On April 17, 2026 Pheast Therapeutics, a clinical-stage biotechnology company advancing macrophage-directed immunotherapies for cancer, reported the presentation of initial Phase 1a clinical data and new preclinical findings for PHST001, an IgG4 anti-CD24 macrophage checkpoint inhibitor, at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026.

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"The data presented at AACR (Free AACR Whitepaper) suggest that PHST001 may address a longstanding challenge in translating the therapeutic potential of macrophage biology into a cancer treatment with the right balance of activity and tolerability," said Roy Maute, Ph.D., CEO and Co-founder of Pheast Therapeutics. "The preclinical data further support rationally designed therapeutic combinations informed by CD24 biology, reinforcing the breadth of PHST001’s development potential."

In the ongoing Phase 1a first-in-human study, PHST001 was generally well-tolerated across dose-escalation cohorts. Most treatment-related adverse events were Grade 1 or 2, with a subset of patients experiencing transient neutrophil decreases that were manageable and not associated with clinical complications. The dataset demonstrated linear pharmacokinetics, increasing CD24 receptor occupancy at higher dose levels, and pharmacodynamic changes consistent with innate immune activation. Early signs of clinical activity were observed, including disease stabilization and tumor shrinkage.

In preclinical studies including patient-derived tumor xenograft models, PHST001 enhanced macrophage-mediated tumor control and prolonged survival in combination with chemotherapies and antibody-drug conjugates. PHST001 also inhibited metastatic spread and reduced metastatic burden across multiple in vivo models.

"Taken together, these clinical and preclinical findings begin to build the profile we are looking for in a macrophage checkpoint inhibitor: favorable tolerability, evidence of biological activity, and meaningful combination potential," said Raphaël Rousseau, M.D., Ph.D., Chief Medical Officer of Pheast Therapeutics. "These data support continued development of PHST001 as a monotherapy and in combination with cytotoxic agents, where it may enhance macrophage-mediated clearance of treatment-damaged tumor cells."

Pheast plans to present updated clinical data from the ongoing PHST001-101 study at a future medical meeting.

The AACR (Free AACR Whitepaper) posters can be viewed at https://www.pheast.com/pipeline.

About CD24

CD24 is a cell surface protein that plays a key role in tumor immune evasion by engaging Siglec-10, an inhibitory receptor on macrophages. This interaction suppresses macrophage-mediated clearance of cancer cells, allowing tumors to evade destruction by the innate immune system. CD24 was identified as a novel macrophage checkpoint through foundational work by Dr. Amira Barkal, principal founder of Pheast. Along with other co-founders, Drs. Irving Weissman, Ravi Majeti, and Roy Maute, Pheast’s research forms the basis for therapeutic strategies targeting CD24 to activate innate immune responses against cancer.

About PHST001

PHST001 is an anti-CD24 macrophage checkpoint inhibitor designed to overcome immune suppression in the tumor microenvironment. CD24 is highly expressed in many human cancers and high expression of CD24 is associated with poor prognosis across multiple tumor types. PHST001 is designed to promote macrophage-mediated phagocytosis of cancer cells and initiate a broader immune response. PHST001-101 is an open-label, multicenter Phase 1 study in patients with advanced solid tumors (ClinicalTrials.gov Identifier: NCT06840886). Primary objectives include safety, tolerability, and dose optimization, with secondary objectives evaluating pharmacokinetics and preliminary anti-tumor activity. PHST001 received FDA Fast Track Designation for the treatment of ovarian cancer in June 2025. The phase 1b portion of the study combining PHST001 with chemotherapies is actively recruiting patients.

(Press release, Pheast Therapeutics, APR 17, 2026, View Source [SID1234664512])

On April 17, 2026 Zymeworks Inc. (Nasdaq: ZYME), a biotechnology company managing a portfolio of licensed healthcare assets while developing a diverse pipeline of novel, multifunctional biotherapeutics, reported six poster presentations featuring new preclinical data from its antibody-drug conjugate (ADC) and payload development programs at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026.

