Orum Therapeutics Presents New Preclinical Data at AACR 2026 on ORM-1153, a CD123-Targeting Degrader-Antibody Conjugate, Highlighting Broad Activity in Acute Myeloid Leukemia and the Potential for Improved Efficacy and Tolerability

On April 17, 2026 Orum Therapeutics ("Orum" or the "Company") (KRX: 475830), a biotechnology company pioneering the field of degrader-antibody conjugates (DACs), reported the presentation of new preclinical data for ORM-1153, a CD123-targeting DAC designed to selectively deliver a proprietary GSPT1-degrading payload, in development for the treatment of AML and other CD123-positive hematological malignancies. The data were presented in two posters at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026.

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"These data show strong preclinical activity and the potential for a differentiated safety and tolerability profile, supporting the advancement of ORM-1153 as a next-generation CD123-targeting degrader-antibody conjugate for acute myeloid leukemia," said Chad May, Ph.D., Chief Scientific Officer of Orum. "Our approach combines a proprietary CD123-antibody and novel GSPT1-targeted protein degrader with the goal of achieving greater selectivity than conventional cytotoxic antibody-drug conjugates. We believe this strategy can enable more effective and better-tolerated therapies for patients with AML."

The first poster (Abstract Number: 1824) highlights how ORM-1153 was engineered with a proprietary CD123-antibody designed for enhanced internalization and reduced Fc-gamma receptor interactions, together with a linker optimized for plasma stability, an approach intended to improve delivery, reduce off-target and immune cell engagement, and support favorable pharmacologic properties. Consistent with that design, ORM-1153 showed strong preclinical anti-leukemia activity at low doses, along with prolonged accumulation in tumors, undetectable systemic free payload, and favorable repeat-dose non-human primate findings supporting a manageable safety and tolerability profile.

Data from the second poster (Abstract Number: 1710) extend Orum’s previously presented findings by showing activity across primary AML patient samples and in models with relevant tumor mutations, including TP53. Taken together, the findings support the potential for broad activity in AML, including in patients with TP53 mutations.

"These AACR (Free AACR Whitepaper) data are particularly encouraging in the context of AML, where many patients, especially those with TP53 mutations, continue to have limited treatment options and poor outcomes," said Olaf Christensen, M.D., Chief Medical Officer of Orum. "The activity we are seeing across primary patient samples and TP53-relevant models, together with a consistent pharmacologic and tolerability profile, supports the continued advancement of ORM-1153 toward clinical development."

Both posters are available on Orum’s website and will be presented at AACR (Free AACR Whitepaper) on Monday, April 20, from 9 am to 12 pm PDT.

About ORM-1153

ORM-1153 is a CD123-targeting degrader-antibody conjugate developed using Orum’s Dual-Precision TPD² approach. The molecule is built from two proprietary elements, a GSPT1-degrading payload and an anti-CD123 antibody engineered for high internalization efficiency, conjugated with a cleavable β-glucuronide linker. By combining tumor-selective antibody delivery with targeted protein degradation, ORM-1153 is designed to induce cancer cell death through degradation of GSPT1, a protein implicated in cell survival, including in TP53-mutant AML, while minimizing effects on normal tissues.

About Orum’s TPD² Approach

Orum’s unique Dual-Precision Targeted Protein Degradation (TPD²) approach builds novel targeted protein degraders combined with the precise cell delivery mechanisms of antibodies to generate innovative, first-in-class, cell-selective TPDs for the treatment of cancer and other serious diseases. Orum has developed new targeted protein degrader payloads to specifically degrade an intracellular target protein within cancer cells via the E3 ubiquitin ligase pathway. Conjugated to antibodies, the payloads are designed to be delivered specifically to target cells and precisely degrade the intracellular target protein of interest.

(Press release, Orum Therapeutics, APR 17, 2026, View Source [SID1234664496])

Pheast Therapeutics Reports Initial Phase 1a Data Showing Early Clinical Activity and Target Engagement for PHST001 at AACR 2026

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])

New data at AACR 2026 demonstrate advancements in Cancerguard® Multi-Cancer Early Detection Test

On April 17, 2026 Abbott (NYSE: ABT) reported it will present new data at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026 demonstrating continued advancements in its multi-biomarker, multi-cancer early detection (MCED) program supporting the commercially available Cancerguard test. Additionally, the AACR (Free AACR Whitepaper) Cancer Prevention Research Award for Outstanding Journal Article will recognize a publication on MCED multiyear outcomes from the DETECT-A study.

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Multi-biomarker approach enables broader and earlier cancer detection
New data demonstrate how combining methylation (M) and protein (P) biomarkers improves cancer detection across stages, with each biomarker contributing independently to overall performance. Cancerguard is currently the only commercially available MCED test designed with a multi-biomarker class approach, combining methylation and protein signals to improve detection.

In a prospectively collected case-control study, nearly half of positive cancer signals were driven by methylation alone (47.1%), with additional detection from protein-only (7.4%) and combined biomarker signals (45.5%), supporting broader detection across cancer types and stages.1 In early-stage disease, many cancer signals were detected by a single biomarker class, demonstrating how each contributes uniquely to overall detection. Notably, none of the 2.6% false-positive results were positive for both biomarkers.1

"We designed Cancerguard as the first-of-its-kind multi-biomarker test because no one signal tells the whole story," said Tom Beer, M.D., chief medical officer, multi-cancer early detection, Abbott’s cancer diagnostics business. "By combining biomarkers, we can detect cancer earlier, when it matters most."

