CREATE Medicines to Showcase Multi-immune In Vivo CAR T, CAR NK, and All-RNA RetroT Platform at AACR 2026

On April 17, 2026 CREATE Medicines, Inc. ("CREATE"), a clinical-stage biotechnology company pioneering in vivo immune cell programming, reported it will present two posters at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, taking place April 17–22, 2026 in San Diego.

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The presentations at AACR (Free AACR Whitepaper) highlight the CREATE platform in action, showcasing new data across CREATE’s multi-immune in vivo CAR portfolio and introducing the first in vivo data for RetroT, the company’s all-RNA genome integration platform designed to enable stable, durable cell engineering without viral components.

The data demonstrates simultaneous engineering of myeloid cells, NK cells, and T cells with tailored CAR mRNAs driving tumor regression and remodeling of the tumor microenvironment in a colorectal cancer model. First-in-vivo evidence for RetroT demonstrates that CAR T cells engineered without double-strand breaks or viral vectors significantly reduced tumor burden in a leukemia model, validating the platform’s potential as a path to stable, durable CAR expression.

"CREATE was built to rapidly iterate directly from our clinical data and unlock the clear advantages of in vivo cell therapy," said Robert Hofmeister, Ph.D., Chief Scientific Officer of CREATE. "The work we are presenting at AACR (Free AACR Whitepaper) underscores this unique capability of our platform, leveraging our experience in over 50 patients to develop the next generation multi-immune CARs or stably integrated mRNA in vivo therapies. These advances position the platform for near-term development of novel scalable therapies across autoimmune and oncology."

CREATE is advancing the broadest portfolio of in vivo CAR therapies, supporting the largest human clinical dataset in the field, built through the application of its integrated mRNA, lipid nanoparticle, and CAR engineering platform. This dataset enables rapid translation from clinical insight to pipeline innovation, informing both current programs and the design of next-generation in vivo CAR therapies.

AACR Poster Presentation Details:

Title: In Vivo CAR mRNA Engineering of T Cells and Myeloid Cells Enables Potent Anti-Tumor Control of Solid Cancers
Date & Time: Sunday, April 19, 2026, 2–5 PM PT
Location: Poster Section 7
Session Category: Immunology
Session Title: Alternative Cell Type and In Situ Cell Therapies
Poster Board #: 18
Abstract #: 144

Title: Stepwise In Vivo CAR T Cell Engineering via Transient RNA Programming and RetroT All-RNA Genome Integration
Date & Time: Monday, April 20, 2026, 9 AM–12 PM PT
Location: Poster Section 53
Session Title: Late-Breaking Research: Immunology 2
Poster Board #: 20
Abstract #: LB155

More information is available on the AACR (Free AACR Whitepaper) Annual Meeting website.

(Press release, Create Medicines, APR 17, 2026, View Source [SID1234664485])

Nested Therapeutics Reports Initial Encouraging Clinical Activity and Favorable Tolerability of NST-628, a Brain-Penetrant Pan-RAF/MEK Molecular Glue, at AACR 2026

On April 17, 2026 Nested Therapeutics, a clinical-stage oncology company developing transformative therapies for RAS/MAPK-driven disorders, reported initial clinical results from its ongoing Phase 1 study evaluating NST-628, a brain-penetrant non-degrading pan-RAF/MEK molecular glue, in patients with advanced solid tumors. Data presented at the AACR (Free AACR Whitepaper) Annual Meeting 2026 demonstrate encouraging single-agent anti-tumor activity and a favorable tolerability profile in a range of RAF and RAS-mutant tumors, including a 38% response rate and 85% disease control rate at the recommended dose in heavily pretreated NRAS and BRAF Class II/III melanoma, a population that represents approximately 33% of cutaneous melanoma patients, for whom no approved targeted therapies are available.

