On July 10, 2026 GSK plc (LSE/NYSE: GSK) licensor Hansoh Pharmaceutical Group Co., Ltd. reported that ARTEMIS-008, its pivotal phase III trial evaluating risvutatug rezetecan (Ris-Rez) in patients with advanced or relapsed small-cell lung cancer (SCLC), met its primary endpoint of overall survival (OS). In the trial, conducted in patients in China, Ris-Rez demonstrated statistically significant and clinically meaningful improvements in OS compared with the standard of care, topotecan. Consistent benefit was also observed across key secondary endpoints, including progression-free survival. These data will be used by Hansoh Pharma for regulatory submission in China.

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These are the first positive phase III overall survival data reported for a B7-H3-targeted antibody-drug conjugate (ADC) in any tumour type. The safety profile is consistent with prior Ris-Rez findings, and no new safety signals were identified.

GSK holds exclusive global rights to develop Ris-Rez outside mainland China, Hong Kong, Macau and Taiwan. GSK’s broad clinical development programme includes studies in lung cancer, prostate cancer and other solid tumours, including the global phase III EMBOLD SCLC-301 trial in relapsed extensive-stage small-cell lung cancer (ES-SCLC) with pivotal data expected next year.

Hesham Abdullah, Senior Vice President, Global Head Oncology, R&D, GSK said: "These results are an important milestone as the first positive phase III overall survival data for a B7-H3-targeted ADC in any tumour type. Together, with other data generated to date, they further support the potential of B7-H3 as a promising target across lung cancer and other solid tumours and reinforce our continued development of Ris-Rez to improve standard of care in areas of high unmet need."

Most patients with ES-SCLC relapse after initial therapy and have limited treatment options, poor prognosis and significant treatment burden.1 B7-H3 is highly expressed in SCLC tumours2,3 and the positive results from ARTEMIS-008 add to the growing body of evidence supporting the encouraging clinical activity and manageable safety profile of Ris-Rez in patients with ES-SCLC.

About risvutatug rezetecan
Ris-Rez is a novel investigational B7-H3-targeted ADC composed of a fully human anti-B7-H3 monoclonal antibody covalently linked to a topoisomerase inhibitor payload. GSK acquired exclusive worldwide rights (excluding China’s mainland, Hong Kong, Macau, and Taiwan) from Hansoh Pharma to progress clinical development and commercialisation of Ris-Rez.

Regulatory designations received for Ris-Rez to date include orphan drug designations from the US Food and Drug Administration (FDA) and Japan’s Ministry of Health, Labour and Welfare in SCLC and the European Medicines Agency (EMA) in a category of cancer that includes SCLC, called pulmonary neuroendocrine carcinoma; Priority Medicines (PRIME) Designation from the EMA for relapsed or refractory ES-SCLC; and Breakthrough Therapy Designations for relapsed or refractory ES-SCLC and relapsed or refractory osteosarcoma from the US FDA.

(Press release, GlaxoSmithKline, JUL 10, 2026, View Source [SID1234669140])

On July 10, 2026 AB Science SA (Euronext – FR0010557264 – AB) reported an update on its clinical development program and announces the discontinuation of certain non-priority clinical studies in order to focus on two clinical programs, the AB8939 program for acute myeloid leukemia and the masitinib program for amyotrophic lateral sclerosis.

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Following the company’s press release dated April 16 [1], three clinical studies—which the company currently considers non-priority and for which patient enrollment had been suspended—are being discontinued, namely:

Phase 2 study (AB20006) of masitinib in mast cell activation syndrome
Phase 3 study (AB15003) of masitinib in mastocytosis
Phase 3 study (AB20009) of masitinib in progressive forms of multiple sclerosis

The discontinuation of these studies is not related to any safety concerns regarding masitinib. The company intends to complete these clinical studies in accordance with applicable regulations.

Stéphane Ledermann, Chairman and CEO of AB Science, stated, "This decision to terminate non-priority studies for which recruitment had been suspended and for which there is no prospect of a rapid resumption reflects compliance with regulatory requirements. It is also consistent with our commitment to allocate all necessary resources to ensure the two priority programs are carried out to the highest standards of quality."

Regarding the AB8939 program for acute myeloid leukemia, the company announced [2] the completion of Phase 1, Step 3, evaluating the combination of AB8939 and venetoclax. The next step is to seek authorization from health authorities—based on a preliminary favorable opinion from the study’s Independent Data Monitoring Committee (IDMC)—to initiate Phase 4 of the study, which will evaluate the triple combination of AB8939, venetoclax, and azacitidine.

