On September 25, 2026 MiraDx, a molecular diagnostics company focused on genetic testing to personalize cancer treatment, reported that research supporting its PROSTOX technology and the role of germline biomarkers in predicting treatment-related adverse events and response will be featured in five presentations and educational sessions at the 2026 American Society for Radiation Oncology (ASTRO) Annual Meeting, taking place September 26-30, 2026, in Boston, Mass.

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The presentations reflect a growing body of evidence about the genetic underpinnings of differences in radiation sensitivity and how they can help physicians identify patients at greater risk of late-onset adverse events as well as treatment responses. This knowledge could support more personalized treatment choices.

A key highlight will be new data presented by Amar Kishan, MD, Professor and Executive Vice Chair for the Department of Radiation Oncology at the David Geffen School of Medicine at UCLA and UCLA Jonsson Comprehensive Cancer Center, and Chair of the American Society for Radiation Oncology (ASTRO) Prostate/GU Resource Panel. These findings, drawn from a cohort of multiple prospective clinical trials including the landmark PACE-B trial, validate the germline biomarker used in MiraDx’s PROSTOX tests to predict late genitourinary (GU) adverse events in a fractionation-specific manner following radiotherapy for localized prostate cancer. A mediation analysis performed on a prospective clinical utility study showed that use of the PROSTOX tests resulted in an absolute 17.5% reduction in 2+ late GU adverse events.

Additional research presented by Joanne Weidhaas, MD, PhD, Professor of Radiation Oncology and Vice Chair of Molecular and Cellular Oncology at the David Geffen School of Medicine at UCLA and co-founder of MiraDx, demonstrates the ability of MiraDx’s PROSTOX test to predict late GU adverse events following stereotactic body radiation therapy (SBRT) to the prostate fossa after radical prostatectomy. Her research also describes the role of microRNA (miRNA) variations identified by PROSTOX testing in the regulation of global messenger RNA (mRNA) and miRNA expression patterns across key cellular pathways.

Beyond prostate cancer, Weidhaas will present research examining genetic signatures associated with adverse events and overall survival in patients with head and neck squamous cell carcinoma receiving radiation therapy and cisplatin chemotherapy. She is also participating in an educational session and presenting on germline miRNA signatures and their role in predicting radiation treatment toxicity.

"As cancer treatment becomes more targeted and complex, we need predictive tools based on an individual’s personal genetics to identify optimal treatment pathways, including those predicting who is at increased risk for treatment-related adverse events," said Dr. Weidhaas. "Our genetics can help determine how susceptible we are to these side effects. Understanding not only which genetic biomarkers contribute to that risk, but also how those biomarkers impact gene expression and biological processes gives insights into why patients receiving the same treatment can experience very different outcomes."

ASTRO 2026 Presentations

EDU 08 – Biomarkers to Predict Radiation Treatment Toxicity
Title: Germline microRNA-Based Signatures to Predict Radiation Treatment Toxicity
Presenter: Joanne Weidhaas, MD, PhD
Date/Time: September 27, 2026, 5:17-5:32 p.m. ET
Location: Room 156

PQA 03 – Digital Health Innovation and Informatics, Patient Safety & Quality, and Radiation and Cancer Biology
Title: mRNA and miRNA Expression Differences Between High- and Low-Risk PROSTOX Patients
Presenter: Joanne Weidhaas, MD, PhD
Date/Time: September 28, 2026, 10:45 a.m.-12:00 p.m. ET
Location: Poster Hall – Exhibit Hall A, Screen 4

SS 36 – Predicting Benefit and Toxicity: Biomarkers in Prostate Radiotherapy
Title: Germline Biomarker for Late Genitourinary Adverse Events after Radiotherapy for Prostate Cancer: Validation in Multiple Prospective Trials
Presenter: Amar Kishan, MD
Date/Time: September 29, 2026, 5:45 p.m. ET
Location: Room 210

QP 28 – Actionable Biomarkers: Guiding Therapy Selection and Deescalation
Title: Germline Biomarker Predicts Adverse Events Following SBRT to the Prostate Fossa After Radical Prostatectomy
Presenter: Joanne Weidhaas, MD, PhD
Date/Time: September 29, 2026, 5:40-5:45 p.m. ET
Location: Room 205

QP 40 – Personalized Therapy and Special Populations in Head and Neck Cancer
Title: Genetic Signatures Predicting Toxicity and Overall Survival in Head and Neck Squamous Cell Carcinoma
Presenter: Joanne Weidhaas, MD, PhD
Date/Time: September 30, 2026, 9:20-9:25 a.m. ET
Location: Room 156

Meet the Investigators

Amar Kishan, MD, Professor and Executive Vice Chair for the Department of Radiation Oncology at the David Geffen School of Medicine at UCLA and UCLA Jonsson Comprehensive Cancer Center, and Chair of the American Society for Radiation Oncology (ASTRO) Prostate/GU Resource Panel, will present research validating a germline biomarker for late GU adverse events following prostate cancer radiotherapy.

