On July 27, 2026 Oryzon Genomics, S.A. (ISIN Code: ES0167733015, ORY), a clinical-stage biopharmaceutical company and a global leader in epigenetics, reported financial results for the three months ended June 30, 2026, and provided a corporate update on recent developments.

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"During the second quarter of 2026, Oryzon reported important clinical progress while strengthening our financial position," said Dr. Carlos Buesa, Oryzon’s Chief Executive Officer. "At the European Hematology Association (EHA) (Free EHA Whitepaper) conference, we presented updated results from the ALICE-2 and FRIDA trials that further support the potential of iadademstat in AML. In first-line AML, the triplet combination of iadademstat with azacitidine and venetoclax continues to demonstrate a highly competitive efficacy profile, including encouraging activity in patients with adverse genetic backgrounds, while maintaining a favorable and manageable safety profile. We are also encouraged by the proportion of patients who have been able to proceed to allogeneic hematopoietic cell transplantation, a potentially curative treatment option that may contribute to improved long-term outcomes. We believe the ALICE-2 results compare favorably with those reported for other emerging triplet regimens and further reinforce the differentiated positioning of iadademstat in this setting."

"We expect to present final data from ALICE-2 and FRIDA by year-end," Dr. Buesa continued. "Subject to confirmation of the current efficacy and safety findings in the final ALICE-2 dataset, we remain on track to engage with the FDA on the design of a potentially registrational study in first-line AML, with the objective of initiating the trial in 2027. We also see iadademstat as an increasingly diversified asset across oncology and hematology, having enrolled the first patient in the IDEAL Phase II trial in essential thrombocythemia."

"We continue to advance vafidemstat toward a Phase III trial in aggression in borderline personality disorder (BPD), as well as a new Phase II trial in aggression in autism spectrum disorder (ASD), while enrollment progresses in the ongoing Phase IIb trial in schizophrenia", Dr. Buesa added. "The recent grant of a U.S. patent significantly extends our IP protection for vafidemstat in BPD and strengthens our longterm development plans for the asset."

"To support our pipeline through the clinical catalysts expected this year and beyond, we raised €12 million through a recent capital increase and entered into a financing agreement with the Social Impact Fund managed by COFIDES," Dr. Buesa concluded. "Under the agreement, the Fund has committed to invest €25 million in future capital increases to support Oryzon’s mental health programs, subject to certain conditions. These additional resources provide us with greater financial flexibility as we work to translate our innovative epigenetic therapies into clinical benefit for patients and long-term value for our stakeholders."

Second Quarter and Recent Highlights

Iadademstat:

Oryzon shared updated positive data from the ongoing ALICE-2 (NCT06357182) Phase Ib clinical trial of iadademstat in combination with azacitidine and venetoclax in patients with newly diagnosed AML at the EHA (Free EHA Whitepaper) 2026 Congress. As reported, the iadademstat-azacitidine-venetoclax triplet combination demonstrated high levels of clinical activity and continued to exhibit a favorable safety profile. Among evaluable patients (n=18), a 100% (18/18) overall response rate (ORR), an 89% (16/18) composite complete remission (CRc) rate and a 78% (14/18) complete response (CR) rate were observed. CRs occurred early, most of them in cycle 1. Efficacy was observed across different genomic risk groups, including TP53 and RAS pathway mutations and patients with complex karyotypes, all considered adverse risk: patients with TP53-mutated disease (2/2) attained CR and showed a reduction in TP53 variant allele frequency (14% to undetected and 22% to 1%, respectively), and patients with RAS pathway mutations (3/3) achieved CR. After a median followup of 8 months, median overall survival (OS) and event-free survival (EFS) were not reached; estimated 12-month OS and EFS were 79% and 71%, respectively. Additionally, 9 patients successfully transitioned to allogeneic HCT, with an estimated 12-month OS of 88%. This investigator-initiated study (IIS) is led by the Oregon Health & Science University (OHSU) Knight Cancer Institute and continues to actively enroll patients. The trial aims to enroll 21 evaluable patients; the 18 evaluable patients reported at EHA (Free EHA Whitepaper) represent around 85% of the target enrollment.