Regarding the Phase 3 program for masitinib in amyotrophic lateral sclerosis, which was approved in 2025 [3] but has not yet begun, the company will update the protocol and its implementation procedures, and will seek authorization from health authorities to resume this study after submitting a substantial amendment.

About AB23005 in ALS

The AB23005 study is a prospective, multicenter, randomized, double-blind, placebo-controlled, two-arm study conducted in patients with amyotrophic lateral sclerosis (ALS), designed to confirm the efficacy and safety of masitinib (at a dose of 4.5 mg/kg/day in combination with riluzole) compared to riluzole plus placebo after 48 weeks of treatment. The study will include 408 patients (randomized in a 1:1 ratio) with ALS who are experiencing normal disease progression (i.e., a functional decline of less than 1.1 points per month) and who have not experienced a complete loss of function (i.e., a score of at least 1 on each of the 12 items of the ALSFRS-R scale). U.S. patients receiving edaravone will also be eligible to participate in the study, as the use of this medication constitutes a stratification factor.

About AB18001 in AML

The AB18001 study, titled "A Phase 1/2 Study to Evaluate the Safety, Pharmacokinetics, and Efficacy of AB8939 Administered Intravenously Daily in Patients with Relapsed/Refractory Acute Myeloid Leukemia," is designed in several phases. The first part is a dose-escalation study designed to assess the safety and tolerability of AB8939 and to determine the recommended dose for the Phase 2 expansion study.

The objective of the Phase 1 study is to determine the maximum tolerated dose (MTD) for the different treatment regimens with AB8939.

Phase 1: Determination of the MTD after 3 consecutive days of treatment with AB8939 alone.
Phase 2: Determination of the MTD after 14 consecutive days of treatment with AB8939 alone.
Phase 3: Determination of the MTD after 14 consecutive days of treatment with AB8939 in combination with venetoclax.
Phase 4: Determination of the maximum tolerated dose (MTD) after 14 consecutive days of treatment with AB8939 in combination with venetoclax and azacitidine.

(Press release, AB Science, JUL 10, 2026, View Source [SID1234669139])

On July 9, 2026 Amplia Therapeutics Limited (ASX:ATX; OTCQB:INNMF), ("Amplia" or the "Company"), reported publication of a new patent application describing chemically novel inhibitors of focal adhesion kinase (FAK) discovered by the Company. The patent application further expands Amplia’s FAK intellectual property portfolio and, if granted, would provide protection for the novel molecules described, and their use, out to 2046.

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Amplia’s patent portfolio covers its lead drug narmafotinib, currently in clinical trials for pancreatic and ovarian cancer, and a second drug candidate (AMP886) being investigated in preclinical studies. The new patent application describes additional chemical compounds closely related to narmafotinib that also demonstrate potent and selective activity against FAK. These molecules broaden Amplia’s development pipeline and may provide future opportunities for evaluation across additional indications. Importantly, the patent application adds depth to the Company’s existing intellectual property estate around its FAK inhibitor program and supports the long-term commercial value of its development assets.

Dr. Chris Burns, CEO and Managing Director of Amplia, commented, "This patent application further strengthens our portfolio of potent FAK inhibitors and highlights the depth of innovation being generated by the Company. In addition to supporting narmafotinib, it creates future development and partnering optionality through a broader suite of novel molecules targeting this important pathway.

(Press release, Amplia Therapeutics, JUL 9, 2026, View Source [SID1234669135])

On July 9, 2026 IN8bio, Inc. (Nasdaq: INAB), a clinical-stage biopharmaceutical company developing innovative gamma-delta (γδ) T cell therapies and T cell engagers for cancer and autoimmune diseases, reported the publication of peer-reviewed clinical data from its Phase 1 trial of INB-200 in The Journal of Clinical Oncology (JCO), one of the most prestigious oncology journals.

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The publication, titled: "Intracranial injection of ex vivo expanded and activated gamma-delta T cells engineered with a MGMT-expressing lentivector in patients with primary glioblastoma," reports results from the first-in-human study of an autologous, genetically modified γδ T cell therapy. The expanded, activated γδ T cells are engineered to be resistant to chemotherapy (DeltEx DRI) and delivered intracranially in combination with standard of care (SOC) temozolomide chemotherapy (TMZ).