Joanne Weidhaas, MD, PhD, Professor of Radiation Oncology and Vice Chair of Molecular and Cellular Oncology at the David Geffen School of Medicine at UCLA and co-founder of MiraDx, will present four studies focused on miRNA-based genetic predictors of radiation outcomes.

(Press release, MiraDx, SEP 25, 2026, View Source [SID1234671096])

On September 25, 2026 IASO Biotechnology ("IASO Bio"), a commercial-stage biopharmaceutical company focused on the discovery, development, manufacturing, and commercialization of novel cell therapies and biologics for hematologic malignancies and autoimmune diseases reported that results from a retrospective analysis of FUMANBA-1 — the pivotal registration study of its world’s first fully human BCMA-targeting CAR-T cell therapy product, FUCASO (equecabtagene autoleucel injection, Eque-cel) — were presented as a poster at the 2026 International Myeloma Society (IMS) Annual Meeting[1] (Abstract No.: PA-469). The results showed that durable persistence of FUCASO CAR-T cells in patients (assessed by vector copy number [VCN] in peripheral blood) was associated with sustained minimal residual disease (MRD) negativity and prolonged time to progression (TTP); moreover, patients with del(17p), high tumor burden, and rapidly progressive disease features were more prone to early CAR-T cell clearance and MRD conversion.

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Study Design: A Retrospective Analysis Focused on "MRD Conversion"

Clinical follow-up data have shown that FUCASO can induce deep MRD negativity in patients with relapsed/refractory multiple myeloma (R/R MM), but some patients experience MRD conversion after achieving MRD negativity. To explore the potential mechanisms underlying MRD conversion and to provide hypothesis-generating evidence for optimizing full-course management following CAR-T cell infusion, this retrospective analysis enrolled 102 patients from the FUMANBA-1 study who had achieved MRD negativity. Based on whether MRD conversion occurred during follow-up, patients were divided into a sustained MRD-negative group (n=61) and an MRD-conversion group (n=41), and baseline characteristics as well as peripheral blood vector copy number (VCN) persistence (with the event defined as peripheral blood VCN below the lower limit of detection) were analyzed for both groups. VCN persistence was assessed using the Kaplan-Meier method and unadjusted Cox regression; the hierarchical correlations among time to progression (TTP), duration of MRD negativity, and VCN persistence were assessed using Kendall’s tau-b coefficient. All analyses were hypothesis-generating in nature.

Patients with MRD Conversion Had Higher-Risk Baseline Features and Shorter VCN Persistence

The analysis showed that patients who experienced MRD conversion presented with higher-risk, more rapidly progressive baseline disease characteristics: a higher proportion with del(17p) (26.8% vs 13.1%), a higher proportion of patients with bone marrow plasma cells ≥50% (26.8% vs 11.5%), a shorter median interval from diagnosis to enrollment (31.1 months vs 54.0 months), and a higher proportion receiving bridging therapy (61.0% vs 41.0%). Regarding VCN persistence, median VCN persistence was 272 days in the MRD-conversion group versus 463 days in the sustained MRD-negative group, a difference of approximately 191 days (HR 0.73, 95% CI 0.42–1.26, P=0.2568). Although the sustained MRD-negative group showed a numerical VCN persistence advantage of approximately 191 days, this difference is not sufficient to draw a statistically significant conclusion given the statistical power of the current data.

Correlation analyses revealed a consistent benefit chain of "VCN persistence — sustained MRD negativity — delayed progression": time to progression (TTP) was strongly correlated with duration of MRD negativity (tau-b=0.736, P<0.0001); time to progression (TTP) was moderately correlated with VCN persistence (tau-b=0.306, P<0.0001); and VCN persistence was correlated with duration of MRD negativity (tau-b=0.185, P=0.006).

