On October 30, 2025 NeoGenomics, Inc. (NASDAQ: NEO), a leading provider of oncology diagnostic solutions that enable precision medicine, reported it will present new research at the International Society of Liquid Biopsy (ISLB) Annual Congress 2025 demonstrating high concordance between its RaDaR ST and RaDaR 1.0 assays for detecting molecular residual disease (MRD) in solid tumors. NeoGenomics will also present on the progress of its NextGen (whole genome-based) MRD research program, as well as three additional posters highlighting the company’s work in liquid biopsy and genomic profiling across solid tumor types.

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The bridging study, "Performance Comparison of RaDaR 1.0 and RaDaR ST Assays for Circulating Tumor DNA Detection Across Solid Tumor Types" (PP.41), evaluated matched samples from 166 patients representing 15 solid tumor types. RaDaR ST demonstrated 97% concordance and maintained equivalent sensitivity with RaDaR 1.0. This study provides analytical confirmation that RaDaR ST maintains the performance of RaDaR 1.0, supporting continuity in MRD assessment as the platform is updated. RaDaR ST is currently covered by Medicare for HR+/HER2- breast cancer (>5 years after diagnosis, recurrence monitoring) and HPV- head and neck carcinoma (adjuvant and recurrence monitoring) and has demonstrated utility across multiple tumor types.

"MRD has become an important part of a patient’s journey for cancer surveillance and monitoring," said Tony Zook, CEO. "This study shows that RaDaR ST delivers equivalent sensitivity as compared to RaDaR 1.0. We are excited to offer clinicians and patients MRD testing optionality with the expected launch of RaDaR ST in Q1 2026. As we continue to invest in novel MRD technologies for the future, the expanding portfolio of MRD solutions will help address unmet needs for sensitive and accurate residual disease detection and monitoring in patients with cancer."

In addition to the RaDaR ST bridging study, NeoGenomics will present four other posters at ISLB:

Performance Characterization of a Novel Whole Genome Sequencing Informed MRD Assay (PP.15), evaluating a whole genome-informed, tumor-specific approach to detect ctDNA at very low levels in solid tumors.
Genomic Profiles of Early-Stage Non-Small Cell Lung Cancer Patients, and Association with Pre-Treatment Blood Circulating Tumor DNA Detection and Levels (PP.74), analyzing genomic features of early-stage lung cancers and investigating the relationship between tumor genomics, ctDNA detectability, and clinical outcomes in these patients.
Validation of NEO │ PanTracer LBx, a Liquid Biopsy Precision Oncology Pan-Solid Tumor Comprehensive Genomic Profiling Assay (PP.05), presenting analytical and clinical validation findings for therapy selection using liquid biopsy.
Non-invasive identification of actionable biomarkers in advanced solid tumors by comprehensive genomic profiling with NEO | PanTracer LBx assay (PP.04), assessing liquid biopsy-based comprehensive genomic profiling to detect actionable variants and support treatment decisions in late-stage cancers.
These presentations contribute to NeoGenomics’ growing body of research in liquid biopsy for MRD detection and genomic profiling. The findings reinforce the company’s strategy to advance next-generation molecular testing platforms and expand the role of ctDNA in clinical research and patient management.

(Press release, NeoGenomics Laboratories, OCT 30, 2025, View Source [SID1234657180])

On October 30, 2025 Parabilis Medicines, a clinical-stage biopharmaceutical company committed to creating extraordinary medicines for people living with cancer, reported preliminary clinical and preclinical findings across its Helicon peptide pipeline at the AACR (Free AACR Whitepaper)-NCI-EORTC AACR-NCI-EORTC (Free AACR-NCI-EORTC Whitepaper) International Conference on Molecular Targets and Cancer Therapeutics (EORTC-NCI-AACR) (Free ASGCT Whitepaper) (Free EORTC-NCI-AACR Whitepaper) in Boston, Massachusetts.

