On June 11, 2026 Vivoryon Therapeutics N.V. (Euronext Amsterdam: VVY; NL00150002Q7) (Vivoryon), a clinical stage company developing small molecule medicines for inflammatory and fibrotic disorders, with a primary focus on kidney diseases, reported financial results for the three-month period ended March 31, 2026, and provided a corporate update.

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"In Q1 2026 our focus remained on strategic discussions with potential partners to support the Phase 2b development of varoglutamstat in advanced DKD. We continue to make substantial progress and remain actively engaged with multiple parties who, like us, understand the need for disease-modifying therapeutics that could improve or stabilize kidney function," said Frank Weber, MD, CEO of Vivoryon. "We have consistently shown that varoglutamstat improves kidney function in elderly patients, in particular those with diabetes, and have established a large pre-clinical and clinical data set to de-risk the planned Phase 2b program. Taken together, these data give us further confidence that, through its differentiated mechanism of action targeting fibrotic and inflammatory pathways, varoglutamstat could have a transformative role in preventing progression of life-limiting kidney diseases."

Q1 2026 and Post-Period Updates

Strategic Priorities
Vivoryon’s key strategic priority for 2026 is to secure the funding necessary to advance varoglutamstat into a Phase 2b clinical study in patients with advanced DKD stage 3b/4 in order to confirm the compelling data observed in the VIVIAD and VIVA-MIND studies. Throughout the reporting period and recent months, the Company has continued to engage in active discussions and due diligence under CDA with multiple potential biopharma partners and strategic investors.

Varoglutamstat Program

Vivoryon’s varoglutamstat Phase 2 program has shown highly consistent, statistically significant and clinically meaningful improvement of kidney function (eGFR) versus placebo in two independent randomized double-blind placebo-controlled studies, VIVIAD and VIVA-MIND. The Company is planning to confirm these results in a dedicated Phase 2b clinical study in patients with DKD stage 3b/4. Initiation of the Phase 2b and all future studies is subject to additional funding and/or partnership, which Vivoryon continues to actively explore.

On March 28, 2026, Vivoryon presented a poster at the World Congress of Nephrology (WCN) in Yokohama, Japan, providing an update on the growing body of evidence validating glutaminyl cyclases (QPCT/L) as promising targets in DKD. The analyses underscored previous reports showing that the effect of varoglutamstat on eGFR observed in VIVIAD and VIVA-MIND was greater in elderly participants with diabetes compared to elderly participants without diabetes. In participants with diabetes and lower baseline eGFR (mean 60 mL/min/1.73m2), the effect size was comparable or higher than in the total population of participants with diabetes. Additionally, analysis of data from a DKD mouse model showed significant improvements of inflammation, glomerulosclerosis and kidney function. These results further support Vivoryon’s rationale for a dedicated Phase 2b clinical study in patients with advanced DKD stage 3b/4.
The Company has actively expanded the pre-clinical data set around varoglutamstat’s mechanism of action (MOA) and recent studies have further elucidated the molecular mechanisms underlying the substantial benefits reported from the VIVIAD and VIVA-MIND studies. On April 22, 2026, the Company published on its website a pre-recorded webcast contextualizing these new data. The webcast includes new data on the role of QPCT and QPCTL in inflammation and fibrosis, including revealing their newly discovered role in collagen maturation, the disruption of which is a key factor in fibrosis, as well as new data on the existing medical need in kidney disease and the positive effect of varoglutamstat treatment on specialized blood-filtering kidney cells (podocytes). The webcast is available here:
View Source
Proposed clinical development plan in DKD
The Company is planning to conduct a randomized, placebo-controlled Phase 2b study in patients with advanced DKD stage 3b/4 to confirm the compelling effects of varoglutamstat on kidney function observed in the VIVAD and VIVA-MIND Phase 2 studies in elderly patients. Initiation of the Phase 2b and all future studies is subject to additional funding and/or partnership, which Vivoryon continues to actively explore.

Financial Results for the First Quarter of 2026

No Revenues were generated in the three months ended March 31, 2026.

