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.

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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])

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.

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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])

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.

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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])

On April 17, 2026 Volastra Therapeutics, a clinical-stage oncology company pioneering therapies targeting chromosomal instability (CIN), reported multiple scientific disclosures coinciding with the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, taking place April 17–22 in San Diego, California. The data define an Rb pathway–driven pan-cancer development framework for KIF18A inhibitors and highlight a proprietary p16 IHC biomarker approach designed to translate that strategy clinically, reinforcing Volastra’s leadership in advancing CIN biology into therapeutic opportunity.

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Separate from its AACR (Free AACR Whitepaper) 2026 presentation, Volastra has posted "KIF18A Inhibition as a Therapeutic Strategy in Cancers with Rb Pathway Inactivation" (Andreu et al. DOI: View Source – preprint publication). Drawing on what is believed to be one of the largest datasets of its kind, the work identifies Rb pathway inactivation as the mechanistic basis of response to KIF18A inhibition and establishes a development path that extends well beyond high-grade serous ovarian cancer.

The study includes clinical data from a substantial cohort of 79 heavily pretreated patients with high-grade serous ovarian cancer treated with either of two distinct KIF18A inhibitors, sovilnesib and VLS-1488. The concordance of the biomarker-defined signal across both agents is particularly compelling and argues against a drug-specific observation. Biomarker-positive tumors were distinguished by marked enrichment for objective responses, durable disease control, and longer progression-free survival, yielding a sharp clinical separation from biomarker-negative disease and strongly supporting both the biomarker strategy and prospective clinical development.

These findings reposition KIF18A inhibition from a histology-defined opportunity into a pan-cancer synthetic lethal strategy centered on one of the most commonly disrupted tumor suppressor pathways in human cancer. This creates a credible path across what is estimated to represent approximately 15% of human cancers. Within that biology, Volastra has identified a proprietary p16 IHC biomarker strategy that enriches for response to its KIF18A inhibitors and provides a practical route to clinical translation.

"The data provide a strong scientific rationale for using p16 status to identify patients most likely to benefit from KIF18A inhibition," said David Southwell, Chief Executive Officer of Volastra Therapeutics. "Importantly, this work reframes KIF18A inhibition from a narrow single cancer-type opportunity into a broader pan-cancer strategy grounded in Rb pathway biology. This p16 biomarker approach provides a practical way to translate that insight into clinical development and patient selection."

AACR Poster Highlights Clear Synergy with Taxanes and Other Microtubule-Targeting Agents

Volastra will also present an official AACR (Free AACR Whitepaper) poster titled "Combination of VLS-1488 and taxanes induces anti-tumor synergistic effect in cancer cells" in the Experimental and Molecular Therapeutics, Novel Antitumor Agents 1 Session on April 19 from 2-5PM Pacific Time (PT) (Poster section 17, poster 18). The presentation will highlight preclinical combination data showing clear synergistic activity between KIF18A inhibition and taxanes and other microtubule-targeting agents. These findings support a development strategy that could extend KIF18A inhibitors into earlier lines of therapy, including combination approaches in frontline settings.

"The totality of these data help define both the monotherapy and combination development paths for KIF18A inhibitors," said Samuel F. Bakhoum, M.D., Ph.D., Co-Founder and Chief Scientific Officer of Volastra Therapeutics. "With this new mechanistic understanding of KIF18A inhibitor sensitivity, it is evident that the biomarker data will help us identify patients most likely to benefit from monotherapy, while the combination findings point to a precision-based approach to identify the most rational therapeutic partners for development in earlier line settings."

Separately, Dr. Bakhoum, also an adjunct faculty member at the Geisel School of Medicine at Dartmouth, will chair an AACR (Free AACR Whitepaper) educational session "Chromosomal Instability in Cancer: From Mechanism to Therapy and Clinical Translation" on Saturday, April 18, 2026, in his academic capacity. The session reflects the field’s growing appreciation of CIN as both a driver of aggressive disease and a source of therapeutic vulnerability.

"This momentum underscores the growing recognition of CIN biology and the increasing importance of CIN-directed therapeutic strategies across oncology," Dr. Bakhoum said.

(Press release, Volastra Therapeutics, APR 17, 2026, View Source [SID1234664476])

On April 17, 2026 Soley Therapeutics, a biotechnology company advancing novel therapeutics informed by integrated cell stress biology, reported the presentation of new preclinical data at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026 highlighting the anti-tumor activity of STX-6398, a first-in-class, oral small-molecule modulator of cytoskeleton-associated protein 2 (CKAP2) pathway. CKAP2 is an intrinsically disordered protein that has been historically considered undruggable and is central to malignant progression.

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"STX-6398 is one of several potential first-in-class candidates rapidly found using our discovery platform," said Yerem Yeghiazarians, M.D., Co-Founder and Chief Executive Officer of Soley. "CKAP2 is implicated in multiple aspects of malignant progression, and its role across tumor types makes it an attractive target for therapeutic intervention. The preclinical profile of STX-6398, including biomarker-linked activity, oral dosing, and in vivo tolerability, supports continued evaluation as a potential therapeutic approach in CKAP2-expressing cancers."

Preclinical studies of STX-6398 demonstrate selective anti-tumor activity. In a 300-tumor cell line panel, sensitivity to STX-6398 correlated with CKAP2 protein abundance across cancer types, supporting a biomarker-linked therapeutic approach in both hematologic and solid tumors. Mechanistic studies showed that STX-6398 modulates CKAP2-associated pathways, including focal adhesion kinase (FAK) signaling, resulting in reduced cell migration, disruption of microtubule dynamics, and induction of cell cycle arrest. Additional studies demonstrated inhibition of angiogenesis and maintenance of activity under hypoxic conditions.

In vivo, oral administration of STX-6398 demonstrated significant anti-tumor activity across multiple xenograft models, including lung and colon cancer, with dose-dependent tumor growth inhibition and regression. The compound was well tolerated in efficacy studies and demonstrated a favorable profile in preclinical safety assessments.

The poster presented at AACR (Free AACR Whitepaper) 2026 titled "CKAP2 Modulation With A Novel Small Molecule Results In Excellent In Vitro And In Vivo Anti-Tumor Activity" is available in the Publications section of the Company’s website at View Source

The poster titled "CKAP2 Modulation With a Novel Small Molecule Results in Excellent In Vitro and In Vivo Anti-Tumor Activity" will be presented at AACR (Free AACR Whitepaper) 2026 on April 20 from 2:00 PM to 5:00 PM PDT in Poster Section 15, Poster Number 3043.

(Press release, Soley Therapeutics, APR 17, 2026, View Source [SID1234664475])