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The findings reinforce the broad potential of FOG-001, the company’s lead investigational therapy and the first-ever direct Wnt/β-catenin:TCF inhibitor, to act across a range of rare and more prevalent solid tumors linked by the same dysregulated biology of the Wnt/β-catenin pathway. Single-agent activity resulting in tumor shrinkage by at least 30% (partial response (PR)) was observed in five low-complexity tumor types, with strong scientific support as well for FOG-001’s potential in combination therapy for more complex tumors, including microsatellite-stable colorectal cancer (MSS CRC).

Together with positive preclinical read-outs demonstrating pharmacologic proof of concept for the company’s discovery-stage Helicon peptides in prostate cancer targeting the ERG and active androgen receptor (ARON) targets, these data highlight how the company’s Helicon platform can repeatably target high-impact "undruggable" targets long considered inaccessible to conventional therapeutic approaches.

"Just one week after presenting the first clinical proof that β-catenin:TCF can be drugged, we are showing the breadth of what this breakthrough could mean for science and for patients," said Mathai Mammen, M.D., Ph.D., Chairman and CEO of Parabilis Medicines. "FOG-001 is demonstrating meaningful signs of clinical activity across multiple Wnt/β-catenin-driven tumors, supporting its continued development in both simpler and more biologically complex Wnt-driven cancers through both monotherapy and combination therapy approaches."

He added, "Together with our preclinical advances in prostate cancer, the data illustrate the potential of Helicons to take on some of the toughest problems in oncology and bring forward transformative medicines that could meaningfully improve outcomes for patients."

FOG-001 Clinical and Preclinical Findings

The Wnt/β-catenin pathway — first identified as a key cancer driver over 30 years ago — is implicated in millions of cancer cases annually, spanning many rare and prevalent solid tumors as well as diseases like familial adenomatous polyposis (FAP) that predispose individuals to certain cancers, including colorectal cancer and desmoid tumors. Despite its central role in cancer biology, the pathway’s critical β-catenin:TCF transcription complex has long been considered "undruggable."

Preliminary data from the ongoing Phase 1/2 trial of FOG-001 (NCT05919264), as of mid-August 2025, show that the therapy is well tolerated with no Grade 4/5 treatment-related adverse events or discontinuations and exhibits a favorable pharmacokinetic profile. As of this early data cut, an objective response rate (ORR) of 43% and a disease control rate (DCR) of 83%, per RECIST 1.1, were observed in non-CRC patients with Wnt pathway activating mutations (WPAM). Evidence of single-agent activity was observed across numerous Wnt/β-catenin–driven tumors, particularly in those with low mutational burden, including desmoid, adamantinomatous craniopharyngioma (ACP), ameloblastoma, salivary gland cancer, and solid pseudopapillary neoplasm (SPN).

In MSS CRC, a 50% DCR was achieved within the efficacious monotherapy dose range, with molecular data confirming on-target pathway inhibition and reprogramming of the tumor microenvironment toward a more immune-active state. Complementary preclinical studies demonstrated that FOG-001 enhances the effects of standard and emerging therapies for MSS CRC—showing in these preclinical models additive or synergistic activity with each of 5-fluorouracil and anti-VEGF regimens, synergy with anti–PD-1 therapy, and combination benefit with pan-RAS and KRAS G12D inhibitors.

Together, these findings highlight FOG-001’s broad pipeline potential — warranting continued development in Wnt pathway–activated low-complexity tumors, and as a backbone for rational combination regimens in more complex cancers. The Phase 1/2 study remains ongoing across a wide range of Wnt-driven rare and common cancers, with additional data readouts expected over the coming months.

Prostate cancer pipeline expansion

Parabilis also presented preclinical data advancing its prostate cancer franchise, focused on two long-standing oncogenic drivers that currently lack effective therapies. ERG-degrading Helicon peptides potently and durably reduced ERG protein levels —overexpressed in 40–50% of prostate cancers — showing in vivo pharmacologic proof-of-concept demonstrating tumor growth inhibition and efficacy comparable to or exceeding standard of care in challenging prostate cancer models.