Research and development expenses decreased by EUR 0.3 million to EUR 0.9 million in the three months ended March 31, 2026, compared to EUR 1.2 million in the three months ended March 31, 2025. This decrease is primarily attributable to EUR 0.2 million lower third-party expenses due to the ramp-down of the Phase 2b clinical studies VIVIAD and VIVA-MIND, reflecting EUR 0.1 million lower clinical costs and EUR 0.1 million lower manufacturing costs.

General and administrative expenses were EUR 0.9 million in the three months ended March 31, 2026, compared to EUR 1.3 million in the three months ended March 31, 2025. The EUR 0.4 million decrease was primarily attributable to lower personnel expenses of EUR 0.2 million and reduced legal costs of EUR 0.2 million. The decline in personnel expenses was mainly due to a EUR 0.2 million reduction in share-based payment expenses.

The net loss for the three months ended March 31, 2026 was EUR 1.8 million compared to EUR 2.5 million for the three months ended March 31, 2025.

As of March 31, 2026, Vivoryon held cash and cash equivalents of EUR 4.0 million compared to cash and cash equivalents of EUR 5.6 million as of December 31, 2025.

Outlook & financial guidance

As published on April 23, 2026, the issuance date of its annual Financial Statements 2025, the Company expects, based on its most recent financial and business plan, that its existing cash and cash equivalents will be sufficient to fund its operating plans into the fourth quarter of 2026, subject to the occurrence of unforeseen circumstances and without taking into account any funds from the SEPA as well as other potential additional financing transactions, if any.

This cash runway guidance reflects an overall reduction in cash utilization while prudently investing in preparing to execute on the Company’s kidney disease strategy. The initiation of the Phase 2b DKD study and all future studies is subject to further additional funding and/or partnership, which the Company continues to actively explore.

The viability of the Company’s business beyond its current guidance is dependent on its ability to raise additional funds to finance its operations which also depends on the success of its research and development activities such as those focusing on exploring opportunities in kidney disease.

The Company expects to have continued operating losses for the foreseeable future and the need to raise additional capital to finance its future operations. The Company has concluded that the ability to continue as a going concern in the financial year 2026, as stated in the Company‘s Annual Report 2025 published on April 23, 2026, depends on the ability to generate additional funding. Please refer to the Company’s Annual Report 2025 for further information.

Conference call and webcast

The Company’s next financial and business update conference call / webcast will be held in conjunction with the publication of its H1 results, anticipated in August.

(Press release, Vivoryon Therapeutics, JUN 11, 2026, View Source [SID1234666572])

On June 11, 2026 Silence Therapeutics plc (Nasdaq: SLN), a global clinical-stage biotechnology company developing novel siRNA (short interfering RNA) therapies, reported follow-up and quality-of-life data from the Phase 1 SANRECO study evaluating divesiran, a first-in-class siRNA therapy targeting TMPRSS6, in 21 phlebotomy-dependent patients with polycythemia vera (PV) at the European Hematology Association (EHA) (Free EHA Whitepaper) 2026 Annual Congress.

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Divesiran data presented at EHA (Free EHA Whitepaper) show improvements in PV-related symptoms and quality-of-life, complementing the substantial reductions in phlebotomy use as previously reported. Additional analyses also showed substantial reductions in phlebotomy use persisted well beyond the final dose.

"Data presented at EHA (Free EHA Whitepaper) continue to reinforce divesiran’s potential to transform the treatment paradigm for patients with polycythemia vera," said Curtis Rambaran, MD, Chief Medical Officer at Silence Therapeutics. "In Phase 1, we observed sustained hematocrit control, symptom improvement, and robust and durable reductions in phlebotomy burden, which persisted after the final dose. These findings further support the potential for less frequent dosing, including the Q12W regimen being evaluated in our ongoing Phase 2 SANRECO study, and we look forward to reporting topline results in August 2026."

Key EHA (Free EHA Whitepaper) 2026 Data Highlights

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In the six months prior to treatment, the 21 enrolled patients required a total of 80 phlebotomies. During the active treatment period, only 5 phlebotomies were required, all occurring in patients classified as "uncontrolled" at baseline with HCT levels greater than 45%.
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During the 16-week follow-up period after the final dose, only 4 phlebotomies were reported, supporting the prolonged duration of divesiran’s effect.
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Among 14 patients with further follow-up data, the median time to first phlebotomy was 287 days.
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The majority of patients experienced improvements in MPN-10 total symptom scores from baseline through Week 34, indicating potential improvements in disease-related symptoms and overall quality of life.
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Divesiran was well tolerated, with no dose-limiting toxicities observed. The most common treatment-emergent adverse events (TEAEs) were mild and transient injection-site reactions. No treatment-related serious adverse events or TEAEs leading to discontinuation were reported.