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"Our AACR (Free AACR Whitepaper) presentations highlight the breadth and depth of our ADC platforms, including multiple novel approaches to targeting RAS-driven cancers," said Paul Moore, Ph.D., Chief Scientific Officer at Zymeworks. "These data reinforce our strategy to develop differentiated therapeutics with the potential to improve efficacy while addressing key limitations of existing treatment approaches."

Poster Presentation Highlights

ZW191 – a differentiated FRα-targeted topoisomerase I antibody drug conjugate active in combination with standard of care drugs
Abstract: 1707
Session: Experimental and Molecular Therapeutics

ZW191 is a clinical-stage (NCT06555744) folate receptor alpha (FRα)-targeting antibody-drug conjugate featuring a novel antibody and a moderate-potency, bystander-active topoisomerase I inhibitor payload (TOPO1i), ZD06519, designed to drive improved efficacy and tolerability versus existing FRα-targeted ADCs. In nonclinical studies, ZW191 demonstrates activity across all levels of FRα expression and shows promising combination potential with standard-of-care therapies, supported by a favorable tolerability profile.

Key non-clinical findings include:

Differentiated by its superior internalizing novel antibody and moderate potency novel TOPO1i payload.
Favorable tolerability profile, attributed to moderate potency TOPO1i payload and moderate stability linker, potentially achieves higher ADC dosing, better tolerability and improved combination potential with standard of care chemotherapeutics.
Nonclinical in vitro and in vivo studies support the efficacious combination of ZW191 with standard of care therapies across multiple modes of action.
A pan-RASi antibody drug-conjugate platform with high activity in RAS sensitive cancers
Abstract: 1642
Session Category: Experimental and Molecular Therapeutics

Zymeworks’ RASi-ADC platform integrates novel tricomplex pan-RAS inhibitors into ADCs to enable tumor-selective delivery and improved therapeutic index.

Key findings include:

Strong regressions observed in multiple tumor models at single doses as low as 1 mg/kg
ADC delivery demonstrates improved tumor selectivity compared to orally administered RAS inhibitors
Favorable tolerability observed in rodents and non-human primates
Platform supports development of broadly applicable ADCs for RAS-mutated cancers
Development of ZW418, a biparatopic PTK7-targeting antibody-drug conjugate incorporating a novel pan-RAS inhibitor payload for the treatment of non-small cell lung cancer
Abstract: 4944
Session Category: Experimental and Molecular Therapeutics

ZW418 is a first-in-class biparatopic ADC targeting PTK7, designed to enhance binding, internalization, and delivery of a pan-RAS inhibitor payload in non-small cell lung cancer (NSCLC).

Key findings include:

Strong anti-tumor activity observed across PTK7-expressing RAS-mutant NSCLC xenograft models, at doses as low as 1 mg/kg
Biparatopic design enhances receptor engagement, internalization, and payload delivery
Selective cytotoxicity in KRAS-mutant tumor cells while sparing normal tissues
Favorable pharmacokinetics and tolerability support further development
ZW427, a Ly6E-targeting antibody-drug conjugate bearing a novel pan-RAS inhibitor payload for the treatment of RAS mutated cancers
Abstract: 7715
Session Category: Experimental and Molecular Therapeutics

ZW427 is a first-in-class ADC targeting Ly6E, designed to deliver a novel pan-RAS inhibitor payload to tumor cells in colorectal (CRC), pancreatic (PDAC), and lung cancers.

Key findings include:

Robust anti-tumor activity observed across CRC, PDAC, and NSCLC xenograft models with a range of Ly6E expression
Targeted delivery enables sustained RAS inhibition in tumors with reduced activity in normal tissues such as skin and colon
Favorable tolerability observed in rodents and non-human primates at exposures exceeding projected efficacious doses
Potential to improve efficacy and safety profile compared to small molecule pan-RAS inhibitors
ZW439, a novel CLDN18.2-targeting pan-RAS inhibitor antibody-drug conjugate for the treatment of RAS mutated pancreatic cancer
Abstract: 4556
Session Category: Experimental and Molecular Therapeutics

ZW439 is a novel ADC targeting CLDN18.2, designed to deliver a pan-RAS inhibitor payload in pancreatic ductal adenocarcinoma.

