On April 19, 2026 Immunocore Holdings plc (Nasdaq: IMCR) ("Immunocore" or the "Company"), a commercial-stage biotechnology company pioneering and delivering transformative immunomodulating medicines to radically improve outcomes for patients with cancer, infectious diseases and autoimmune diseases, reported that KIMMTRAK (tebentafusp-tebn) five-year overall survival (OS) was presented in an oral session at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) 2026 meeting.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

This is the longest, prospective Phase 3 randomized trial in patients with unresectable or metastatic uveal melanoma (mUM) – a disease with a very poor prognosis and a historical survival rate of <5% at 5 years1. KIMMTRAK doubled the likelihood of being alive at five years, with an OS for KIMMTRAK of 16% versus 8% in the control arm (hazard ratio [HR] of 0.67 [95% CI: 0.54-0.85]). These results also represent the longest follow-up reported for any T cell engager in a solid tumor.

In the trial, 378 patients were randomized to tebentafusp (252) or investigator’s choice (126; 82% pembrolizumab). The median OS was 21.6 months on KIMMTRAK, versus 16.9 months on investigator’s choice (IC). The Kaplan–Meier survival curves separated early and remained separated over time, confirming the durability of the benefit with extended follow-up.

"These important results allow us, for the first time, to speak with real confidence to patients about the possibility of long-term survival," said Professor Paul Nathan, Consultant Medical Oncologist, Mount Vernon Cancer Centre, UK. "Before tebentafusp, such conversations simply weren’t possible for metastatic uveal melanoma patients."

"These long-term overall survival results further solidify KIMMTRAK as the first-line standard of care for HLA-A*02:01 positive patients with metastatic uveal melanoma," said Mohammed Dar, Immunocore Chief Medical Officer. "The survival benefit was evident even in patients with known poor prognostic factors, including those with large tumors and extrahepatic disease."

The data confirmed that the OS benefit was primarily driven by tebentafusp rather than subsequent therapies. Among patients treated with KIMMTRAK who were alive at five years, nearly half (44%) received only KIMMTRAK, while among patients in the control arm alive at the same time point, 86% subsequently received tebentafusp.

Importantly, the OS benefit with KIMMTRAK was observed regardless of known poor prognostic factors at baseline (high tumor burden [≥10cm]; elevated lactate dehydrogenase [LDH]) or tumor location (hepatic only; hepatic and extra-hepatic). OS benefit was also observed in patients with a best response of progressive disease, including those with >20% tumor growth as best change on treatment.

More patients continued treatment beyond progression in the KIMMTRAK arm than in the control arm (57% vs 25%) – with the trial allowing this option in both arms. Patients on KIMMTRAK achieved nearly a 7-fold higher rate of tumor reduction with treatment beyond initial progression compared to IC patients (27% vs 4%). In fact, patients who continued tebentafusp treatment beyond tumor progression experienced longer post-progression survival compared to those who stopped treatment, even after accounting for variations in patient characteristics.

In tebentafusp-treated patients, longer OS was associated with undetectable ctDNA at baseline or ctDNA reductions ≥50% by week 9. Among 21 ctDNA-evaluable patients who survived ≥ 5 years, 71% had undetectable baseline ctDNA and 29% had ctDNA clearance by week 9. Deep reductions in ctDNA were seen across all RECIST categories. Early ctDNA molecular response continues to be a more sensitive marker of tebentafusp activity than radiographic measurements.

The data were presented today in an oral session during the AACR (Free AACR Whitepaper) 2026 meeting:

Title: Five-year survival with tebentafusp in previously untreated metastatic uveal melanoma in a Phase 3 trial (CT029)
Presenting author: Paul Nathan
Session: Advanced Cellular and Immune-Based Therapeutics

(Press release, Immunocore, APR 19, 2026, View Source [SID1234664542])

On April 19, 2026 Immunocore Holdings plc (Nasdaq: IMCR) ("Immunocore" or the "Company"), a commercial-stage biotechnology company pioneering and delivering transformative immunomodulating medicines to radically improve outcomes for patients with cancer, infectious diseases and autoimmune diseases, reported that KIMMTRAK (tebentafusp-tebn) five-year overall survival (OS) was presented in an oral session at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) 2026 meeting.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

This is the longest, prospective Phase 3 randomized trial in patients with unresectable or metastatic uveal melanoma (mUM) – a disease with a very poor prognosis and a historical survival rate of <5% at 5 years1. KIMMTRAK doubled the likelihood of being alive at five years, with an OS for KIMMTRAK of 16% versus 8% in the control arm (hazard ratio [HR] of 0.67 [95% CI: 0.54-0.85]). These results also represent the longest follow-up reported for any T cell engager in a solid tumor.