The 2026 EHA (Free EHA Whitepaper) poster presentation is linked here.

The ongoing Phase 2 SANRECO study (NCT05499013) is evaluating divesiran using Q6W and Q12W dosing regimens in patients with PV. Topline data are expected in August 2026.

SANRECO Phase 1 Study Design

The Phase 1 portion of SANRECO was a 34-week, open-label study evaluating divesiran (3 mg/kg, 6 mg/kg and 9 mg/kg) administered subcutaneously (s.c.) Q6W for four doses, with a 16-week follow-up period following the date of the last administered dose in 21 PV patients. Key inclusion criteria included a PV diagnosis and a history of requiring at least three phlebotomies in the last six months or five in the last year prior to screening. Patients were allowed to be on stable doses of cytoreductive agents. Given the exploratory nature of this Phase 1 study, both well-controlled patients – defined as those with HCT levels ≤ 45% – as well as those with HCT levels > 45% at baseline on current standard-of-care treatment were enrolled.

SANRECO Phase 2 Study Design

The Phase 2 portion of SANRECO is an ongoing, three-part, global, randomized, placebo-controlled, double-blind study evaluating divesiran in 48 phlebotomy-dependent PV patients. The trial is evaluating the safety and efficacy of divesiran 6 mg administered s.c. Q6W or Q12W in patients with uncontrolled HCT who are phlebotomy-dependent despite standard-of-care treatment which could include hydroxyurea, interferon and/or ruxolitinib. The primary endpoint of the study is the proportion of patients achieving a response during weeks 18-36, which is defined as the absence of "phlebotomy eligibility." To meet phlebotomy eligibility, patients in the study are required to have HCT ≥ 45%. Following the placebo-controlled portion of the trial, patients enter the 3-year, double-blind and open label extension periods.

About PV

PV is a rare, myeloproliferative neoplasm – a type of blood cancer – characterized by the excessive production of red blood cells, often resulting in elevated hematocrit levels. Elevated hematocrit above 45-percent is associated with a four-times higher rate of death from cardiovascular and thrombotic events. PV is associated with a range of burdensome symptoms including fatigue, cognitive disturbance and pruritus and additionally, longer term can transform to myelofibrosis and Acute Myeloid Leukemia. The aim of treatment is to maintain hematocrit less than 45%, a level that is associated with a reduced incidence of thrombosis and CV-associated death. The current standard of care includes repeated phlebotomies to reduce hematocrit and/or cytoreductive agents to reduce red blood cell production. There are currently no approved therapies that specifically target red blood cells and hematocrit.

About Divesiran

Divesiran is Silence’s wholly owned siRNA product candidate developed from its proprietary mRNAi GOLD platform that "silences" TMPRSS6 expressed almost exclusively in the liver. TMPRSS6 is a negative regulator of hepcidin, the body’s master regulator of iron metabolism including its absorption, distribution, and storage. By silencing TMPRSS6 in PV patients, divesiran aims to increase hepcidin production and release by liver hepatocytes, leading to the restriction of iron to the bone marrow and, thus, reducing the excessive production of red blood cells, a process dependent on availability of iron. Divesiran is currently in Phase 2 development for PV and has FDA Fast Track and Orphan Drug designations for PV.

(Press release, Silence Therapeutics, JUN 11, 2026, View Source [SID1234666571])

On June 11, 2026 Purple Biotech Ltd. ("Purple Biotech" or the "Company") (NASDAQ/TASE: PPBT), a clinical-stage oncology company developing a next-generation immunotherapy platform designed to maximize anti-cancer potency while minimizing toxicity, reported the presentation of new preclinical data from its lead CAPTN-3 program, IM1240, at the European Association for Cancer Research (EACR) 2026 Annual Congress, being held June 8-11, 2026, in Budapest, Hungary.