Conclusion

This analysis suggests that more durable in vivo persistence of FUCASO CAR-T cells is associated with sustained MRD negativity and prolonged time to progression (TTP), supporting peripheral blood VCN persistence as a candidate pharmacodynamic (PD) marker of durable disease control; patients with del(17p), high tumor burden, and rapidly progressive disease are more prone to early CAR-T cell clearance and MRD conversion. These findings are hypothesis-generating in nature and may inform strategies to prolong CAR-T cell persistence as well as the use of CAR-T therapy in earlier lines of treatment.

Professor Lugui Qiu

Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences

"We are very pleased to report this follow-up analysis of FUMANBA-1 focusing on MRD conversion at this year’s IMS Annual Meeting, and the results are encouraging. MRD negativity is an important hallmark of deep response, yet some advanced patients still experience MRD conversion after achieving MRD negativity — an issue of long-standing clinical focus. This analysis suggests that durable in vivo persistence of CAR-T cells may be one of the key factors in maintaining long-term MRD negativity and delaying disease progression; patients with high-risk cytogenetic features and high tumor burden are more prone to early CAR-T cell clearance and MRD conversion. These hypothesis-generating findings point the way for research into strategies to prolong cell persistence, and also support clinical exploration of the value of CAR-T therapy at earlier stages of disease."

(Press release, IASO Biotherapeutics, SEP 25, 2026, View Source;updated-fumanba-1-analysis-of-iaso-bios-fucaso-reveals-that-in-vivo-durable-persistence-of-car-t-cells-is-associated-with-sustained-mrd-negativity-and-delayed-disease-progression-302890352.html [SID1234671095])

On September 25, 2026 Nutshell Therapeutics (Shanghai) Co., Ltd. ("Nutshell Therapeutics"), an innovative biotech company focused on AI-driven allosteric drug discovery, reported FDA IND clearance for NTS231, a covalent allosteric molecular glue degrader of NRF2, to launch clinical development in the United States.

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NTS231 is the first NRF2 degrader molecule from China and second globally to enter clinical development. This program represents a significant advancement in efforts to therapeutically target the NRF2 pathway, a key driver of tumor survival and treatment resistance in multiple cancer types.

AI-Driven Discovery of a Novel NRF2-Targeting Molecular Glue

The discovery of NTS231 was powered by Nutshell Therapeutics’ proprietary AI-driven allosteric drug discovery platform, ALLOSTAR, which integrates computer-aided drug design (CADD), medicinal chemistry and cutting-edge experimental techniques.

By leveraging the ALLOSTAR platform, Nutshell Therapeutics successfully identified NTS231 as a highly potent and selective novel small molecule that covalently binds to KEAP1 and induces the degradation of NRF2. Mechanistically, NTS231 irreversibly links to the Cys151 residue of KEAP1 and stabilizes the KEAP1 structural conformation conducive to CUL3 interaction as well as the assembly of functional KEAP1–CUL3 E3-ligase complex, thereby driving NRF2 degradation, suppressing NRF2 signaling pathway, and inhibiting cancer cell viability. The team accomplished IND approval within 24 months from target nomination, highlighting AI-enabled acceleration of drug discovery.

Robust Preclinical Antitumor Activity and Desirable Safety Profile

In preclinical studies, NTS231 exhibits non-inferior in vitro activities to VVD-130037[1], a clinical-stage compound under the same targeting mechanism, while possessing superior pharmacokinetic properties. Across multiple cell-derived xenograft (CDX) and patient-derived xenograft (PDX) models harboring diverse NRF2/KEAP1/CUL3 mutations or NRF2 hyperactivation, NTS231 has demonstrated dose-dependent antitumor efficacy as a single agent in a range of solid tumors, including lung squamous cell carcinoma (LUSC), lung adenocarcinoma (LUAD), esophageal squamous cell carcinoma (ESCC), and head and neck squamous cell carcinoma (HNSCC).

NTS231 has also demonstrated the potential for combination therapies. Synergistic antitumor effects were observed when combining NTS231 with chemotherapy, targeted therapies, and antibody-drug conjugates (ADCs). Notably, in chemotherapy-resistant LUSC PDX models harboring KEAP1 and other mutations, the combination of NTS231 and paclitaxel significantly enhanced tumor growth inhibition relative to single agents; in a proof-of-concept CDX model of NFE2L2-amplified LUAD, combined treatment with NTS231 and a TROP2 ADC dramatically improved efficacy and led to tumor regression, accompanied by decreased expression of NRF2-regulated efflux transporters, which might sensitize tumors to ADC payloads and mitigate resistance.