The Phase 1 trial is a frequency-escalation study of DeltEx DRI in GBM patients in combination with the SOC Stupp regimen (surgical resection followed by chemoradiation and maintenance chemotherapy). A total of 13 patients were enrolled and treated across three cohorts with subjects in their respective cohorts receiving 1, 3, or up to 6 doses of DeltEx DRI in 28-day cycles during maintenance chemotherapy. Evaluations included the safety and feasibility of repeated intracranial administration during maintenance chemotherapy.

GBM is the most common malignant primary brain tumor in adults and one of the most aggressive and difficult cancers to treat, with overall survival of only ~11 months and a five-year survival of ~5%. Despite overall advances across numerous cancer therapies, survival in GBM has been almost unchanged in more than 20 years with no new drug approvals and only a single device approval. Recurrence is nearly universal with GBM patients facing rapid decline, very limited treatment options, and poor outcomes.

In the Phase 1 study, DeltEx DRI in combination with SOC demonstrated a well-tolerated safety profile with no DLTs, no cytokine release syndrome (CRS), and no immune effector cell-associated neurotoxicity (ICANS) observed. The therapy also showed compelling signals of clinical activity. Across all 13 treated patients, mPFS was 9.9 months, and a 43.5% improvement over the 6.9 months typically reported with SOC alone. The results were most striking in repeat-dose patients (those receiving 3 to 6 doses) where mPFS reached 16.1 months, more than double the SOC benchmark. Overall survival (OS) was equally notable: median OS in repeat-dose patients was 19.5 months, compared to a historical SOC mOS of approximately 14.6 months in this patient population.

"These peer-reviewed results validate the scientific foundation of our DeltEx platform and highlight the transformative potential of γδ T cells in treating solid tumors," said William Ho, Chief Executive Officer and Co-founder of IN8bio. "Glioblastoma remains one of the most devastating cancers, and patients urgently need new treatment options. By enabling immune cells to remain active alongside conventional chemotherapy and delivering them directly to the tumor, DeltEx DRI is designed to drive meaningful synergies, improve patient outcomes, and change the treatment paradigm for this disease."

"Publication in The Journal of Clinical Oncology represents a significant milestone for this program and for the broader effort to bring effective immunotherapies to patients with glioblastoma," said Burt Nabors, M.D., Professor of Neurology, Director of Neuro-Oncology at the O’Neal Comprehensive Cancer Center at the University of Alabama at Birmingham, and lead investigator of the study. "This trial demonstrates that intracranial delivery of chemotherapy-resistant γδ T cells is feasible and well tolerated. The encouraging signals of prolonged disease control and absence of immune-mediated toxicity, particularly with repeated dosing, provide a compelling rationale for continued clinical development of this novel therapeutic approach."

Despite aggressive SOC treatment, residual tumor cells persist in nearly all GBM patients, a key reason the disease remains almost universally fatal. The DeltEx DRI technology directly addresses this challenge: γδ T cells are engineered to resist being killed by the chemotherapy that is administered concurrently, then delivered intracranially to the tumor site, where they can attack residual cancer cells and potentially achieve deeper, more durable tumor responses. These JCO-published results offer meaningful evidence that this strategy can extend disease control in these patients with significant unmet need and support its continued advancement as a potential new treatment paradigm for solid tumors. IN8bio expects to provide additional updates to the DeltEx DRI program in newly diagnosed GBM later this year.

About INB-200 and INB-400 (DeltEx Drug Resistant Immunotherapy)

INB-200 and INB-400 are an autologous, genetically modified gamma-delta T cell therapy engineered with an MGMT-expressing lentivector designed to resist alkylating chemotherapy. The therapy is administered intracranially and is intended to work in combination with temozolomide to target residual tumor cells, enhance immune activation, and prolong disease control in patients with glioblastoma.

(Press release, In8bio, JUL 9, 2026, View Source [SID1234669134])

On July 9, 2026 Confluence Genetics reported the launch of Cas-CLEAR, Collaterally Enhanced Activated Ribonuclease, a new CRISPR technology platform for the treatment of cancers carrying defined genetic signatures, with lead programs in development for hepatocellular carcinoma (HCC). Unlike gene editing CRISPR systems that cut and modify DNA at a single site, Cas-CLEAR uses Cas12a2 nucleases to recognize cancer-specific genetic signatures and trigger broad collateral cleavage of cellular DNA and RNA, resulting in the selective elimination of cells carrying the targeted signature. The launch coincides with two independent Nature publications validating the platform’s selective cancer cell-killing mechanism: a peer-reviewed publication from the laboratory of Nobel laureate Jennifer Doudna at the University of California, Berkeley featuring in vivo mouse model data, and another led by researchers at Utah State University and University of Utah Health.