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A non-GLP toxicology study in NHPs validates the CAPTN-3 masking strategy and supports the planned advancement of IM1240 toward a first-in-human clinical study in 2027. Additionally, efficacy data in patient-derived samples from PD-1-resistant head and neck squamous cell carcinoma (HNSCC) metastatic lymph nodes, NSCLC and bladder cancer, generated in collaboration with the laboratory of Dr. Amir Horowitz at the Tisch Cancer Institute at the Icahn School of Medicine at Mount Sinai, highlight the essential role of the NKG2A arm in IM1240-mediated anti-tumor immunity and further strengthen CAPTN-3’s differentiation and clinical potential.

Poster Title: Toxicology study results in NHP validated improved PK and safety profile of CAPTN-3 masking design, revealing an extended therapeutic window

Abstract: EACR26-0695

Session: Immunotherapy

Date: Wednesday, June 10, 2026

Summary of data presented at EACR 2026:

● IM1240 induced apoptosis of PD-1-resistant patient-derived biopsies from six HNSCC metastatic lymph node samples and one enfortumab vedotin/pembrolizumab-resistant muscle-invasive bladder cancer sample, with both the CD3 and NKG2A functional arms required for full activity.

● In a PD-1/chemotherapy-resistant NSCLC patient-derived explant, IM1240 induced mature tertiary lymphoid structures (TLS) – immune cell organizations associated with effective anti-tumor immunity and favorable clinical prognosis – while increasing CD8 T cell and NK cell abundance and reducing regulatory T cells (Tregs) and tumor cells. These effects were not observed with IM1340, the NKG2A loss-of-function variant, underscoring the essential and differentiated contribution of the NKG2A arm.

● In a non-GLP dose-range finding toxicology study in NHPs, IM1240 demonstrated markedly superior pharmacokinetics (PK) compared to the non-capped variant IM1222, including an approximately 8-fold longer half-life and 16-fold greater systemic exposure. IM1240 showed dose-proportional PK with a broad therapeutic window, as systemic exposure associated with tumor regression in mouse models remained well below the tolerated levels in NHPs.

● The CAPTN-3 masking strategy effectively mitigated peripheral T-cell activation and prevented systemic cytokine release in NHPs, which is associated with one of the main safety challenges of T-cell engagers, cytokine release syndrome (CRS):

○ IM1240 induced minimal IL-6 and TNF-α at 10 mg/kg dose, whereas the non-capped IM1222 induced robust cytokine release at just 0.03 mg/kg – a more than 300-fold difference in the dose required to trigger cytokine release.

○ The IM1240 capping design also improved the PK profile by reducing the CD3-mediated antigen sink effect and incorporating human serum albumin to further extend half-life, as compared to the non-capped variant IM1222.

○ IM1240 demonstrated ~14-fold slower clearance than active non-capped IM1222, supporting extended exposure and potential efficacy; rapid clearance of peripherally released non-capped IM1222 reduces systemic accumulation and lowers CRS risk and off-tumor toxicity.

"The preclinical data we are presenting at EACR 2026 demonstrate the full strength of the CAPTN-3 design. In NHPs, our masking strategy delivered markedly superior pharmacokinetics and an improved safety profile compared to the non-capped variant, establishing a broad therapeutic window that supports our planned path to the clinic." said Dr. Hadas Reuveni, VP R&D of Purple Biotech. "In collaboration with Dr. Amir Horowitz from Mount Sinai, we explored IM1240’s activity and mechanism of action in patient-derived tumors from PD-1/SoC-resistant patients. Data generated in Dr. Horowitz’s lab demonstrated cancer cell apoptosis induced by IM1240 across multiple PD1-resistant biopsies from HNSCC metastatic LN and muscle-invasive bladder cancer, where functional NKG2A and CD3 arms were both required for full activity, highlighting the potential of IM1240 design for patients who progressed on previous line/s of treatment. Additionally, we present for the first time tissue profiling analyses of NSCLC patient-derived explants showing that IM1240 treatment – unlike the NKG2A loss-of-function variant – drives substantial immune remodeling, characterized by the formation of mature tertiary lymphoid structures (TLS), a hallmark of effective anti-tumor immunity and favorable prognosis, along with increased CD8 T and NK cell abundance and reduced Treg levels.. These immune changes correlate with robust anti-tumor activity and underscored the critical contribution of the NKG2A arm, and further support IM1240’s potential to reprogram the tumor microenvironment and deliver meaningful clinical benefit in immunotherapy-resistant tumors."