Updated positive data from the fully enrolled Phase Ib FRIDA (NCT05546580) clinical trial of iadademstat in combination with gilteritinib in patients with relapsed or refractory (R/R) FLT3-mutated AML were also presented at EHA (Free EHA Whitepaper) 2026. Updated data from the expansion cohort at the selected pharmacological active dose (PAD, 75 μg iadademstat) included 18 patients evaluable for response. The iadademstat+gilteritinib combination showed a favorable safety profile and a CRc rate of 67% (12/18) in a heavily pre-treated patient population. These results compare favorably with gilteritinib monotherapy responses in contemporary real‑world cohorts enriched for heavily pre‑treated patients, which are reported to be 28% CR+CRi.

Enrollment has continued across additional ongoing iadademstat clinical studies, conducted under the Cooperative Research and Development Agreement (CRADA) with the U.S. National Cancer Institute (NCI) in first-line AML, myeloproliferative neoplasms and extensive-disease small cell lung cancer (ED-SCLC), as well as investigator-initiated studies in myelodysplastic syndrome and EDSCLC.

Oryzon has initiated and enrolled the first patient in the IDEAL Phase II trial to evaluate iadademstat in adult patients with essential thrombocythemia (ET) who are resistant/intolerant to hydroxyurea. The study is designed to evaluate the safety, tolerability and clinical activity of iadademstat, including its efficacy in reducing the percentage of adult ET patients with abnormal platelet counts. Iadademstat will be administered for up to 24 weeks, with an additional 24-week extension period available for those benefiting from treatment.

Oryzon continues to advance the RESTORE Phase Ib trial of iadademstat in adult patients with sickle cell disease (SCD). The study will evaluate the safety and tolerability of iadademstat, establish the Recommended Phase II dose (RP2D), and investigate iadademstat’s effect on inducing fetal hemoglobin (HbF) expression, a clinically meaningful endpoint in SCD. The trial is actively enrolling patients.

Vafidemstat:

Oryzon continues active regulatory and development activities to support the advancement of the Phase III PORTICO-2 trial with vafidemstat in aggression in BPD. Following receipt of written FDA feedback regarding study endpoints and certain non-clinical considerations, the Company is actively generating additional supporting information and protocol refinements required for resubmission. These activities include qualitative research and endpoint-validation work intended to further support the proposed clinical outcome measures.
Patient enrollment is ongoing in the EVOLUTION Phase IIb trial of vafidemstat in schizophrenia. The study is primarily assessing its effects on negative symptoms, with cognitive impairment and positive symptoms included as secondary endpoints. Initially launched in Spain, EVOLUTION is being extended to additional European countries (Bulgaria, Poland, Romania and Slovakia).
Oryzon is finalizing preparations for the HOPE-2 Phase II study of vafidemstat for the treatment of aggression in autism spectrum disorder (ASD). The trial will focus on genetically-defined ASD subpopulations, in particular individuals with Phelan-McDermid syndrome (PMS). The study will initially be conducted in Spain and forms part of the activities supported by the Med4Cure IPCEI EU initiative.
Oryzon continues to reinforce its IP portfolio for vafidemstat, as the United States Patent and Trademark Office (USPTO) recently granted U.S. Patent No. 12,673,044, entitled "Methods of treating borderline personality disorder". The granted claims cover methods of treating non-aggressive symptoms of borderline personality disorder (BPD) using LSD1 inhibitors, including vafidemstat, complementing Oryzon’s patent portfolio covering the treatment of aggression. The patent is expected to expire in March 2043, including 1,095 days of Patent Term Adjustment (PTA) awarded by the USPTO to compensate for delays during patent prosecution. This estimate does not include any potential Patent Term Extension (PTE) that may become available following regulatory review, if applicable. A corresponding patent application has also been allowed in Canada.
Earlier stage programs:

ORY-4001, Oryzon’s highly selective histone deacetylase 6 (HDAC6) inhibitor for neurological disorders, continues IND-enabling studies to enable future clinical trials. The program remains focused on potential applications in Amyotrophic Lateral Sclerosis (ALS), Charcot-Marie-Tooth disease (CMT) and other neurological disorders.
Financial Update: First half 2026 Financial Results

Research and development (R&D) expenses were $6.3 million and 11.4 million for the quarter and six months ended June 30th, 2026, compared to $3.0 and $5.8 million for the quarter and six months ended June 30th, 2025.

General and administrative expenses were $1.3 and $2.8 million for the quarter and six months ended June 30th, 2026, compared to $1.4 and $2.7 million for the quarter and six months ended June 30th, 2025.

Net losses were $1.6 and $3.6 million for the quarter and six months ended June 30th, 2026, compared to $1.7 and $3.4 million for the quarter and six months ended June 30th, 2025. The result is as expected, given the biotechnology business model where companies in the development phase typically have a long-term maturation period for products and do not have recurrent income.

Negative net result was $1.6 million (–$0.02 per share) for the six months ended June 30th, 2026, compared to a negative net result of $1.8 million (–$0.03 per share) for the six months ended June 30th, 2025.

Cash, cash equivalents, and marketable securities totaled $16.7 million (€14.7 million) as of June 30, 2026.

After quarter-end, Oryzon raised gross proceeds of €12.0 million ($13.7 million) through a capital increase, without the issuance of warrants, as announced on July 1, 2026.

On the same date, the Company announced that it had entered into a share subscription agreement with the Social Impact Fund, managed by Compañía Española de Financiación del Desarrollo (COFIDES), an entity attached to the Spanish Ministry of Inclusion, Social Security and Migration. Under the agreement, the Social Impact Fund has committed, as an anchor investor, to subscribe for newly issued Oryzon shares in a future financing for an aggregate investment of €25 million, subject to the satisfaction of certain corporate, financial, business, and social impact-related conditions.

(Press release, Oryzon, JUL 27, 2026, View Source;utm_medium=email&utm_campaign=NdP.20+27-07-2026+Resultados+2Q26+ENG842 [SID1234669435])

On July 27, 2026 VERAXA Biotech AG (NASDAQ: VRXA; "VERAXA" or the "Company"), an emerging leader in designing novel cancer therapies, reported the advancement of bispecific ADC (bsADC) program VXA-222, following successful achievement of a key technical milestone in its alliance with OmniAb, Inc. (NASDAQ: OABI, "OmniAb"). The program is moving into its next collaboration phase with OmniAb’s discovery work successfully concluded. VXA-222 utilizes an "AND-gate" logic to address two different target antigens present on solid tumors with one molecule. Established in May 2025, the alliance and joint discovery collaboration brought together OmniAb’s cutting-edge suite of transgenic antibody discovery solutions and screening technologies with VERAXA’s proprietary antibody drug conjugate (ADC) linker technology and conjugation expertise to support next-generation therapeutic discovery.

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"We are pleased to announce this important achievement and the advancement of this program from our alliance with OmniAb for the development of a novel AND-gated bsADC utilizing our conjugation and linker technology," commented Christoph Erkel, Ph.D., Chief Scientific Officer of VERAXA. "This successful partnership has united two highly complementary technologies to establish a new therapeutic candidate in VXA-222, representing a powerful opportunity for a best-in-class bispecific ADC to address solid tumor indications with high unmet medical need. We look forward to advancing this program and acknowledge OmniAb’s partnership and contributions in delivering a diverse set of highly promising antibodies."