Key findings include:

Strong anti-tumor activity observed in CLDN18.2-expressing RAS-mutant xenograft models, at doses as low as 1 mg/kg
Target-dependent delivery of pan-RAS inhibitor payload with potent RAS pathway inhibition and cytotoxicity
Robust bystander activity supports activity in heterogeneous tumors
Favorable pharmacokinetics and tolerability compared to small molecule RAS inhibitors
Design and evaluation of mRNA translation inhibitors for use as antibody drug conjugate payloads
Abstract: 2062
Session Category: Experimental and Molecular Therapeutics

Zymeworks presented a novel class of eIF4A inhibitor payloads designed to inhibit mRNA translation and enable a new mechanism for ADC therapies.

Key findings include:

Over 40 novel eIF4A inhibitor payloads synthesized spanning a range of potency and hydrophilicity
Hydrophilic linker designs improve both efficacy and tolerability in vivo
Demonstrated robust anti-tumor activity across multiple targets including HER2, TROP2, EGFR, Ly6E, and PTK7
Represents a novel payload class with potential to overcome resistance to existing ADC payloads
Posters are available on the Company’s website located at View Source." target="_blank" title="View Source." rel="nofollow">View Source

Oral Presentation Details

Results from Part 1 dose escalation of ZWI-ZW191-101 study: Phase 1 first-in-human multicenter open-label study of ZW191, a folate receptor α (FRα)–targeting antibody-drug conjugate (ADC), in participants with advanced solid tumors
Abstract: CT306
Session: Advances in Precision Oncology

Lead author Patricia LoRusso, DO, PhD (hc), FAACR will present an updated data cut from the late breaking abstract on Tuesday, April 21, 2026 at 2:30 – 4:30 pm Pacific Standard Time (PST). The presentation will be available on the Company’s website located at View Source at the time of the session.

(Press release, Zymeworks, APR 17, 2026, View Source [SID1234664511])

On April 17, 2026 Xilio Therapeutics, Inc. (Nasdaq: XLO), a clinical-stage biotechnology company discovering and developing masked immuno-oncology therapies for people living with cancer, reported new preclinical data for XTX601, a masked T cell engager targeting claudin 18.2 (CLDN18.2), at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, taking place from April 17–22, 2026 at the San Diego Convention Center in San Diego, California.

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"The data to be presented at AACR (Free AACR Whitepaper) underscore the significant potential of our clinically-validated masking technology to address the central challenge that has limited the advancement of T cell engagers in solid tumors – namely, the inability to achieve meaningful anti-tumor activity without inducing severe systemic toxicities," said Uli Bialucha, Ph.D., chief scientific officer of Xilio Therapeutics. "XTX601 has demonstrated a promising preclinical profile, including potent tumor cell killing across multiple CLDN18.2-expressing tumor models and a favorable tolerability profile in non-human primates, supporting its potential to achieve a wide therapeutic index. Importantly, our modular architecture for masked T cell engagers provides flexibility to rapidly evaluate multiple designs in parallel, including masking of the CLDN18.2 binding domain and/or the addition of a co-stimulatory domain, which enables us to seek to optimize the molecule for the best possible clinical profile."

Masked T Cell Engager Design

XTX601 is a potentially first-in-class masked T cell engager designed to selectively target CLDN18.2, a tumor-associated antigen expressed in gastric, pancreatic and esophageal cancers. XTX601 incorporates Xilio’s clinically-validated masking technology and advanced tumor-activated cell engager (ATACR) format, which consists of a T cell engager with a masked CD3 targeting domain, with the goal of minimizing systemic T cell engagement in healthy tissue and overcoming the significant systemic toxicities that have limited non-masked T cell engagers targeting CLDN18.2. In addition, XTX601 is designed with a conditional half-life modulation element for antibody-like pharmacokinetics in its masked state and a short half-life upon activation in the tumor microenvironment to further limit peripheral exposure.