In parallel, allosteric ARON Helicon degraders that bind a conserved site distinct from the androgen ligand pocket, were designed to selectively target the active, agonist-bound androgen receptor. These Helicon degraders block proliferation in AR-amplified prostate cancer cells, offering a strategy to overcome resistance driven by AR mutations or amplification. Importantly, this approach also allows for effective combinations with approved and emerging treatments that target the testosterone ligand pocket. Together, these data demonstrate the repeatability of the Helicon platform in addressing high-value, historically undruggable targets in oncology.

"Our Helicons are delivering against three of the most challenging and compelling targets in oncology, from β-catenin:TCF to ERG to ARON," said Fawzi Benzaghou, M.D., Chief Medical Officer of Parabilis Medicines. "By pursuing bold science that makes the undruggable druggable, we’re opening new therapeutic possibilities for patients with few or no options. These data reinforce the power of our α-helical peptide platform to repeatedly unlock difficult targets and advance medicines with the potential for extraordinary patient impact."

About the Phase 1/2 trial of FOG-001
FOG-001 is being evaluated in a first-in-human Phase 1/2 multicenter, open-label study (NCT05919264) assessing its safety, tolerability, pharmacokinetics, pharmacodynamics, and antitumor activity. The trial includes dose-escalation and dose-expansion phases and is testing FOG-001 both as a monotherapy and in combination with other anticancer agents in patients with advanced or metastatic solid tumors likely or known to harbor a Wnt pathway–activating mutation (WPAM).

About FOG-001
FOG-001 is an investigational first-in-class competitive inhibitor of β-catenin interactions with the T-cell factor (TCF) family of transcription factors and is currently in clinical development. By directly targeting the β-catenin:TCF protein-protein interaction, FOG-001 is intended to block the Wnt signaling pathway irrespective of the various APC and β-catenin mutations that typically drive disease.

FOG-001 combines key features that distinguish it from previously reported Wnt/β-catenin pathway modulators: FOG-001 acts inside the cell where it binds directly to the key oncogenic driver β-catenin; and FOG-001 blocks the Wnt pathway at the key downstream node, disrupting the interaction between β-catenin and the TCF transcription factors, thereby abrogating the signal transmission by which Wnt pathway mutations are believed to drive oncogenesis.

FOG-001 is currently being evaluated in a first-in-human Phase 1/2 clinical trial in patients with locally advanced or metastatic solid tumors.

(Press release, Parabilis Medicines, OCT 30, 2025, View Source [SID1234657179])

On October 30, 2025 Intensity Therapeutics, Inc. (Nasdaq: INTS) ("Intensity" or "the Company"), a late-stage clinical biotechnology company focused on the discovery and development of proprietary cancer therapies using its non-covalent, drug-conjugation technology that creates drug products designed to kill tumors and increase immune system recognition of cancers, reported that eBioMedicine, a Lancet Discovery Science journal, has published the Company’s phase 1/2 IT-01 clinical study manuscript for the treatment of metastatic or refractory cancers. The full text article, "Safety and Efficacy of Intratumourally Administered INT230-6 in Adult Patients with Advanced Solid Tumours: Results from an Open-Label Phase 1/2 Dose Escalation Study," can be viewed via Online First 105980 October 29, 2025.

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Jacob Stephen Thomas, M.D. Assistant Professor of Clinical Medicine at Keck School of Medicine of the University of Southern California (USC) and medical oncologist with USC’s Norris Comprehensive Cancer Center, is the first author. Anthony El-Khoueiry, M.D., Associate Director for Clinical Research and Chief of Section of Developmental Therapeutics/Phase I Program at USC Norris, is the senior and corresponding author.