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"These initial data support our hypothesis that targeting RAF/MEK signaling with a single-agent, fully brain-penetrant pan-RAF/MEK molecular glue can deliver meaningful clinical benefit with a tolerability profile that supports sustained dosing even in comparison to what may be expected from combination regimens," said Darrin Miles, Chief Executive Officer of Nested Therapeutics. "We are particularly encouraged by the durable responses in NRAS and BRAF Class II/III melanoma – large patient populations with historically poorer outcomes and for whom there are no approved targeted therapy options – as well as early signals of clinical activity beyond melanoma, including in KRAS-mutant solid tumors and evidence of brain penetrance. Together, these clinical findings, in addition to robust preclinical evidence and favorable drug properties, support the potential for NST-628 to address significant unmet need across RAS/MAPK-driven cancers and to serve as a foundational therapy in both monotherapy and combination settings."

Key Data Highlights

As of the data cutoff date of February 1, 2026, NST-628 has been administered to 69 patients: 64 patients in dose-escalation and 5 patients in the expansion phase. Key findings are summarized below.

Monotherapy Clinical Activity in evaluable patients (with at least one tumor assessment or who discontinued the study) at Recommended Dose for Expansion (RDE)

NST-628 monotherapy demonstrated a 38% response rate in BRAF Class II/III and NRAS-mutant melanoma (N=13) and 33% response rate overall (N=18); response rates include one unconfirmed partial response
Disease control rate was 85% in the melanoma subgroup and 72% overall
With a median follow-up of 6.4 months, the median duration of response in melanoma was not yet reached
Anti-Tumor Activity Beyond Melanoma

Responses to NST-628 were observed across multiple tumor types and genotypes, including KRAS-mutant ovarian and cervical cancers – highlighted by an ongoing partial response in a KRAS G12V-mutant cervical cancer patient with a treatment duration exceeding one year – as well as NRAS/BRAF Class III-mutant colorectal cancer and BRAF Class II-mutant thymic cancer
A patient with high-grade astrocytoma (BRAF V600E), previously treated with multiple lines of RAF/MEK-targeted therapy, demonstrated 70% tumor shrinkage on NST-628 monotherapy, consistent with NST-628’s preclinical brain penetration profile
Reductions in ctDNA correlated with radiographic response
Safety and Tolerability

Adverse events were consistent with the mechanism of action and predominantly Grade 1-2
Most common treatment-related adverse events included dermatologic, gastrointestinal, CK elevation, constitutional, and ocular events
Grade ≥3 TRAEs were infrequent; most common was CK elevation
No Grade 5 events reported
At the RDE:
Discontinuation rate: 9%
Dose intensity (actual dose delivered vs. intended): 82%
"The anti-tumor activity observed with NST-628 monotherapy is encouraging," said Philip Komarnitsky, MD, PhD, Chief Medical Officer of Nested Therapeutics. "A safety profile that supports continuous dosing at 82% dose intensity with a 9% discontinuation rate, combined with the response rate of 38% and disease control rate of 85% in NRAS and BRAF Class II/III melanoma patients at the recommended dose, is promising for this patient population with no approved targeted therapies. The clinical evidence of activity in malignancies with BRAF class III mutations, an emerging resistance mechanism to RAS inhibitors, and of brain penetrance consistent with preclinical findings is particularly noteworthy. These data support the continued development of NST-628 as monotherapy and its evaluation in rational combinations."

Nested plans to continue enrollment in the ongoing Phase 1 expansion cohort and evaluate NST-628 in additional malignant and non-malignant MAPK-driven diseases and combination settings, including mutant-selective RAS and other inhibitors.

Poster Presentation Details

Title: Preliminary results from a Phase 1a/b dose-escalation and expansion trial of the pan-RAF-MEK molecular glue NST-628 in patients (pts) with advanced or refractory RAF, KRAS, and NRAS-mutant solid tumors

Presenter: Ahmad A. Tarhini, MD, PhD, Moffitt Cancer Center

Presentation Date and Time: Monday, April 20, 2026, 2:00 PM-5:00 PM PT

Session: PO.CT01.01 – Phase 0 and First-in-Human Phase I Clinical Trials

Location: Section 51

About the Phase 1 Study of NST-628, NST-628-001

The ongoing Phase 1 open-label, single-arm, two-part study (NCT06326411) is investigating the safety, pharmacokinetics (PK), pharmacodynamics (PD), and preliminary efficacy of single-agent NST-628 in adult patients with RAS-MAPK pathway mutated/dependent advanced solid tumors, especially diverse KRAS, NRAS, and BRAF alterations, who have exhausted standard treatment options. The study includes two parts: dose escalation (Part A), which enrolled 64 patients across seven dose regimens, followed by dose expansion (Part B) at the recommended dose for expansion. Part B is currently enrolling. For more information, visit clinicaltrials.gov.