AACR recognizes impactful MCED research with journal award
The AACR (Free AACR Whitepaper) Cancer Prevention Research Award for Outstanding Journal Article will be presented to the authors of a 2024 Cancer Prevention Research publication reporting multi-year outcomes from the DETECT-A study, the first large prospective interventional trial of a blood-based MCED test. The study identified nine cancer types, including several without routine screening, and showed that, after a median follow-up of approximately four years, all patients treated for stage I or II cancers remained alive and cancer-free.2,3

The award recognizes the significance of these multi-year outcomes data in advancing evidence for the clinical impact of MCED, an area where long-term outcomes data have historically been limited.

"Long-term follow-up provides critical insight into how multi-cancer early detection can shape the future of cancer screening," said Beer. "With nearly 70 percent of cancers occurring in types without recommended screening, these findings highlight the potential for MCED to increase early detection and improve outcomes."4

About the DETECT-A study
The DETECT-A (Detecting cancers Early Through Elective mutation-based blood Collection and Testing) study was the first-ever large, prospective, interventional study to use a blood test to detect multiple types of cancer in a real-world setting. The DETECT-A study enrolled more than 10,000 women with no history of cancer to determine if a blood test in combination with standard-of-care screenings could detect cancers before signs and symptoms appeared. The CancerSEEK test, the MCED test studied in DETECT-A, was the forerunner to the Cancerguard test.

About the Cancerguard test
Cancerguard is a laboratory-developed test (LDT) designed to detect multiple cancers, including the most aggressive cancers, in early stages from a simple blood draw. It integrates two classes of biomarkers to enable broader detection and follows a streamlined, imaging-based diagnostic pathway to help reduce unnecessary follow-up procedures. Developed with high specificity to minimize false positives, the test helps detect a wide range of cancers, including those that lack guideline-recommended screening options.5 The Cancerguard test has not been cleared or approved by the U.S. Food and Drug Administration or any other regulatory authority. To learn more, visit cancerguard.com.

(Press release, Abbott, APR 17, 2026, View Source [SID1234664465])

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

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

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

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

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

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

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

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

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

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

Efficacy Parameter
(RECIST v1.1, BICR)

Prior repotrectiniba

Prior taletrectinibb

ORR, % (n/n)

[95% CI]

41% (19/46)

[27, 57]

47% (9/19)

[24, 71]

CR, n (%)

7% (3/46) c

5% (1/19)

mDOR, months d

[95% CI]

15.7

[5.6, NE]

NR

[5.2, NE]

ROS1 G2032R resistance mutation

ORR, % (n/n)

[95% CI]

67% (8/12)

[35, 90]

50% (2/4) e

[7, 93]

CR, n (%)

8% (1/12)

0 %

mDOR, months d

[95% CI]

15.7

[3.5, NE]

NR

[NE, NE]

Intracranial Activity f

IC-ORR, % (n/n)

[95% CI]

44% (8/18)

[22, 69]

71% (5/7)

[29, 96]

IC-CR, n (%)

11% (2/18)

43% (3/7)

mIC-DOR, months d

[95% CI]

NR

[5.2, NE]

NR

[5.2, NE]

IC-DOR ≥6 months d

86%

[33, 98]

80%

[20, 97]

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

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

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

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

d Kaplan-Meier estimates.

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

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

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

New Preclinical Data for Zidesamtinib

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

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

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

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

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

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

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

SingleCell Biotechnology Presents Data at AACR Annual Meeting Demonstrating High-Throughput Single-Cell Assay Linking Clonal Growth Phenotypes to Molecular Profiles

On April 17, 2026 SingleCell Biotechnology, a biotechnology company developing technologies to measure tumor cell behavior at single-cell resolution, reported the presentation of new data at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026 demonstrating an integrated, high-throughput assay capable of measuring clonal tumor cell growth across thousands of individual microenvironments while preserving the full distribution of proliferative behaviors.

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The data show the platform can consistently measure differences in how individual tumor cells grow across multiple glioblastoma models. Importantly, it captures cell states that are often missed by traditional assays. It also enables tracking of single cells over time and recovery of specific cell populations for further analysis, allowing researchers to connect how cells behave with their underlying biology.

Tumor heterogeneity remains a major challenge in oncology drug development. Traditional preclinical approaches often rely on average responses across large groups of cells, which can miss the smaller populations that drive treatment resistance and disease progression. As a result, it remains difficult to identify and study the cells most responsible for relapse.

Presentation Details:
Poster Title: An Integrated High-throughput Assay for Proliferative Phenotypic and Omics
Presenter: Shiska Raut, Machine Learning Engineer
Poster ID: LB029
Session Date/Time: Sunday, April 19, 2026, 2:00 PM – 5:00 PM
Location: Poster Section 51, Board #9, San Diego Convention Center, San Diego, CA

(Press release, SingleCell Biotechnology, APR 17, 2026, View Source [SID1234664497])