In the trial, 378 patients were randomized to tebentafusp (252) or investigator’s choice (126; 82% pembrolizumab). The median OS was 21.6 months on KIMMTRAK, versus 16.9 months on investigator’s choice (IC). The Kaplan–Meier survival curves separated early and remained separated over time, confirming the durability of the benefit with extended follow-up.

"These important results allow us, for the first time, to speak with real confidence to patients about the possibility of long-term survival," said Professor Paul Nathan, Consultant Medical Oncologist, Mount Vernon Cancer Centre, UK. "Before tebentafusp, such conversations simply weren’t possible for metastatic uveal melanoma patients."

"These long-term overall survival results further solidify KIMMTRAK as the first-line standard of care for HLA-A*02:01 positive patients with metastatic uveal melanoma," said Mohammed Dar, Immunocore Chief Medical Officer. "The survival benefit was evident even in patients with known poor prognostic factors, including those with large tumors and extrahepatic disease."

The data confirmed that the OS benefit was primarily driven by tebentafusp rather than subsequent therapies. Among patients treated with KIMMTRAK who were alive at five years, nearly half (44%) received only KIMMTRAK, while among patients in the control arm alive at the same time point, 86% subsequently received tebentafusp.

Importantly, the OS benefit with KIMMTRAK was observed regardless of known poor prognostic factors at baseline (high tumor burden [≥10cm]; elevated lactate dehydrogenase [LDH]) or tumor location (hepatic only; hepatic and extra-hepatic). OS benefit was also observed in patients with a best response of progressive disease, including those with >20% tumor growth as best change on treatment.

More patients continued treatment beyond progression in the KIMMTRAK arm than in the control arm (57% vs 25%) – with the trial allowing this option in both arms. Patients on KIMMTRAK achieved nearly a 7-fold higher rate of tumor reduction with treatment beyond initial progression compared to IC patients (27% vs 4%). In fact, patients who continued tebentafusp treatment beyond tumor progression experienced longer post-progression survival compared to those who stopped treatment, even after accounting for variations in patient characteristics.

In tebentafusp-treated patients, longer OS was associated with undetectable ctDNA at baseline or ctDNA reductions ≥50% by week 9. Among 21 ctDNA-evaluable patients who survived ≥ 5 years, 71% had undetectable baseline ctDNA and 29% had ctDNA clearance by week 9. Deep reductions in ctDNA were seen across all RECIST categories. Early ctDNA molecular response continues to be a more sensitive marker of tebentafusp activity than radiographic measurements.

The data were presented today in an oral session during the AACR (Free AACR Whitepaper) 2026 meeting:

Title: Five-year survival with tebentafusp in previously untreated metastatic uveal melanoma in a Phase 3 trial (CT029)
Presenting author: Paul Nathan
Session: Advanced Cellular and Immune-Based Therapeutics

(Press release, Immunocore, APR 19, 2026, View Source [SID1234664527])

On April 19, 2026 Ascentage Pharma Group International (NASDAQ: AAPG; HKEX: 6855), a global, commercial stage, integrated biopharmaceutical company engaged in the discovery, development and commercialization of novel, differentiated therapies to address unmet medical needs in cancer, reported that it will present four preclinical studies in poster format at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) 2026 Annual Meeting, held April 17 to 22, 2026 in San Diego, CA, USA.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

These posters feature three of the Company’s drug candidates, Olverembatinib (HQP1351), a novel BCR-ABL inhibitor; APG-2449, a FAK/ALK/ROS1 triple tyrosine kinase inhibitor; and APG-5918, a PRC2/EED inhibitor.

Yifan Zhai, M.D., Ph.D., Chief Medical Officer of Ascentage Pharma, said, "These preclinical findings reflect our continued commitment to advancing innovative therapies across multiple cancer types. The four studies demonstrate the breadth and versatility of our pipeline, exploring the therapeutic potential of our key assets in combination with other approved treatment options in both hematologic malignancies and solid tumors.

Notably, the research examines Olverembatinib’s potential beyond its approved use in China for chronic myeloid leukemia (CML), exploring new applications in areas such as endometrial carcinoma and mantle cell lymphoma, including combination approaches with BTK inhibitors. In addition, our evaluation of APG-2449 in BRAF-mutant tumors, and APG-5918 in small-cell lung cancer, underscores our strategic focus on addressing resistance mechanisms and exploring combination strategies.