The manuscript includes the following data results:

In heavily pretreated patients with advanced disease having over 20 different types of cancer who had progressed following multiple prior lines of therapy, intratumoral INT230-6 achieved:
A disease control rate of 75% (48/64 patients) and median overall survival (mOS) of 11.9 months; these results compare favorably in phase 1/2 studies that historically reported an mOS of 4 to 7 months
In a metastatic sarcoma subset population receiving only INT230-6, the median overall survival was 21.3 months

In an exploratory analysis comparing patients receiving INT230-6 at a total dose (in mL) that treated greater than 40% of the patient’s total tumour burden ("TTB") compared to those treated with less than 40% of their TTB, the:
Disease control rate was 83.3% (40/48) compared to 50% (8/16)
Median overall survival was 18.7 months (95% CI: 11.5–23.5) compared to 3.1 months (95% CI: 1.6–5.9) with a hazard ratio (HR) of 0.17 (95% CI: 0.081–0.342); P<0.0001 (see Figure 1 below)
Improved survival was consistent across a range of low to high tumor burden and tumor sizes

Approximately 20% of patients in the >40% group had uninjected tumors shrink, abscopal effects
Fifteen of 64 patients survived for more than 21 months
INT230-6 induced a qualitative decrease in proliferating cancer cells in injected tumors and a qualitative increase in activated T-cells infiltrating the tumor microenvironment
No dose-limiting toxicities were reported among 64 monotherapy patients; seven patients had a grade 3 (10.9%) with no grade 4 or 5 treatment-related adverse events
Pharmacokinetic results showed that greater than 95% of the active cytotoxic agents remained in the injected tumors
"INT230-6 is a local treatment that kills cancer using a diffusion process following direct injection into tumors. The trial demonstrated favorable safety and promising efficacy in patients with advanced metastatic cancers who had failed a median of three prior lines of therapy. The disease control rates and median survival compare favorably to those historically seen for such a diverse set of refractory cancer types in a phase 1/2 study," said Jacob S. Thomas, M.D. "There were also several learnings about INT230-6 dosing and safety gained during this trial. The pharmacokinetic data indicated that high rates of the drug are absorbed by the injected tumor, with minimal leakage, even at doses as high as 175 mL administered to a single tumor. These results are consistent with the low incidence of grade 3 adverse events observed."

"The mechanism by which cancer is killed through the diffusion of cytotoxic agents following intratumoral injection of INT230-6 and systemic immune activation, as observed in preclinical models, translated well in the human setting. Uninjected tumors shrinking from a locally administered therapy, referred to as abscopal effects, are generally rare for local therapies. Yet, an abscopal effect was observed in at least 20% of 48 patients who received drug volumes above 40% of their tumor burden. In addition, in thirteen of fourteen matched pair biopsy slides, a notable increase in activated CD4+ and CD8+ T cells was observed in the tumor microenvironment in response to INT230-6 treatment. Representative images can be found in the paper," said Anthony El-Khoueiry M.D. "The abscopal effects and immune cell infiltration observed in this study highlight this intratumoral therapy’s potential to drive both a local and systemic anti-cancer activity."

"This comprehensive paper is the culmination of over a decade of nonclinical and clinical research. The article describes the development of a new technology to destroy tumors using molecular agents that can disperse potent anti-cancer compounds within injected tumors and deliver them into cancer cells. We believe these are the first clinical results where a locally administered therapy used alone could potentially extend survival for patients with metastatic disease," said Lewis H. Bender, Founder, President, and CEO of Intensity Therapeutics, Inc. "As Drs. Thomas and El-Khoueiry noted, our paper reports that INT230-6 injected into visible tumors in metastatic patients at an amount based on the size of the injected tumors supports the hypothesis that INT230-6 causes immunologic cancer cell death, even in cancers that are considered immunologically cold. Given the drug’s mechanism of action and the data reported in this paper from over 20 types of metastatic solid cancers, such as breast, sarcoma, pancreatic, lung, and head and neck, we believe the study results show the potential of INT230-6 to achieve clinical benefit for metastatic patients of multiple cancer types with or without the use of radiation, systemic drugs or immunotherapy. As a result, we have initiated randomized controlled studies, including a Phase 3 study in sarcoma (NCT06263231)."

The Company will be hosting a conference call featuring two key authors of the study on Friday, October 31, 2025 at 9:00AM ET to discuss the results. Interested parties can access the call by clicking here: View Source Participants are encouraged to log on at least 10 minutes prior to the start of the event.