In the 28-day Good Laboratory Practice (GLP) toxicology studies conducted in rats and dogs, NTS231 demonstrated a favorable safety profile and a wide safety margin. These findings provide important preclinical support for the continued clinical development of NTS231.

Targeting a Significant Unmet Need in NRF2-Driven Cancers

Constitutive activation of NRF2 has been observed in many human cancers as a result of genetic alterations in the NRF2-encoding gene NFE2L2 and its regulatory genes KEAP1 and CUL3. Approximately 12% of cancer patients profiled in The Cancer Genome Atlas (TCGA) database carry mutations in at least one of the three genes NFE2L2, KEAP1 or CUL3, particularly prevalent in >30% LUSC and >20% LUAD. Preliminary estimates indicate over 1.5 million annual new cancer cases worldwide harbor NRF2/KEAP1/CUL3 alterations or other aberrant NRF2 pathway activation.[2]

This patient population is largely ineligible for most targeted therapies, given that NRF2/KEAP1/CUL3 alterations are mutually exclusive with EGFR, ALK, ROS1, and BRAF genetic lesions. Immunotherapy likewise yields limited efficacy, since such mutations are strongly associated with an immunologically cold tumor microenvironment (TME) that leads to therapeutic resistance. Constant activation of the NRF2 pathway resulting from mutations in NRF2, KEAP1 or CUL3 can also confer resistance to standard chemotherapy. Collectively, these factors underscore the substantial unmet medical need for effective therapies targeting NRF2-driven tumor biology.

By directly targeting the KEAP1–NRF2 regulatory axis, NTS231 has the potential to provide a new therapeutic approach for patients with NRF2, KEAP1, or CUL3 mutations, as well as tumors characterized by NRF2 pathway hyperactivation.

(Press release, Nutshell Therapeutics, SEP 25, 2026, View Source [SID1234671094])

On September 25, 2026 Daiichi Sankyo (TSE: 4568) and Merck’s (NYSE: MRK), known as MSD outside of the United States and Canada reported that the Biologics License Application (BLA) seeking accelerated approval in the U.S. for ifinatamab deruxtecan (I-DXd) for the treatment of adult patients with extensive-stage small cell lung cancer (ES-SCLC) with disease progression on or after platinum-based chemotherapy has been voluntarily withdrawn.

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The decision to withdraw the BLA is based on discussions with the U.S. Food and Drug Administration (FDA) that data supporting the application, including from the IDeate-Lung01 Phase 2 trial, do not satisfy requirements needed to support an accelerated approval for the proposed indication.

Patient enrollment continues in the IDeate-Lung02 Phase 3 trial evaluating the efficacy and safety of ifinatamab deruxtecan versus treatment of physician’s choice of chemotherapy (amrubicin, lurbinectedin or topotecan) in patients with relapsed ES-SCLC following disease progression with only one prior line of platinum-based chemotherapy.

"Extensive-stage small cell lung cancer is a challenging disease to treat, leaving patients in need of new options," said Abderrahmane Laadem, MD, head, therapeutic area oncology development, Daiichi Sankyo. "Enrollment into the IDeate-Lung02 Phase 3 trial is near completion and we look forward to assessing the potential for a future filing of ifinatamab deruxtecan with the FDA and other global regulatory authorities based on those results."

"While we are disappointed that the current dataset are not supportive of an approval at this time, we are continuing to evaluate the role of ifinatamab deruxtecan in patients with extensive-stage small cell lung cancer and other types of difficult-to-treat cancer," said Marjorie Green, MD, senior vice president and head of oncology, global clinical development, Merck Research Laboratories. "We would like to thank the patients, their families and investigators who have participated or continue to participate in these studies."

In addition to the IDeate-Lung02 Phase 3 trial, there are two additional Phase 3 trials underway with ifinatamab deruxtecan in advanced/metastatic disease, including IDeate-Prostate01 for castration-resistant prostate cancer (CRPC) and IDeate-Esophageal01 for esophageal squamous cell carcinoma (ESCC).