These preclinical investigations are designed to inform our clinical development strategies and complement our ongoing global registrational trials as we bring new treatment options to patients with significant unmet medical needs."

Detailed data presented at AACR (Free AACR Whitepaper) 2026 Annual Meeting are summarized below:

(Abstract #4583)

Multitarget kinase inhibitor Olverembatinib (HQP1351) is efficacious and synergizes with chemotherapy in preclinical models of endometrial carcinoma (EC)

Background:

EC is the most common gynecologic malignancy in developed countries, with an incidence that is steadily increasing globally. Patients with advanced-stage, high-risk non-endometrioid EC subtypes or recurrent disease have a poor prognosis and limited treatment options.
Olverembatinib is a tyrosine kinase inhibitor approved by the National Medical Products Administration (NMPA) of China for the treatment of patients with CML. It targets multiple kinases, including VEGFR1–3, FGFR1–4, Src family kinases, RAF, KIT, RET, and PDGFR.
Drug sensitivity screening of 883 human cancer cell lines using the PRISM (Profiling Relative Inhibition Simultaneously in Mixtures) platform showed that EC is one of the tumor types most sensitive to Olverembatinib. This study further explored the antitumor effects of Olverembatinib alone or in combination with standard-of-care chemotherapy in preclinical EC models.

Summary:

In a broad range of preclinical in vitro and in vivo EC models, Olverembatinib was efficacious and synergized with chemotherapy agents to promote antitumor effects.
Mechanistically, Olverembatinib combined with chemotherapy suppressed FGFR2, PI3K/AKT, and MEK/ERK signaling pathways, induced DNA damage, and resulted in enhanced cell apoptosis.
These findings support future clinical evaluation of Olverembatinib and its combination with other approved treatment options in EC.

(Abstract #5875)

Multikinase inhibitor Olverembatinib (HQP1351) is efficacious and synergizes with BTK inhibitor acalabrutinib in mantle cell lymphoma (MCL) preclinical models

Background:

MCL is a rare, aggressive type of non-Hodgkin lymphoma. Although BTK inhibitors have transformed MCL treatment, response to monotherapy is limited, and efforts are underway to develop combination therapies.
Olverembatinib, an investigational multikinase inhibitor (approved in China for CML), inhibits Src-family kinases (e.g., Lyn, Fyn, YES1) and BTK, which are essential for B-cell receptor (BCR) signaling and B-cell proliferation, differentiation, and activation.
Hypothesizing that dual inhibition of Lyn and BTK pathways could enhance antitumor effects, this study evaluated Olverembatinib in combination with acalabrutinib in preclinical MCL models and explored potential mechanisms of action.

Summary:

Olverembatinib potently inhibited MCL cell proliferation both in vitro and in vivo and showed synergistic effects when combined with acalabrutinib. The combination significantly promoted apoptosis and induced G0/G1 cell cycle arrest.
Mechanistically, Olverembatinib inhibited phosphorylation of Lyn and its downstream BTK, while the combination further downregulated NF-kB activity.
These data provide a scientific rationale for further clinical evaluation of this novel combination therapy in patients with MCL.

(Abstract #1858)

FAK inhibition by APG-2449 enhances the antitumor activity of MAPK pathway blockade in BRAF V600E-mutant tumor models

Background:

BRAF mutations occur in approximately 4% to 8% of all cancers, most frequently in colorectal cancer (CRC), melanoma, and non-small-cell lung cancer. The V600E mutation is the most common and functionally activating form, leading to constitutive activation of the mitogen activated protein kinase (MAPK) signaling cascade.
Combined BRAF and MAPK kinase (MEK) inhibition has shown substantial clinical benefit in BRAF V600Emutant melanoma and CRC. However, resistance frequently develops through feedback reactivation of extracellular signal-regulated kinase (ERK) or compensatory activation of the phosphoinositide-3 kinase (PI3K)-AKT signaling pathway.
Recent evidence indicates that focal adhesion kinase (FAK) signaling is also adaptively reactivated upon MAPK inhibition, contributing to therapeutic resistance.
This study evaluated the effects of APG-2449, a potent and selective multi-kinase inhibitor that also targets FAK, on the antitumor activities of the BRAF inhibitor dabrafenib and the MEK inhibitor trametinib in BRAF V600E-mutant CRC and melanoma preclinical models.