(Press release, Purple Biotech, JUN 11, 2026, View Source [SID1234666570])

On June 11, 2026 Propanc Biopharma, Inc. (Nasdaq: PPCB) ("Propanc" or the "Company"), a biopharmaceutical company focused on developing novel treatments for chronic diseases, including recurrent and metastatic cancer, reported it has approved a share repurchase program authorizing the Company to repurchase up to $5.0 million of its common stock.

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"With our recent advancements of the Company’s lead asset, PRP, towards entering the clinic with a novel, first-in-class cancer therapy to treat and prevent metastatic cancer from solid tumors with a pivotal Phase 1b, First-In-Human study in 30 to 40 advanced cancer patients, the management team believes we are entering a transformative stage for the Company. The work we’ve undertaken throughout this recent period, publishing key scientific data, filing patentable discoveries, forming partnerships with CRO’s, CDMO’s and suppliers, has us well positioned to advance PRP meaningfully and efficiently to achieve significant clinical milestones. This is further supported by US FDA Orphan Drug Designation for the treatment of pancreatic cancer which provides us with seven-year exclusivity in the market, post approval. The foundation is clearly there and as a result, we believe we are undervalued significantly," said Mr. James Nathanielsz, Propanc’s Chief Executive Officer. "Furthermore, this decision reflects our commitment to disciplined, flexible capital allocation. Repurchases will be considered when we believe the market price meaningfully understates intrinsic value and when buybacks compete favorably relative to other uses of capital. We believe we are approaching such a position. Importantly, when executed thoughtfully, buybacks allow continuing shareholders to increase their ownership in the Company’s underlying assets, improve per share economics over time, and signal management’s confidence in the long-term value of the business, while still preserving the financial flexibility needed to pursue attractive opportunities as they arise."

Under the share repurchase program, the Company may buy back its common stock from time to time, in amounts, at prices, and at such times as the Company deems appropriate, subject to market conditions, pursuant to Rule 10b5-1 of the Securities Exchange Act of 1934, as amended, and federal and state laws governing such transactions, through a variety of methods, which may include open market purchases, privately negotiated transactions, block trades, accelerated share repurchase transactions, purchases through 10b5-1 trading plans, or by any combination of such methods. The repurchase program does not oblige the Company to acquire any specific number of shares and may be modified, discontinued, or suspended at any time.

(Press release, Propanc, JUN 11, 2026, View Source [SID1234666569])

On June 11, 2026 Nurix Therapeutics, Inc. (Nasdaq: NRIX), a clinical-stage biopharmaceutical company focused on the discovery, development and commercialization of targeted protein degradation medicines, reported updated clinical data from the Company’s ongoing NX-5948-301 Phase 1a/b clinical trial evaluating bexobrutideg (NX-5948), an investigational oral CNS-penetrant BTK degrader, in patients with chronic lymphocytic leukemia (CLL). The data will be presented during an oral presentation at the 2026 EHA (Free EHA Whitepaper) Congress taking place June 11–14, 2026, in Stockholm, Sweden.

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"These updated data continue to demonstrate the differentiated profile of bexobrutideg, including durable responses in heavily pretreated patients and encouraging activity in patients earlier in their treatment journey," said Talha Munir, M.B. Ch.B., Ph.D., consultant hematologist at Leeds Teaching Hospitals NHS Trust and deputy chair of the United Kingdom National Cancer Research Institute CLL Study Group. "Importantly, responses were observed across patients with difficult-to-treat disease characteristics, including BTK inhibitor resistance mutations, high-risk molecular features and CNS involvement, while maintaining a favorable tolerability profile."

"With longer follow-up in relapsed/refractory CLL and expansion into earlier-line treatment settings, we continue to see a consistent efficacy and safety profile for bexobrutideg," said Paula O’Connor, M.D., chief medical officer of Nurix. "The durability of responses observed in heavily pretreated patients together with the promising activity seen in BCL2i-naïve and BTKi-naïve patients further support the broad potential of BTK degradation across all lines of therapy in CLL."