About NST-628

NST-628 is a brain-penetrant, non-degrading molecular glue designed to inhibit RAF and MEK signaling by stabilizing RAF-MEK complexes in a catalytically inactive form. This mechanism is intended to prevent pathway reactivation, a common liability of existing RAS/MAPK-targeted therapies, and enable more durable pathway suppression across RAS/MAPK-driven cancers.

(Press release, Nested Therapeutics, APR 17, 2026, View Source [SID1234664484])

Accent Therapeutics Presents Data Reinforcing Therapeutic Potential of Novel KIF18A Inhibitor, ATX-295, at the 2026 American Association for Cancer Research Annual Meeting

On April 17, 2026 Accent Therapeutics, a clinical-stage biopharmaceutical company pioneering novel small molecule precision cancer therapies, reported preclinical data supporting its potentially best-in-class KIF18A inhibitor, ATX-295, at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026 taking place April 17-22 in San Diego, California.

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"The strength and consistency of the preclinical results supporting our KIF18A program reinforce our confidence in ATX-295 as a novel therapeutic targeting a fundamental vulnerability in cancers with high levels of chromosomal instability," said Serena Silver, Ph.D., Chief Scientific Officer of Accent Therapeutics. "We are further advancing our commitment to maximize ATX-295’s potentially transformative impact for cancer patients by exploring AI-guided tools to assess chromosomal instability."

The company’s presentation includes preclinical data demonstrating the strong anti-tumor activity of ATX-295 across multiple solid tumor indications with high levels of chromosomal instability. The molecule showed potent in vitro activity in high-grade serous ovarian cancer (HGSOC), squamous non-small cell lung cancer (sqNSCLC), and triple-negative breast cancer (TNBC) cell lines, leading to cell cycle arrest and apoptosis. ATX-295 showed robust and durable tumor regression in patient-derived xenograft models of HGSOC, sqNSCLC and TNBC exhibiting whole-genome doubling (WGD), supporting WGD and chromosomal instability as predictive markers of tumor sensitivity to ATX-295. The results also include proof of concept for a novel, artificial intelligence (AI)-based method capable of rapidly detecting WGD in clinical samples, providing the foundation for a clinically feasible biomarker.

ATX-295 is currently under investigation in a first-in-human, Phase 1/2, open-label, dose escalation and expansion study, designed to evaluate the molecule’s safety, tolerability, and preliminary efficacy in patients with locally advanced or metastatic solid tumors, including HGSOC and sqNSCLC (NCT06799065).

Details for the presentation are as follows:

Poster Title: Robust anti-tumor activity of the novel KIF18A inhibitor, ATX-295, in preclinical models of chromosomally instable tumors
Abstract Number: 6641
Session Title: Multi-Axis Antineoplastic Agents
Session Date and Time: Tuesday, April 21: 2:00 PM – 5:00 PM PT
Location: Poster Section 14
Poster Board Number: 2
Presenter: Laura Ghisolfi, Ph.D.
About ATX-295
Accent’s lead program, ATX-295, is a potential best-in-class inhibitor for KIF18A, a mitotic kinesin motor protein critical for cell division in select tumors with chromosomal instability. KIF18A inhibitor treatment results in rapid cell death for cancers with an abnormal number of chromosomes (aneuploid) in vitro and in vivo, while cells with normal numbers of chromosomes (euploid) are unaffected. ATX-295 may address a large patient population across several cancer indications, including ovarian and squamous non-small cell lung cancer. Accent retains full worldwide rights to the KIF18A program, currently being evaluated in an ongoing Phase 1/2 clinical study (NCT06799065) enrolling patients with locally advanced or metastatic solid tumors, including high-grade serous ovarian cancer and squamous non-small cell lung cancer.