Summary:

The results showed selective sensitivity of BRAF V600E-mutant cancer cell lines to APG-2449.
APG-2449 suppresses compensatory signaling activation induced by MAPK pathway blockade and synergistically enhances the antitumor activity of dabrafenib + trametinib in preclinical models.
These results warrant clinical development of APG-2449 for patients with melanoma or CRC harboring the BRAF V600E mutation.

(Abstract #4500)

Embryonic ectoderm development (EED) inhibitor APG-5918 synergizes with topoisomerase I inhibitors in preclinical small-cell lung cancer (SCLC) models through epigenetic priming of chemosensitivity

Background:

Although SCLC initially responds to platinum-based chemotherapy, it rapidly develops resistance, resulting in a poor prognosis.
PRC2-mediated epigenetic silencing represses Schlafen 11 (SLFN11), a biomarker of sensitivity to DNA-damaging therapies, thereby contributing to treatment resistance.
EZH2, the catalytic subunit of PRC2, promotes chemoresistance in part through SLFN11 repression. EED, another core PRC2 component, stabilizes the complex and maintains its methyltransferase activity, making it an attractive therapeutic target in SCLC.
Topoisomerase I inhibitors, such as topotecan and irinotecan, are used in relapsed SCLC; however, their efficacy is limited when SLFN11 is epigenetically suppressed.
APG-5918 is a selective and investigational EED inhibitor that disrupts PRC2 function. This study evaluated the antitumor activity of APG-5918 in combination with topoisomerase I inhibitors in preclinical SCLC models.

Summary:

In preclinical SCLC models, combination treatment with APG-5918 and topoisomerase I inhibitors synergistically inhibited cell proliferation and induced apoptosis.
In vivo, APG-5918 combined with irinotecan demonstrated synergistic antitumor activity in the NCI-H446 SCLC cell-derived xenograft (CDX) model without significant body-weight loss, indicating favorable tolerability.
Mechanistically, APG-5918 reduced the repressive histone mark H3K27me3, indicating on-target inhibition of PRC2 activity. Consistent with this effect, APG-5918 treatment increased SLFN11 and p21 expression. Notably, treatment with topotecan or SN-38 increased H3K27me3 levels, whereas APG-5918 reduced this effect. Combination treatment further decreased expression of PRC2 core components, suppressed cell-cycle progression, and enhanced DNA damage and apoptotic signaling, supporting a synergistic proapoptotic effect.
The findings support clinical investigation of APG-5918 in combination with DNA-damaging agents as a promising therapeutic strategy for SCLC.

(Press release, Ascentage Pharma, APR 19, 2026, View Source [SID1234664528])

On April 19, 2026 Revolution Medicines, Inc. (Nasdaq: RVMD), a late-stage clinical oncology company developing targeted therapies for patients with RAS-addicted cancers, reported updated Phase 1 (RMC-9805-001) clinical data for zoldonrasib, an oral RAS(ON) G12D-selective inhibitor, in patients with previously treated KRAS G12D non-small cell lung cancer (NSCLC). Results were highlighted in the official press program at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting and will be featured in a plenary oral presentation today, April 19, 2026, at 1:30 p.m. PDT.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

"Patients with RAS G12D non-small cell lung cancer remain a population with a significant unmet medical need for targeted therapeutic options," said Jonathan Riess M.D., medical director of thoracic oncology at UC Davis Comprehensive Cancer Center and principal investigator for the RMC-9805-001 trial. "The manageable safety profile and evidence of clinical activity in this Phase 1 trial are encouraging and support the continued clinical development of zoldonrasib."

"We believe these updated data further strengthen the profile of zoldonrasib as a potentially important targeted therapy for patients with RAS G12D non-small cell lung cancer where historical treatment options, such as chemotherapy, have offered limited benefit, and are often associated with considerable toxicity," said Alan Sandler, M.D., chief development officer of Revolution Medicines. "The emerging profile supports advancing zoldonrasib across monotherapy and combination settings in lung cancer and other RAS G12D-driven cancers."

Summary of Phase 1 Zoldonrasib Data at AACR (Free AACR Whitepaper) 2026 (Abstract # CT021)

RMC-9805-001 is a multicenter, open-label, dose escalation and dose expansion Phase 1 trial designed to evaluate zoldonrasib in patients with advanced solid tumors harboring a KRAS G12D mutation. The data to be presented at the AACR (Free AACR Whitepaper) Annual Meeting are as of a December 1, 2025 data cutoff, and included 40 patients with KRAS G12D NSCLC treated with zoldonrasib 1200 mg once daily, the recommended Phase 2 dose, and who were evaluable for safety. Efficacy analyses were conducted in a subset of patients with prior immune checkpoint inhibitor and platinum chemotherapy and no prior docetaxel treatment who had sufficient follow-up for response assessment (n=27).