Under the terms of the May 2025 agreement, VERAXA initiated a novel bsADC program addressing two attractive target molecules in cancer medicine. The Company utilized OmniAb’s suite of transgenic antibody discovery solutions, including OmniClic, a common light-chain transgenic chicken developed to facilitate the generation of bispecific antibodies, to source high-quality human antibody leads, which are naturally optimized through in vivo affinity maturation. VERAXA will subsequently establish the bsADC lead candidate by applying its proprietary linker technology and conjugation routine and will be responsible for in vitro and in vivo validation. VERAXA holds exclusive rights to develop and commercialize products incorporating the OmniAb-derived antibodies under the collaboration, with OmniAb entitled to a share of specified revenue generated from those products.

"We’re delighted to see this bispecific ADC program cross this important threshold," said Bill Harriman, Ph.D., Senior Vice President of Discovery Partnership Management and Technology Development and Operations at OmniAb. "Continuation of the discovery phase at VERAXA underscores the productive collaboration and alliance between our scientific and business teams, and highlights the complementary strengths of OmniAb’s technologies and VERAXA’s expertise in ADC conjugation and development. We look forward to seeing our partners at VERAXA advance this exciting program."

(Press release, Veraxa Biotech, JUL 27, 2026, View Source [SID1234669450])

On July 27, 2026 Akeso, Inc. (9926.HK) ("Akeso" or the "Company") reported that the first patient has been dosed in a Phase Ib/II clinical study (AK138D1-201) evaluating its internally developed next-generation differentiated HER3 ADC, AK138D1, as monotherapy or in combination with ivonescimab (PD-1/VEGF bispecific antibody) for advanced non-small cell lung cancer (NSCLC).

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The study aims to evaluate the potential of Akeso’s IO2.0 + ADC2.0 regimen across multiple settings in advanced NSCLC, including: first-line treatment, treatment after EGFR-TKI resistance, and treatment after immuno-chemotherapy resistance.

HER3 expression is strongly linked to the development, progression, and treatment resistance in patients with NSCLC. Traditional HER3 ADCs have faced limitations in clinical use due to toxicity concerns, and none have been approved to date. Akeso designed the next-generation HER3 ADC, AK138D1, with an unique and innovative approach that minimizes uptake in normal tissues to reduce off-target toxicity and broaden the therapeutic window. This approach also prevents surface aggregation on tumor cells to improve deep and uniform tumor penetration, effectively overcoming the binding site barrier. Early clinical studies conducted in China and Australia have demonstrated that AK138D1 monotherapy delivers potent anti-tumor activity in patients with lung cancer, along with a favorable safety profile featuring low hematologic toxicity and no reported cases of interstitial lung disease (ILD).

Ivonescimab, a first-in-class PD-1/VEGF bispecific antibody, has shown strong clinical results compared to PD-1 inhibitor-based therapies across multiple Phase III studies. The combination of AK138D1 with ivonescimab is expected to further amplify ivonescimab’s immune-activating effects. This combination enables ivonescimab to exert synergistic anti-tumor activity with the next-generation HER3 ADC, potentially delivering superior clinical efficacy across various NSCLC subtypes while maintaining a favorable safety profile.

Leveraging its technological leadership in bispecific and multi-specific antibodies, Akeso is systematically building a comprehensive global IO2.0 + ADC2.0 therapeutic matrix.

In the immuno-oncology field, Akeso has two approved bispecific antibodies for cancer treatment. The Company is actively evaluating ivonescimab and cadonilimab in combination with the Company’s proprietary next-generation ADC candidates. Increasingly, global partners recognize both ivonescimab and cadonilimab as preferred agents for combination regimens and breakthrough therapy explorations across a wide spectrum of tumor types.

In the ADC space, Akeso has built a differentiated pipeline of next-generation candidates, including AK146D1 and AK138D1, both of which have entered into Phase II clinical studies, and AK157D1 and AK158D1 (a bispecific ADC), both of which will soon enter clinical studies.

Currently, multiple Phase II clinical studies are underway evaluating ivonescimab and cadonilimab in combination with AK138D1, AK146D1, and other assets. These combination studies from Akeso’s own approved therapies and pipelines continue to drive global treatment paradigms upgrades for major malignancies, including lung cancer and breast cancer.