(Press release, Accent Therapeutics, APR 17, 2026, View Source [SID1234664483])

Lunit to Present Six AI Studies at AACR 2026 Highlighting Advances in Precision Oncology and Real-World Clinical Application

On April 17, 2026 Lunit (KRX:328130), a leading provider of AI for cancer diagnostics and precision oncology, reported six studies at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, taking place from April 17 to 22 in San Diego, California.

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The presentations highlighted Lunit’s continued advancements in AI-driven biomarker development, tumor microenvironment (TME) analysis, and real-world clinical applicability. Several studies were conducted in collaboration with global partners, including Agilent Technologies.

In a study conducted with Agilent Technologies and Ajou University Medical Center, researchers used Lunit SCOPE IO and uIHC to analyze over 25,000 non-small cell lung cancer (NSCLC) samples. The results showed that tumors with high c-MET expression exhibited a significant reduction in immune cell density within 30 μm of tumor cells (p<0.001), revealing a spatial immune exclusion pattern not captured by conventional analysis. These findings suggest a potential link between c-MET overexpression and immune evasion, supporting combination strategies involving MET-targeted therapy and immunotherapy.

Researchers also present findings from an exploratory analysis of the phase II MOUNTAINEER trial, demonstrating that AI- quantified HER2 expression is strongly associated with treatment response in patients with HER2-positive metastatic colorectal cancer treated with tucatinib plus trastuzumab. The overall objective response rate (ORR) was 43.4%, increasing to as high as 80% in patients with higher HER2 expression, indicating a clearer dose-dependent relationship. Tumor-Infiltrating Lymphocyte (TIL) density independently predicted progression-free survival. Notably, patients with low stromal TIL levels showed no response (ORR 0%) and a significantly higher risk of disease progression.

These findings highlight the increasing complexity of biomarker assessment, where both tumor characteristics and immune context need to be considered, underscoring the potential role of AI in supporting treatment decision-making.

In addition to these representative studies, Lunit presented additional research abstracts at AACR (Free AACR Whitepaper) 2026, further demonstrating the breadth of its AI-powered oncology research. These include studies on

AI-based analysis of tumor-infiltrating lymphocyte in NSCLC in collaboration with Dr. David Rimm’s lab at Yale University School of Medicine
AI-based target discovery for bi-specific antibodies
Biomarker research in CD47-targeted therapies
"Our AACR (Free AACR Whitepaper) presentations reflect how AI is increasingly translating into real-world clinical impact" said Brandon Suh, CEO of Lunit. "Across these studies, we demonstrate how AI-driven biomarkers can enhance precision, deepen our understanding of tumor biology and increasingly support treatment decision-making in clinical practice."

Visit Lunit at Booth #2248 during AACR (Free AACR Whitepaper) 2026 to learn more about its latest research and AI-powered solutions in cancer diagnostics and therapeutics.

Lunit’s featured presentations at AACR (Free AACR Whitepaper) 2026 include:

[Poster #0011/11] Artificial intelligence-based spatial analysis of the local tumor microenvironment in relation to c-MET expression in non-small cell lung cancer
April 19, 2:00 PM – 5:00 PM, Section 1

[Poster #7735/26] HER2 expression and tumor-infiltrating lymphocytes predict response to tucatinib plus trastuzumab in HER2-positive metastatic colorectal cancer (MOUNTAINEER): Exploratory analysis of a multicenter, Phase II trial
April 22, 9:00 AM – 12:00 PM, Section 41

[Poster #4415/23] AI-powered analysis of millions of IHC images identifies 19 spatially highly co-expressed protein pairs to enable bispecific antibody development
April 21, 9:00 AM – 12:00 PM, Section 11

[Poster #0080/11] Quantitative assessment of tumor-infiltrating lymphocytes using AI in non-small cell lung cancer and association with immunotherapy response
April 19, 2:00 PM – 5:00 PM, Section 4

[Poster #4355/26] Cryo EM-based structural characterization of IMC-002, a next-generation anti-CD47 antibody with a unique binding site and biomarker candidates, supporting evidence of enhanced safety and efficacy
April 21, 9:00 AM – 12:00 PM, Section 9

(Press release, Lunit, APR 17, 2026, View Source [SID1234664482])

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])