About ifinatamab deruxtecan
Ifinatamab deruxtecan is an investigational potential first-in-class B7-H3 directed ADC. Designed using Daiichi Sankyo’s proprietary DXd ADC Technology, ifinatamab deruxtecan is comprised of a humanized anti-B7-H3 IgG1 monoclonal antibody attached to a number of topoisomerase I inhibitor payloads (an exatecan derivative, DXd) via tetrapeptide-based cleavable linkers.

Ifinatamab deruxtecan has been granted orphan drug designation (ODD) by the U.S. FDA, European Commission, Japan Ministry of Health, Labor and Welfare and Taiwan Food and Drug Administration for the treatment of SCLC. Ifinatamab deruxtecan also was granted ODD for the treatment of esophageal cancer by the FDA.

A comprehensive global clinical development program is underway evaluating the efficacy and safety of ifinatamab deruxtecan monotherapy and in combination with other cancer medicines across multiple cancers. The program is currently comprised of three Phase 3 trials in advanced/metastatic disease, including SCLC (IDeate-Lung02), CRPC (IDeate-Prostate01) and ESCC (IDeate-Esophageal01).

About IDeate-Lung01
IDeate-Lung01 (ClinicalTrials.gov, NCT05280470) is a Phase 2 global, multicenter, randomized, open-label, two-part trial evaluating the safety and efficacy of ifinatamab deruxtecan in patients with ES-SCLC who were previously treated with at least one prior line of platinum-based chemotherapy and a maximum of three prior lines of therapy. IDeate-Lung01 enrolled 187 patients in Asia, Europe and North America. Patients with asymptomatic brain metastases (untreated or previously treated) were eligible to participate. Patients with a history of ILD/pneumonitis requiring treatment with steroids or current ILD/pneumonitis at screening, clinically severe pulmonary compromise resulting from intercurrent pulmonary illnesses, were not eligible.

In the first part of the trial (dose optimization), patients were randomized 1:1 to receive ifinatamab deruxtecan (8 or 12 mg/kg) given intravenously once every three weeks. In the second part of the trial (dose expansion), patients received ifinatamab deruxtecan (12 mg/kg) intravenously at the same dosing interval.

The primary endpoint is objective response rate (ORR) as assessed by blinded independent central review (BICR) per RECIST v1.1. Secondary endpoints include duration of response, progression-free survival, disease control rate, time to response, overall survival, pharmacokinetics and safety. Intracranial ORR was assessed by BICR as an exploratory analysis.

About small cell lung cancer
Approximately 250,000 patients are diagnosed with small cell lung cancer (SCLC) each year globally. There were approximately 27,000 new cases of SCLC in the U.S. in 2025, accounting for about 12% of all lung cancer cases. SCLC is aggressive and progresses rapidly to the distant metastatic stage, which has a low five-year survival rate. While conventional standard of care treatments for patients with advanced SCLC may help improve outcomes, there is a need for additional subsequent treatment approaches

About B7-H3
B7-H3 is a transmembrane protein that belongs to the B7 family of proteins, which bind to the CD28 family of receptors that includes PD-1. B7-H3 is highly expressed in a wide range of cancer types, including SCLC, and its overexpression has been shown to correlate with poor prognosis, making B7-H3 a promising therapeutic target. There are currently no B7-H3 directed medicines approved for the treatment of cancer.

(Press release, Merck & Co, SEP 25, 2026, View Source [SID1234671093])

On September 25, 2026 SELLAS Life Sciences Group, Inc. (NASDAQ: SLS) ("SELLAS’’ or the "Company"), a late-stage clinical biopharmaceutical company focused on the development of novel therapies for a broad range of cancer indications, reported preclinical data from studies evaluating SLS009 (tambiciclib), its highly selective cyclin-dependent kinases 9 (CDK9) inhibitor, in patient-derived organoid models of pancreatic ductal adenocarcinoma (PDAC). The data are being presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Conference on Pancreatic Cancer: New Frontiers in Biology and Therapeutic Development, being held September 25–28, 2026, in San Diego. The timing of this announcement reflects AACR (Free AACR Whitepaper)’s embargo policy, under which the data presented at the conference were restricted from publication until 1:00 p.m. ET today.

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The studies, conducted in collaboration with researchers at the University of Wisconsin–Madison, evaluated SLS009 in MYC-amplified PDAC models, including a model resistant to the recently approved RAS inhibitor daraxonrasib (RMC-6236), as well as in combination with the BET inhibitor ZEN3694. MYC amplification is a biologically recognized mechanism of RAS targeting resistance.