About AK138D1
Injectable AK138D1 is a HER3-targeted antibody-drug conjugate (ADC), with a fully humanized anti-HER3 IgG1 antibody, patritumab. It is conjugated to the topoisomerase I inhibitor DXd through a cleavable linker, MC-AAA (maleimide-alanine-alanine-alanine). After binding to HER3 on tumor cells, the ADC is internalized into the tumor cells, where the linker is cleaved, releasing the membrane-permeable DXd. This leads to DNA damage and subsequent cell apoptosis. Early study results have shown that AK138D1 possesses potent biological activity and a favorable safety profile. A phase II clinical trial is currently ongoing to investigate AK138D1 combined with cadonilimab and ivonescimab in patients with solid tumors. This regimen is a critical part of Akeso’s IO2.0 + ADC 2.0 combination approach.

(Press release, Akeso Biopharma, JUL 27, 2026, View Source;adc2-0-strategy-makes-another-advancement-first-patient-dosed-in-phase-ibii-study-of-her3-adc-ak138d1-combined-with-ivonescimab-in-lung-cancer-302835843.html [SID1234669436])

On July 27, 2026 Insilico Medicine ("Insilico", HKEX:3696), a clinical-stage, generative AI-driven drug discovery company, reported that first-in-human Phase 1 trial data for ISM6331, its novel AI-designed pan-TEAD inhibitor, has been accepted for a Rapid Oral presentation at the European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) Congress 2026, taking place October 23–27, 2026, in Madrid, Spain.

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"TEAD has long been recognized as an attractive target in hard-to-treat solid tumors, but small-molecule inhibition has historically posed significant design challenges, said Feng Ren, Ph.D., Co-CEO and Chief Scientific Officer of Insilico Medicine. "The selection of ISM6331 for a Rapid Oral presentation at ESMO (Free ESMO Whitepaper) 2026 highlights the potential of our AI-generated platform to target complex oncogenic drivers like the Hippo pathway and represents a promising pan-TEAD approach that we are eager to share with the community."

Details of the Rapid Oral Presentation

Title: First-in-human Multicenter Phase 1 Study of ISM6331, an AI-Designed Pan-TEAD Inhibitor, in Patients with Mesothelioma or Other Advanced Solid Tumors
Abstract Number: #997
Session Name: Rapid Oral Presentation: Developmental Therapeutic
Location: Cordoba Auditorium – Hall 4
Date/Time: Sunday 25.10.2026 08:30 – 10:00
"Presenting our first-in-human Phase 1 study at ESMO (Free ESMO Whitepaper) marks an important clinical milestone for ISM6331," said Halle Zhang, Ph.D., Vice President, Clinical Development – Oncology at Insilico Medicine. "Patients with advanced mesothelioma and other Hippo-driven solid tumors face limited therapeutic options. These preliminary clinical findings provide early encouragement as we evaluate ISM6331’s safety, pharmacokinetics, and initial antitumor activity to inform our ongoing clinical development strategies."

About ISM6331

ISM6331 is a novel, potent, small-molecule pan-TEAD inhibitor discovered and designed using Insilico Medicine’s proprietary generative AI-powered drug discovery platform, Chemistry42. The molecule targets TEAD transcription factors, the principal downstream effectors of the Hippo signaling pathway, a critical regulator of cell proliferation, survival, tissue homeostasis, and therapeutic resistance across a broad range of solid tumors. Although the Hippo pathway has long been recognized as a promising therapeutic target in oncology, developing effective small-molecule TEAD inhibitors has remained a significant medicinal chemistry challenge. ISM6331 was designed to selectively inhibit pan-TEAD activity and is being evaluated in a global, multicenter Phase 1 clinical trial in patients with malignant mesothelioma and other advanced solid tumors. The study is assessing ISM6331 safety, tolerability, pharmacokinetics, and preliminary antitumor activity to inform its continued clinical development.