"These latest findings continue to reinforce our belief that bexobrutideg has the potential to redefine BTK-directed therapy and emerge as a potentially best-in-class treatment for CLL," said Arthur T. Sands, M.D., Ph.D., president and chief executive officer of Nurix Therapeutics. "The updated data to be presented at EHA (Free EHA Whitepaper) across Phase 1 cohorts continue to support the launch of a broad Phase 3 monotherapy program and strengthen the rationale for exploring the use of combination regimens in first- and second-line patients. We look forward to advancing these programs through our recently announced collaboration with Roche."

Growing Safety Cohort Continues to Support Differentiated Profile
Across all Phase 1a/b CLL patients (n=142), bexobrutideg was well tolerated, consistent with prior disclosures, with safety findings generally comparable between patients treated at the 600 mg RP2D and the broader study population.

As of the January 1, 2026, data cutoff:
•No dose-limiting toxicities were observed
•No treatment-related Grade 5 adverse events were reported
•Treatment discontinuations due to adverse events occurred in only 5.6% of patients
•The most common treatment-emergent adverse events included purpura/contusion, neutropenia, petechiae, diarrhea, and fatigue.

Updated Phase 1a Data in Relapsed/Refractory CLL Continue to Support Durable Responses
The Phase 1a dose escalation study enrolled 48 patients with relapsed/refractory CLL/SLL treated with bexobrutideg at doses ranging from 50 mg to 600 mg once daily. Patients were heavily pretreated, having received a median of four prior lines of therapy (range 2–12), including prior BTK inhibitors (97.9%), prior BCL2 inhibitors (83.3%), and prior non-covalent BTK inhibitors (27.1%). Baseline high-risk features included BTK inhibitor resistance mutations (38.3%), TP53 mutations (44.7%), PLCG2 mutations (14.9%), and central nervous system (CNS) involvement (10.4%).

As of the January 1, 2026, data cutoff:
•Median follow-up was 22.4 months
•Median progression-free survival (PFS) was 22.1 months (95% CI: 14.0–NR)
•Objective response rate (ORR) was 83.0% (95% CI: 69.2–92.4)
•Responses included two complete responses, one nodal partial response, and 36 partial responses.
•Responses were observed across patients with BTK inhibitor resistance mutations, high-risk molecular features, and CNS involvement

Phase 1b Data Supports High ORR in Earlier-Line Cohorts
Nurix also presented new data from two of the Phase 1b cohorts evaluating bexobrutideg in earlier lines of treatment, including patients who had received prior BTKi treatment but were BCL2i-naïve (Cohort 5) and patients who were BTKi-naïve, including treatment-naïve patients (Cohort 15).

In Cohort 5 (n=19), patients had received prior BTK inhibitor therapy but no prior BCL2 inhibitor:
•ORR was 92.9% (95% CI: 66.1–99.8) among evaluable patients (n=14)
•18 of 19 patients remained on treatment at data cutoff
•Median follow-up was 5.2 months
•Five patients have not yet reached their first scan but remain on treatment

In Cohort 15 (n=20), which included BTKi-naïve and treatment-naïve patients:
•ORR was 84.2% (95% CI: 60.4–96.6) among evaluable patients (n=19)
•19 of 20 patients remained on treatment at data cutoff
•Median follow-up was 4.9 months
•Three patients with stable disease remain on treatment

About Bexobrutideg
Bexobrutideg (NX-5948) is an investigational, orally bioavailable, brain-penetrant, highly selective small-molecule degrader of Bruton’s tyrosine kinase (BTK) being developed by Nurix and Roche as a potential best-in-class therapy across oncology, immunology and neurology.

Bexobrutideg is currently being evaluated in the DAYBreak CLL-201 clinical trial (NCT07221500), a pivotal single-arm Phase 2 study in patients with relapsed or refractory chronic lymphocytic leukemia (CLL), and in the NX-5948-301 Phase 1a/1b clinical trial (NCT05131022) in patients with relapsed or refractory B-cell malignancies. A new tablet formulation of bexobrutideg is also being evaluated in a first-in-human single-ascending-dose and multiple-ascending-dose study in healthy volunteers (NCT06717269) to support future development in immunology and neurology indications. Additional information about ongoing clinical trials can be found at clinicaltrials.gov.

(Press release, Nurix Therapeutics, JUN 11, 2026, View Source [SID1234666567])