"These findings provide encouraging preclinical evidence that CDK9 inhibition may enhance the activity of RAS-directed therapy in pancreatic cancer, including in the setting of MYC-associated resistance," said Dragan Cicic, MD, Senior Vice President, Clinical Development of SELLAS. "In a daraxonrasib-resistant patient-derived model, SLS009 demonstrated substantially greater activity than daraxonrasib alone and further increased apoptosis and necrosis when the two agents were combined. Together with the synergistic activity observed with BET inhibition, these data support a broader strategy of using SLS009 to disrupt transcriptional programs that may contribute to resistance to RAS-targeted therapies and provide a strong rationale for further evaluation in pancreatic cancer patients."

In a MYC-amplified, daraxonrasib-resistant patient-derived PDAC organoid model, SLS009 at 200 nM, daraxonrasib at 100 nM, and the combination of both agents were evaluated. Daraxonrasib was administered continuously, while SLS009 was removed after 24 hours to approximate its in vivo pharmacokinetic profile, with apoptosis and necrosis assessed at 72 hours.

A separate MYC-amplified patient-derived PDAC organoid model evaluated SLS009 in combination with the BET inhibitor ZEN3694. The combination demonstrated synergistic activity, including increased cancer cell death and sustained suppression of MYC transcription. Notably, these effects were observed at a ZEN3694 concentration substantially below reported physiologically achievable exposure levels.

Key findings:

SLS009 demonstrated substantially greater single-agent activity than daraxonrasib in the daraxonrasib-resistant model, inducing 17.9% apoptosis versus 2.8% with daraxonrasib and 14.5% necrosis versus 2.7%.
The combination of SLS009 and daraxonrasib further increased cancer cell death, inducing 36.5% apoptosis and 30.6% necrosis, compared with 17.9% and 14.5%, respectively, with SLS009 alone and 2.8% and 2.7%, respectively, with daraxonrasib monotherapy.
SLS009 combined with ZEN3694 demonstrated synergistic activity, producing greater apoptosis and necrosis than either agent alone.
The SLS009/ZEN3694 combination produced sustained suppression of MYC RNA and reduced expression of MYC and MCL-1 proteins, consistent with disruption of transcriptional pathways supporting tumor cell survival.

Together, the findings support further investigation of CDK9 inhibition as a strategy to enhance RAS-directed therapy and potentially address MYC-associated resistance in pancreatic cancer. The BET combination data provide additional mechanistic support for SLS009-based approaches designed to disrupt MYC-dependent transcriptional programs and suggest the potential to enhance BET inhibition at lower drug exposures.

"MYC is a particularly challenging oncogenic driver because it has historically been difficult to target directly," said Jeremy D. Kratz, MD, Assistant Professor of Medicine and Principal Investigator at the University of Wisconsin–Madison. "Across these studies, CDK9 inhibition produced substantial activity in MYC-amplified pancreatic cancer models through two distinct therapeutic strategies. The activity of SLS009 supports its activity in a model with de novo daraxonrasib-resistance and together with the synergistic transcriptional suppression observed with BET inhibition, provides a strong rationale for further investigation of SLS009-based combinations in molecularly defined subsets of pancreatic cancer."

Poster presentation details:

Title: Elucidating MYC allelic imbalance and therapeutic response in pancreatic ductal adenocarcinoma via patient-derived organoids
Authors: Sawyer AG, Flannagan LE, Esguerra PN, Hossan MS, Kratz JD
Poster Number: A036 – September 27, 2026: 5-7pm PST

Title: Synthetic Lethality Through Combined BET and CDK9 Inhibition in MYC-Amplified Pancreatic Ductal Adenocarcinoma
Authors: Esguerra PN, Cadarso M, Livingwell S, Hossan MD, Wong O, Kratz JD
Poster Number: B127 – September 27, 2026: 5-7pm PST

Title: Targeting dual CDK9 and KRASG12D selective inhibition as a novel combination therapy in pancreatic ductal adenocarcinoma
Authors: Cadarso M, Esguerra P, Flannagan L, Hossan MS, Kratz JD
Poster Number: B043 – September 27, 2026: 5-7pm PST

The posters will be available on SELLAS’ website following the conference.

(Press release, Sellas Life Sciences, SEP 25, 2026, View Source [SID1234671092])