Zoldonrasib was generally well tolerated and demonstrated a safety profile consistent with previously reported findings. Treatment-related adverse events (TRAEs) of any grade occurring in at least 15% of patients were nausea (43%), vomiting (33%), diarrhea (30%), and rash (18%). The majority of TRAEs were Grade 1 in severity. Grade 3 TRAEs occurred in 13% of patients and resolved following dose interruption; TRAEs led to treatment discontinuation in 5% of patients. No Grade 4 or Grade 5 TRAEs were observed. Zoldonrasib demonstrated a favorable mean dose intensity of 94%.

Zoldonrasib demonstrated encouraging clinical activity in patients with KRAS G12D NSCLC previously treated with immune checkpoint inhibitor and platinum chemotherapy and no prior docetaxel. Among this subset of patients (n=27), the confirmed objective response rate was 52% (confidence interval (CI): 32, 71) and the disease control rate was 93% (CI: 76, 99). Median time to response was 1.4 months and median duration of response was not yet estimable (95% CI: 8.3, not estimable). Median progression-free survival (PFS) was 11.1 months (95% CI: 5.3, not estimable), with an estimated 12-month PFS rate of 48% (95% CI: 27, 66). Overall survival (OS) data were immature at the time of analysis, and median OS was not yet reached with median potential follow-up of 13.1 months (range: 9.1–19.9). Estimated survival rate at 12 months was 73% (95% CI: 52, 86), suggesting encouraging early survival outcomes.

About Non-Small Cell Lung Cancer
Non-small cell lung cancer (NSCLC) accounts for 80%-85% of all lung cancers, with more than 229,000 people diagnosed in the U.S. each year.1,2 Despite treatment advancements, NSCLC remains a leading cause of cancer-related mortality worldwide, primarily due to its late-stage diagnosis and limited response to conventional therapies. KRAS G12D is the most common oncogenic driver of human cancers and represents 4% of NSCLC cases.3

About Zoldonrasib
Zoldonrasib is a tri-complex inhibitor that binds to cyclophilin A, creating a complex that selectively recognizes and inhibits the active, oncogenic RAS G12D(ON) mutant. KRAS G12D is the most prevalent RAS mutation, accounting for 29% of all RAS cancers, and currently lacks an approved targeted therapy.4 Across tumor types, approximately 61,000 new patients with RAS G12D cancers are estimated each year in the United States.5 Zoldonrasib is currently being evaluated as a monotherapy and in combination with other therapies, including with Revolution Medicines’ RAS(ON) multi-selective inhibitor daraxonrasib (RMC-6236), as well as standard of care regimens in lung and gastrointestinal cancers.

(Press release, Revolution Medicines, APR 19, 2026, View Source [SID1234664519])

On April 19, 2026 Sutro Biopharma, Inc. (Sutro or the Company) (NASDAQ: STRO), a clinical-stage oncology company pioneering site-specific and novel-format antibody drug conjugates (ADCs), reported promising preclinical data across its pipeline of next- generation ADCs in five posters and one oral presentation at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026. Of note, results from a preclinical study of STRO-004, its DAR8 Topo1 ADC targeting Tissue Factor (TF), were reviewed today in an oral presentation titled "STRO-004, an exatecan-based next-generation tissue factor (TF)-targeted ADC, demonstrates superior efficacy across TF-expressing solid tumors in a comprehensive single-mouse PDX trial."

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

In the preclinical study, STRO-004 demonstrated robust and consistent antitumor activity across a broad range of TF-expressing solid tumor patient-derived xenograft (PDX) models, with improved efficacy compared to benchmark ADCs. At a single, clinically relevant dose of 5 mg/kg, STRO-004 achieved remarkable disease control and tumor reduction across multiple tumor types. STRO-004’s favorable tolerability, with a highest non-severely toxic dose (HNSTD) of 50 mg/kg, and pharmacokinetic profile are expected to enable increased drug exposure and payload delivery, supporting the Company’s belief that STRO-004 will demonstrate superior depth and durability of response in the clinic. Exploratory biomarker analyses provide preliminary insight into STRO-004’s mechanism of action, suggesting potential for combination studies addressing specific indications in either early or late lines of treatment.