Preclinical Data Highlights Presented at AACR (Free AACR Whitepaper)

In preclinical studies, XTX601 demonstrated the potential to achieve a wide therapeutic index.

XTX601 demonstrated protease-dependent activation and tumor cell killing in high- and low-expression settings for CLDN18.2, with effective masking of the anti-CD3 domain.
XTX601 exhibited robust, dose-dependent anti-tumor activity in multiple murine cell line-derived xenograft models, including GSU gastric carcinoma and OE19 esophageal adenocarcinoma models engrafted with human T cells.
Consistent with its masked design, XTX601 was well tolerated in non-human primates (NHP) with no evidence of cytokine release syndrome and no changes in liver enzymes.
Integration of drug exposure data from murine tumor models and NHP studies indicated a favorable, positive therapeutic index for XTX601 and supports the potential for XTX601 to achieve meaningful anti-tumor activity at doses that are well-tolerated systemically.

Xilio plans to advance its masked T cell engager program targeting CLDN18.2 into investigational new drug (IND)-enabling studies and submit an IND application for this program in 2027.

Presentation Details

Xilio’s poster presentation at AACR (Free AACR Whitepaper) is listed below, and a copy of the presentation will be available under the "Our Approach—Presentations & Publications" section of the company’s website at www.xiliotx.com.

Title: Discovery and Optimization of XTX601, a Masked Claudin 18.2-Targeting T Cell Engager
Session Category: Immunology
Session Title: T Cell Engagers 1
Session Date and Time: Monday, Apr. 20, 2026, from 9:00 a.m. to 12:00 p.m. PST
Location: Poster Section 10, Poster Board 11
Abstract Number: 1619

(Press release, Xilio Therapeutics, APR 17, 2026, View Source [SID1234664510])

On April 17, 2026 Cardiff Oncology, Inc. (Nasdaq: CRDF), a clinical-stage biotechnology company leveraging PLK1 inhibition to develop novel therapies across a range of cancers, reported it will present new preclinical data in a poster at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, taking place April 17–22 in San Diego, California. These data highlight the potential of Cardiff’s highly specific oral PLK1 inhibitor, onvansertib, in combination with the HER2-targeted antibody-drug conjugate (ADC), trastuzumab deruxtecan (T-DXd), demonstrating robust antitumor activity and the ability to overcome resistance in HER2-low breast cancer models.

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"These preclinical findings highlight a potential new opportunity for onvansertib, demonstrating its ability to enhance the activity of ADCs, which are becoming mainstays in oncology across multiple indications," said Tod Smeal, Ph.D., Chief Scientific Officer of Cardiff Oncology. "By enhancing and prolonging DNA damage, this combination appears to drive greater apoptosis than either agent alone, offering a promising new approach for patients whose cancers have become resistant to standard-of-care treatments."

Poster Presentation Highlights:

Onvansertib + T-DXd synergistically inhibited the viability of HER2-low breast cancer cell lines, including fulvestrant- and CDK4/6i-resistant cells
In the resistant triple-negative breast cancer model and two hormone receptor-positive models, the combination drove tumor regression in nearly all mice, with complete response rates up to 62%
Increased tumor regression, improved tumor growth inhibition, and extended event-free survival across models
Combination showed favorable tolerability in vivo
Following the presentation on April 19, 2026 from 2:00–5:00 PM PT, the poster titled "PLK1 inhibitor onvansertib potentiates the antitumor efficacy of trastuzumab deruxtecan (T-DXd) and reverses its resistance in therapy-resistant HER2-low breast cancer models" will be available on the Scientific Publications page of the Company’s website.

About Onvansertib
Onvansertib is a highly specific, oral PLK1 inhibitor currently in mid-stage clinical development for RAS-mutated metastatic colorectal cancer. It is also being evaluated in multiple other cancers through investigator-initiated studies, including metastatic pancreatic ductal adenocarcinoma (mPDAC), small cell lung cancer (SCLC), triple-negative breast cancer (TNBC), and chronic myelomonocytic leukemia (CMML).