About INT230-6
INT230-6, Intensity’s lead proprietary investigational product candidate, is designed for direct intratumoral injection. INT230-6 was discovered using Intensity’s proprietary DfuseRx℠ technology platform. The drug consists of two proven, potent anti-cancer agents, cisplatin and vinblastine sulfate, and a diffusion and cell penetration enhancer molecule ("SHAO") that non-covalently conjugates to the two payload drugs, facilitating the dispersion of potent cytotoxic drugs throughout tumors and allowing the active agents to diffuse into cancer cells. These agents remain in the tumor, resulting in a favorable safety profile. In addition to local disease control and direct tumor killing, INT230-6 causes a release of a bolus of neoantigens specific to the malignancy, leading to immune system engagement and systemic anti-tumor effects. Importantly, these effects are mediated without immunosuppression, which often occurs with systemic chemotherapy.

(Press release, Intensity Therapeutics, OCT 30, 2025, View Source [SID1234657177])

About Study Intensity’s Clinical Study IT-01
IT-01 was Intensity’s first-in-human, open-label, single-arm phase 1/2 study (NCT03058289) using INT230-6. The study was conducted in patients with advanced, refractory, or metastatic solid tumors at six clinical sites in addition to USC. Other investigators were from Johns Hopkins University, Princess Margaret Hospital in Toronto, Columbia Presbyterian in New York, The Fox Chase Cancer Center in Philadelphia, Houston Methodist, and UMass Memorial. The study was comprised of adults with histologically or cytologically confirmed advanced or metastatic solid tumors who did not respond to or were not candidates for standard therapies and had accessible superficial and/or deep tumors for injection. Dose escalation was achieved by increasing the initial and subsequent total dose volumes (total injected amount), the maximum injected volume per any single tumor, the ratio of drug-volume to tumor-size, the number of injected tumors per session, and the dose frequency (once per month vs. every 2 weeks). Maintenance dosing was added in protocol amendments. A tumor’s dose was set as a percentage of the volume of the target tumor, which was calculated from radiologic measurements. There were six monotherapy dose cohorts.

On October 30, 2025 ChemDiv, a global provider of integrated drug discovery solutions, reported kinase inhibitor design enhancements to its discovery platform. The new capabilities strengthen support for partners developing reversible pan‑EGFR inhibitors for EGFR‑mutant NSCLC (non‑small cell lung cancer). This upgrade integrates AI‑guided chem‑bio design, kinome‑wide selectivity modeling, and parallel synthesis to deliver candidates with broad coverage across driver and on‑treatment resistance mutations while minimizing inhibition of wild‑type (WT) EGFR—a profile aimed at improving therapeutic window, safety, and tolerability.

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As a result of these upgrades, a partner collaboration has progressed from late lead‑optimization into process route scouting and multi‑gram scale‑up, with early CMC (solid‑form assessment, analytical method development, and pre‑formulation) now underway.

"Wild‑type sparing is the needle to thread in next‑generation EGFR therapy," said Ilya Baimetov, COO/CTO at ChemDiv. "Our platform brings together structure‑enabled, reversible chemistry space exploration and kinome selectivity risk‑mitigation to help partners design pan‑EGFR molecules that hit the right mutants—and leave WT EGFR largely alone—so the safety margin moves in the right direction."

What’s new in ChemDiv’s pan‑EGFR support

Mutant‑centric design loops: AI/ML and physics‑based engines prioritize potency against classical and resistance mutations while penalizing WT EGFR liabilities. Integrated ADME/DMPK prediction balances potency with exposure and brain/lung distribution targets as defined by program strategy.

Reversible chemistry toolkits: Focused make‑on‑demand libraries and scaffold families for non‑covalent EGFR binding—engineered for tunable residence time, metabolic stability, and efflux navigation.

Kinome‑wide selectivity modeling: Early off‑target risk scoring against a broad kinase panel to drive SAR decisions toward cleaner profiles that support tolerability and combination potential.