(Press release, Insilico Medicine, JUL 27, 2026, View Source [SID1234669437])

On July 27, 2026 IDEAYA Biosciences, Inc. (NASDAQ: IDYA), a leading precision medicine oncology company, reported that initiation of Part 2 monotherapy expansion has been achieved in its Phase 1/2 clinical trial evaluating IDE892, a potential best-in-class methylthioadenosine (MTA)-cooperative inhibitor of PRMT5, in MTAP-deleted solid tumors, with a focus on non-small cell lung cancer (NSCLC) and pancreatic ductal adenocarcinoma (PDAC). IDE892 Phase 1/2 monotherapy expansion has been initiated at projected efficacious target human exposures where 24-hours target EC90 coverage have been achieved. The IDE892 maximum tolerated dose (MTD) has not yet been reached in the ongoing dose escalation.

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"We are excited to initiate monotherapy expansion evaluating IDE892 in MTAP-deleted PDAC and NSCLC. We designed IDE892 to be a potential best-in-class PRMT5 inhibitor, including approximately 1,400-fold selective MTA-PRMT5 cooperative binding versus SAM-PRMT5 cooperative binding, lack of brain penetrance, and favorable drug-like properties intended to maximize its therapeutic window as both a monotherapy agent and in combination. We are well positioned to have the industry’s deepest MTAP-deletion pipeline, with IDE892, MAT2A inhibitor IDE397 in Phase 2, and the potential first-in-class CDKN2A lead molecule advancing in preclinical toxicology studies for a target IND in the first half of 2027," said Yujiro S. Hata, President and Chief Executive Officer, IDEAYA Biosciences.

Loss of MTAP leads to the accumulation of MTA and increased dependence on PRMT5 and MAT2A, two key enzymes involved in methylation and RNA splicing. In MTAP-deleted tumors, this biology establishes a robust synthetic lethal vulnerability that underpins the mechanistic rationale for combining IDE892 and IDE397, where the first-patient-in (FPI) was achieved in mid-2026. IDEAYA also entered into a clinical collaboration with Roche evaluating IDE892 in combination with RG6505, Roche’s Phase 1 pan-RAS inhibitor, in MTAP-deleted pancreatic ductal adenocarcinoma (PDAC) to target the genetic co-alterations of MTAP and KRAS in this indication. Next, IDEAYA is advancing a third proprietary and potential first-in-class program for MTAP-deleted solid tumors targeting CDKN2A, the most common co-alteration of MTAP-deletion, through ongoing preclinical toxicology studies to support an investigational new drug (IND) application in the first half of 2027. IDEAYA anticipates that rational combination doublets may be pursued with IDEAYA’s CDKN2A lead molecule and IDE892 to target the co-alterations of MTAP and CDKN2A, and pan-RAS inhibitors, as the key tumor suppressor gene CDKN2A has been reported to be deficient in approximately 70% of PDAC.

MTAP deletion is estimated to occur in approximately 15% of all solid tumors, including 15 to 20% of NSCLC and up to 40% of PDAC. There are no approved therapies for MTAP-deleted cancers, highlighting the significant unmet need and opportunity for new precision therapies for these patients.

IDE892 has potential best-in-class properties, including approximately 1,400-fold selective MTA-PRMT5 cooperative binding versus SAM-PRMT5 cooperative binding and lack of brain penetrance intended to maximize its therapeutic window, and favorable drug-like properties to enable rational combinations with IDE397, pan-RAS inhibitors, KRAS G12D therapies, and IDEAYA’s CDKN2A lead molecule. IDE892 has a CYP3A4 IC50 greater than 45 micromolar and did not show time dependent inhibition of any of the 7 major cytochrome P450s (CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP3A4) based on full kinetic CYP inactivation assays, positioning IDE892 as a potential best-in-class MTA-cooperative PRMT5 combination partner.

(Press release, Ideaya Biosciences, JUL 27, 2026, View Source [SID1234669438])