(Press release, Cardiff Oncology, APR 17, 2026, View Source [SID1234664509])

On April 17, 2026 Olema Pharmaceuticals, Inc. ("Olema" or "Olema Oncology", Nasdaq: OLMA), a clinical-stage biopharmaceutical company focused on the discovery, development, and commercialization of targeted therapies for breast cancer and beyond, reported new preclinical data for palazestrant, a complete estrogen receptor antagonist (CERAN) and selective estrogen receptor degrader (SERD), alone and in combination with OP-3136, a novel small molecule that potently and selectively inhibits acetyltransferase 6 (KAT6) inhibitor. The data will be presented in two poster presentations at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting taking place April 17-22 in San Diego, California.

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"We are very excited to share, for the first time ever, data that confirm the mechanism by which palazestrant completely blocks estrogen receptor transcription and signaling by recruiting the corepressor protein NCoR1," said David C. Myles, Ph.D., Chief Scientific Officer of Olema Oncology. "Further, the synergistic anti-tumor activity of OP-3136 combined with palazestrant in preclinical models highlights the role that both complete ER antagonism and KAT6 inhibition play in addressing acquired resistance associated with metastatic disease. We are pleased to continue to explore the potential of this combination in our ongoing Phase 1 study of OP-3136 and look forward to announcing top-line data from our Phase 3 OPERA-01 trial of palazestrant monotherapy, which is anticipated this fall."

Poster Presentation Details
Title: Palazestrant directly recruits the corepressor protein NCoR1 in vitro leading to complete antagonism of estrogen receptor alpha
Poster/Abstract: 2950
Session: Experimental and Molecular Therapeutics: Cellular Responses to Anticancer Drugs
Date/Time: April 20, 2026, from 2:00pm-5:00pm PT / 5:00pm-8:00pm ET

Key findings:

Palazestrant completely blocks estrogen-driven transcription and demonstrates robust anti-tumor activity in vitro.
In a split-luciferase assay, palazestrant was shown to fully recruit the corepressor, NCoR1, enabling complete estrogen receptor (ER) antagonism.
In both ESR1 wild-type and mutant models, palazestrant more potently suppressed ER-regulated and cell-cycle genes, including PGR and GREB1, than selective estrogen receptor modulators (SERMs), delivering complete inhibition of tumor cell proliferation without partial agonist effects.

These findings position palazestrant as a differentiated endocrine therapy designed to achieve deeper, more consistent ER pathway suppression in estrogen receptor-positive, human epidermal growth factor receptor 2-negative (ER+/HER2-) breast cancer.

Title: Palazestrant, a CERAN, in combination with OP-3136, a KAT6 inhibitor, synergistically downregulates cell proliferation and metastasis related gene signatures
Poster/Abstract: 2949
Session: Experimental and Molecular Therapeutics: Cellular Responses to Anticancer Drugs
Date/Time: April 20, 2026, from 2:00pm-5:00pm PT / 5:00pm-8:00pm ET

Key findings:

Combining OP-3136 with palazestrant drives synergistic anti-tumor activity in in vivo ER+/HER2- breast cancer models, which is mediated by suppression of cell-cycle and estrogen receptor-driven oncogenic signaling processes.
The combination of OP-3136 plus palazestrant downregulates genes associated with MYC, E2F, and G2M more effectively than either agent alone or OP-3136 in combination with fulvestrant.
Combining OP-3136 with palazestrant or fulvestrant suppresses expression of genes associated with MTORC1 signaling, indicating that targeting KAT6 and ER-alpha can suppress mechanisms of acquired resistance.

These findings provide a strong biological rationale for advancing palazestrant in combination with OP-3136 for the treatment of ER+ metastatic breast cancer.

Copies of these posters will be available on the Publications page of Olema’s website in alignment with the AACR (Free AACR Whitepaper) embargo. Additional information, including abstracts, is available on the AACR (Free AACR Whitepaper) Annual Meeting website.

(Press release, Olema Oncology, APR 17, 2026, View Source [SID1234664508])