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"For more than a decade, gene editing has defined how CRISPR is applied in cell and gene therapy, yet for cancer that approach has been slow to translate into treatments," said Matt Begemann, Senior Director of R&D at Confluence Genetics. "Cas-CLEAR works differently: instead of repairing or replacing a cancer-driving mutation, it uses that mutation as a recognition signal to eliminate the cells that carry it. With advances in precision medicine, cancer-specific signatures can now be identified patient by patient, and Cas-CLEAR is built to act on them. For indications like HBV-derived HCC, where the cancer carries a distinct genetic marker, that represents a meaningfully different mode of action for the cell and gene therapy field."

A new Nature publication "Targeting Cancer-Specific Mutations with RNA-Triggered Chromatin Shredding" by the laboratory of Nobel laureate Jennifer Doudna at the Innovative Genomics Institute (IGI) at UC Berkeley provides additional independent validation of Confluence’s SuCas12a2 nuclease for oncology applications. The study features SuCas12a2 throughout its main findings, including selective elimination of cells carrying mutations in the historically "undruggable" p53 tumor suppressor gene, and reports in vivo mouse model data in two cancer types: liver cancer, directly relevant to Confluence’s lead HCC program, and lung cancer.

In addition, the Nature publication "RNA-triggered cell killing with CRISPR-Cas12a2" characterized the cancer cell-killing mechanism across multiple Cas12a2 nucleases, including Confluence’s SuCas12a2. Led by researchers at Utah State University and University of Utah Health, the study demonstrated that SuCas12a2 can discriminate cancer cells carrying a single-base-pair KRAS mutation from non-cancerous cells. The findings provide independent peer-reviewed validation of the core mechanism Confluence Genetics is advancing through Cas-CLEAR for oncology applications.

Confluence Genetics holds foundational composition-of-matter and methods of use patents on Cas12a2 nucleases, including SuCas12a2 (U.S. Patent No. 9,896,696), supported by an extensive global patent portfolio of issued patents and pending applications.

Coinciding with today’s launch, Confluence Genetics scientists posted a preprint to bioRxiv [View Source characterizing nine newly discovered Cas12a2 nucleases. The work identifies a lead nuclease, designated RsCas12a2, with cytotoxic activity comparable to or exceeding that of SuCas12a2. The work also includes a second high-activity nuclease, SdCas12a2, which is designed to access target sites previously unreachable with SuCas12a2, including the S37 CTNNB1 hotspot mutation associated with hepatocellular carcinoma. Hepatocellular carcinoma is one of the leading causes of cancer-related death worldwide, with limited treatment options for advanced disease. Hotspot mutations in CTNNB1 and HBV-derived HCC account for a substantial share of liver cancer globally and present a particularly clear cancer-specific genetic signature for Cas-CLEAR recognition. RsCas12a2 and related nucleases are covered by additional patent applications, including U.S. Patent Application No. 2026/0085301.

About Cas-CLEAR

Cas-CLEAR is a CRISPR-based oncology platform that uses Cas12a2 nucleases to eliminate cancer cells carrying cancer-specific genetic signatures while sparing healthy cells. The Cas-CLEAR mechanism was discovered and patented by Confluence Genetics scientists and originally characterized in bacteria before being extended to human cancer cell systems. The mechanism of action has now been described in four peer-reviewed Nature publications (Bravo et al., 2023; Dmytrenko et al., 2023; Scholz et al., 2026; Zeng et al., 2026). The Cas-CLEAR platform is built on foundational composition-of-matter and methods of use patents originally developed by Confluence Genetics scientists. Lead programs are in development for the treatment of hepatocellular carcinoma (HCC), including HBV-derived HCC.

Confluence Genetics is actively seeking co-development partners for Cas-CLEAR oncology programs and for plant defense applications of the underlying Cas12a2 nuclease technology, which is also available for full licensing in antimicrobial development and molecular diagnostics. For more information, visit cas-clear.com.

(Press release, Confluence Genetics, JUL 9, 2026, View Source [SID1234669133])