Rapid synthesis + learn cycles: Parallel synthesis and micro‑scale PK accelerate SAR hypotheses; "success criteria" dashboards track mutant coverage, WT‑sparing index, and developability in each sprint.

CMC‑aware discovery: Route‑scouting heuristics, green‑chemistry flags, and salt/solid‑form optionality are considered during hit‑to‑lead to de‑risk later manufacturing.
"By aligning mutant coverage, selectivity index, and developability from day one, we’re seeing cleaner, faster paths into scale‑up and CMC." said Roman Timakhov, Research Director at ChemDiv.

Collaboration progress toward scale‑up and CMC

Following demonstration of a differentiated reversible pan‑EGFR profile in lead series (broad mutant activity with WT sparing in cellular assays; favorable PK in preclinical models), ChemDiv and its partner have initiated:

Multi‑gram scale‑up with route scouting and solvent/impurity risk assessment;

Solid‑form and salt screening to support stability and formulation flexibility;

Phase‑appropriate analytical methods (purity, potency, related substances); and

Pre‑formulation to enable non‑GLP and GLP toxicology material supply.
These activities are designed to support pre‑IND readiness while maintaining optionality for combination studies.

(Press release, ChemDiv, OCT 30, 2025, View Source [SID1234657176])

On October 30, 2025 Pilatus Biosciences, a biopharmaceutical company developing novel metabolic checkpoint immunotherapies for liver and gastrointestinal cancers, reported the Company will present new preclinical data on its lead product candidate, PLT012, in a poster presentation at the upcoming Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) 2025 Annual Meeting, being held November 5-9, 2025 in National Harbor, Maryland.

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"Immunometabolism is a key lever for overcoming resistance in solid tumors," said Dr. Yi-Ru Yu, Lead Scientist at Pilatus Biosciences and presenting author. "Our preclinical results demonstrate that PLT012, a first-in-class anti-CD36 monoclonal antibody, exerts a dual mechanism of action by reprogramming immune-metabolic pathways—suppressing immunosuppressive Tregs while enhancing CD8⁺ T-cell responses in lipid-rich tumors. These combined effects have been shown to drive durable and superior anti-tumor efficacy across multiple cancer models, outperforming anti–PD-1/PD-L1 blockade and inducing long-lasting immune memory that sustains tumor control and protects against rechallenge." Dr. Raven Lin, CEO of Pilatus Biosciences, added "Alongside a favorable GLP toxicology profile, these data support our planned Phase I study, with first patient in (FPI) targeted for Q1 2026."

Details of the SITC (Free SITC Whitepaper) poster presentation are as follows:

Abstract Title: PLT012, a Humanized CD36-Blocking Antibody, Induces Durable Anti-Tumor Immunity via Immunometabolic Reprogrammig
Presenting Author: Yi-Ru Yu, Ph.D., Lead Scientist, Pilatus Biosciences
Date: Friday, November 7, 2025
Time: 12:15 p.m. – 1:45 p.m. EST
Poster Number: 1205

The abstract for this presentation will be available on SITC (Free SITC Whitepaper)’s website on November 4, 2025, and the poster presentation will be available on Pilatus’ website following the meeting.

About PLT012

PLT012 is a humanized monoclonal antibody designed to selectively block CD36-mediated lipid uptake, a key mechanism driving immunosuppression and immune exclusion within the tumor microenvironment. By targeting lipid metabolism, PLT012 exerts a unique mechanism of action: it depletes immunosuppressive cell populations, including Tregs and pro-tumor macrophages, while simultaneously enhancing anti-tumor activities of intratumoral NK cell and cytotoxic CD8+ T cell that are otherwise susceptible to lipid-induced exhaustion. In preclinical studies, PLT012 has demonstrated potent monotherapy efficacy in models of liver malignancies, with a favorable safety profile across species. Leveraging its distinct mechanism of action, PLT012 further acts as a potent sensitizer in combination with anti–PD-L1 therapies, effectively overcoming drug resistance in immune "cold" tumors and liver metastases.

(Press release, Pilatus Biosciences, OCT 30, 2025, View Source [SID1234657175])