"The STRO-004 preclinical data presented today underscore the potential of our next-generation ADCs to drive meaningful activity across multiple solid tumors," said Jane Chung, Sutro’s Chief Executive Officer. "As STRO-004 advances in the clinic – with initial results from our Phase 1 study expected in mid-2026 – these preclinical data further strengthen our confidence in its potential across indications. More broadly, they underscore the versatility of our platform to generate differentiated ADCs across many targets and payloads, supporting a pipeline designed to address significant unmet need in cancer."

In addition to the oral presentation, Sutro will present multiple posters highlighting advances across its ADC pipeline and discovery platforms, the full details of which are included below.

Select Poster Highlights:

Preclinical data for STRO-006, an integrin β6-targeting ADC (DAR 8 exatecan), demonstrated robust, dose-dependent antitumor activity across multiple solid tumor models at a single, clinically relevant dose of 5 mg/kg, including non-small cell lung cancer (NSCLC) and head and neck cancers. The program also shows a favorable pharmacokinetic and tolerability profile, supporting its potential as a differentiated next-generation ADC with IND submission planned for 2026.
Preclinical data for STRO-227, a PTK7-targeting dual-payload ADC (DAR 10; 8 exatecan + 2 MMAE), demonstrated robust, dose-dependent antitumor activity across multiple solid tumor models, including breast, ovarian and NSCLC, with improved efficacy versus single-payload ADCs. The program also shows favorable pharmacokinetics, stable payload delivery, and tolerability comparable to benchmark ADCs, supporting the potential of its dual-payload design. These findings position STRO-227 as a differentiated ADC with broad applicability across solid tumors. Sutro expects to file an IND for STRO-227, its first wholly-owned dual-payload ADC, in late 2026.

Full Poster Presentation Details:

Poster: "Phase 1 open-label study to evaluate safety, pharmacokinetics, and preliminary anti-tumor activity of STRO-004 in adults with refractory/recurrent metastatic solid tumors"
Session Date and Time: Monday, April 20, 2026; 9:00 AM-12:00 PM PT
Poster: "STRO-006: An Integrin beta-6–targeting ADC demonstrates favorable safety profile and potent antitumor activity in preclinical solid tumors"
Session Date and Time: Monday, April 20, 2026; 9:00 AM-12:00 PM PT
Poster: "Preclinical characterization of STRO-227: A PTK7-targeting dual-payload ADC with topoisomerase 1 and tubulin inhibitors"
Session Date and Time: Monday, April 20, 2026; 9:00 AM-12:00 PM PT
Poster: "The HER2-targeting dual-payload antibody-drug conjugate combining a topoisomerase I inhibitor and a microtubule inhibitor demonstrates superior efficacy and overcomes resistance to single-payload ADCs in xenograft models"
Session Date and Time: Monday, April 20, 2026; 9:00 AM-12:00 PM PT
Poster: "Sutro’s Site-Specific Dual-Payload ADCs Combining TOPO1i and DNA Damage Response Inhibitors to Enhance Efficacy, Overcome Resistance, and Improve Safety"
Session Date and Time: Tuesday, April 21, 2026; 9:00 AM-12:00 PM PT

In addition to these presentations, Sutro’s strategic partner, Astellas Pharma, also reviewed preclinical results from its TROP2-targeted iADC program at AACR (Free AACR Whitepaper) today. The oral presentation, titled "ASP2998, a TROP2-targeted immunostimulatory antibody-drug conjugate (iADC) with dual payloads, demonstrates potent efficacy and a favorable safety profile in nonclinical models," highlighted the company’s progress in the development of next-generation iADCs leveraging Sutro’s cell-free protein synthesis platform. ASP2998 is a first-in-class iADC that combines cytotoxic and immune-stimulatory mechanisms to enhance antitumor efficacy. Inclusion of a STING agonist augments the antitumor efficacy, immune activation and durable tumor immunity of ASP2998, supporting its superior activity over toxin-only anti-TROP2 ADCs. Preclinically, ASP2998 demonstrated a favorable safety profile, supporting a promising therapeutic index. ASP2998 entered the clinic earlier this year and is actively dosing patients.

Following the congress, the Company’s presentations will be made available in the Scientific Publications section of Sutro Biopharma’s website at www.sutrobio.com.

(Press release, Sutro Biopharma, APR 19, 2026, View Source [SID1234664520])