ceralasertib) and PARP (olaparib) inhibitor (CAPRI) trial in acquired PARP inhibitor-resistant homologous recombination-deficient ovarian cancer. Clin Cancer Res. 2023;29(15):2800-2807. doi:10.1158/1078-0432.CCR-22-2444. PMID: 37097611. PMCID: PMC11934101. PubMed record
2. Mahdi H, Hafez N, Doroshow D, et al. Ceralasertib-mediated ATR inhibition combined with olaparib in advanced cancers harboring DNA damage response and repair alterations. JCO Precis Oncol. 2021;5:1432-1442. doi:10.1200/PO.20.00439. PMID: 34527850. PMCID: PMC8437220. PubMed record
3. Westin SN, Coleman RL, Fellman BM, et al. EFFORT: Efficacy of adavosertib in PARP resistance: a randomized two-arm non-comparative phase II study of adavosertib with or without olaparib in women with PARP-resistant ovarian cancer. J Clin Oncol. 2021;39(15_suppl):5505. doi:10.1200/JCO.2021.39.15_suppl.5505. ClinicalTrials.gov identifier NCT03579316. ASCO abstract
4. Yap TA, Fontana E, Lee EK, et al. Camonsertib in DNA damage response-deficient advanced solid tumors: phase 1 trial results. Nat Med. 2023;29(6):1400-1411. doi:10.1038/s41591-023-02399-0. PMID: 37277454. PubMed record
5. Aggarwal R, Italiano A, Domchek SM, et al. Ceralasertib monotherapy in patients with ATM-altered advanced solid tumors or metastatic castration-resistant prostate cancer: data from the phase IIa PLANETTE study. Cancer Res Commun. 2026;6(7):1546-1556. doi:10.1158/2767-9764.CRC-26-0184. PMID: 42219553. PubMed record
6. Tsung I, Smith DC, Heath EI, et al. Multicenter phase II study of olaparib and the ATR inhibitor ceralasertib in metastatic castration-resistant prostate cancer (TRAP). JCO Precis Oncol. 2025;9:e2500457. doi:10.1200/PO-25-00457. PMID: 40956994. PubMed record
7. ClinicalTrials.gov. NCT05128825. A study of azenosertib (ZN-c3) in subjects with platinum-resistant high-grade serous ovarian, fallopian tube or primary peritoneal cancer (DENALI). Last update posted July 1, 2026. Accessed August 7, 2026. ClinicalTrials.gov record
8. ClinicalTrials.gov. NCT07546500. A study of azenosertib versus investigator’s choice chemotherapy in subjects with platinum-resistant high-grade serous ovarian, primary peritoneal, or fallopian tube cancers positive for Cyclin E1 protein expression (ASPENOVA). Last update posted May 19, 2026. Accessed August 7, 2026. ClinicalTrials.gov record
9. Yap TA, Aggarwal R, Fontana E, et al. First data disclosure of the phase I trial of the first-in-class combination of WEE1 inhibitor zedoresertib with PKMYT1 inhibitor lunresertib in patients with advanced solid tumors harboring CCNE1, FBXW7, or PPP2R1A genomic alterations. Cancer Res. 2026;86(8_Suppl):CT022. doi:10.1158/1538-7445.AM2026-CT022.
10. Shah PD, Wethington SL, Pagan C, et al. Combination ATR and PARP inhibitor (CAPRI): a phase 2 study of ceralasertib plus olaparib in patients with recurrent, platinum-resistant epithelial ovarian cancer. Gynecol Oncol. 2021;163(2):246-253. doi:10.1016/j.ygyno.2021.08.024. PMID: 34620496. PMCID: PMC9614917.
11. Fu S, Yao S, Yuan Y, Previs RA, Elias AD, Carvajal RD, et al. Multicenter phase II trial of the WEE1 inhibitor adavosertib in refractory solid tumors harboring CCNE1 amplification. J Clin Oncol. 2023;41(9):1725-1734. doi:10.1200/JCO.22.00830. PMID: 36469840. PMCID: PMC10489509. PubMed record
12. Lheureux S, Cristea MC, Bruce JP, et al. Adavosertib plus gemcitabine for platinum-resistant or platinum-refractory recurrent ovarian cancer: a double-blind, randomized, placebo-controlled, phase 2 trial. Lancet. 2021;397(10271):281-292. doi:10.1016/S0140-6736(20)32554-X. PMID: 33485453. PMCID: PMC10792546. PubMed record
13. ClinicalTrials.gov. NCT04972110. Study of RP-3500 (camonsertib) with niraparib or olaparib in advanced solid tumors (ATTACC). Status: terminated. Last update posted October 30, 2025. Accessed August 7, 2026. ClinicalTrials.gov record
14. Zentalis Pharmaceuticals, Inc. Quarterly Report on Form 10-Q for the quarter ended March 31, 2026. U.S. Securities and Exchange Commission. Accessed August 7, 2026. SEC Form 10-Q
15. Zentalis Pharmaceuticals, Inc. Zentalis Pharmaceuticals provides an update on azenosertib clinical development program. June 18, 2024. Accessed August 7, 2026. Regulatory update
16. Debiopharm. Following oral presentation of phase I data at AACR 2026, Debiopharm announces FDA Fast Track designation for lunresertib in combination with zedoresertib for genomic-defined platinum-resistant ovarian cancer. April 20, 2026. Accessed August 7, 2026. Regulatory announcement