On June 12, 2026 Atossa Therapeutics, Inc. (Nasdaq: ATOS) ("Atossa" or the "Company"), a clinical-stage biopharmaceutical company developing novel therapies in oncology and other areas of high unmet clinical need, reported the closing of its previously announced registered direct offering of 1,363,637 shares (the "Shares") of its common stock, par value $0.18 per share ("Common Stock") (or common stock equivalents in lieu thereof), Series A warrants to purchase up to 1,363,637 shares of Common Stock and short-term Series B warrants to purchase up to 1,363,637 shares of Common Stock (such warrants, collectively, the "Series Warrants") and accompanying Series Warrants. The Series Warrants are exercisable six months following the date of issuance. The Series A warrants expire on the five and one-half (5.5) year anniversary of the date of issuance. The short-term Series B warrants expire on the two (2) year anniversary of the date of issuance.

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Rodman & Renshaw LLC acted as the exclusive placement agent for the offering.

The aggregate gross proceeds to the Company from the offering were approximately $4.5 million before deducting the placement agent’s fees and other estimated offering expenses payable by the Company. The potential additional gross proceeds to the Company from the Series Warrants, if fully exercised on a cash basis, will be approximately $12 million. No assurance can be given that any of the Series Warrants will be exercised, or that the Company will receive cash proceeds from the exercise of the Series Warrants. The Company currently intends to use the net proceeds from the offering for clinical development of its product candidates, working capital and general corporate purposes.

The securities described above were offered and sold by the Company in a registered direct offering pursuant to a "shelf" registration statement on Form S-3 (File No. 333-279367) that was filed with the Securities and Exchange Commission (the "SEC"), on May 13, 2024, and declared effective by the SEC on May 23, 2024. The securities offered in the registered direct offering were offered only by means of a prospectus, including a prospectus supplement, forming a part of the effective registration statement. A prospectus supplement and the accompanying base prospectus relating to the registered direct offering were filed with the SEC and are available on the SEC’s website at www.sec.gov. Electronic copies of the prospectus supplement and the accompanying base prospectus may also be obtained from Rodman & Renshaw LLC at 600 Lexington Avenue, 32nd Floor, New York, NY 10022, by telephone at (212) 540-4414, or by email at [email protected].

This press release shall not constitute an offer to sell or the solicitation of an offer to buy any of the securities described herein, nor shall there be any sale of these securities in any state or jurisdiction in which such offer, solicitation or sale would be unlawful prior to the registration or qualification under the securities laws of any such state or jurisdiction.

(Press release, Atossa Therapeutics, JUN 12, 2026, View Source [SID1234666610])

On June 12, 2026 BeOne Medicines Ltd. (Nasdaq: ONC; HKEX: 06160; SSE: 688235), a global oncology company, reported new data from its foundational hematology franchise at the 2026 European Hematology Association (EHA) (Free EHA Whitepaper) Congress in Stockholm. Updated results from tacabrutideg (BGB-16673), a potential best-in-class Bruton’s tyrosine kinase (BTK) degrader, demonstrated durable responses in pretreated relapsed/refractory (R/R) chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), with early activity also seen in BTK inhibitor–naïve patients. These data are complemented by results from the all-oral combination of BRUKINSA (zanubrutinib) plus next-generation BCL2 inhibitor BEQALZI (sonrotoclax; ZS), which continue to demonstrate rapid, deep, durable responses across multiple B-cell malignancies.

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Amit Agarwal, M.D., Ph.D., Chief Medical Officer, Hematology, BeOne Medicines, said:
"BTK inhibition has reshaped the treatment of B-cell cancers, and we believe degradation is the next leap forward. At EHA (Free EHA Whitepaper), tacabrutideg is showing durable responses in heavily pretreated CLL, where patients have limited options, with early data suggesting potential in earlier lines of treatment. At the same time, the depth and consistency of responses we’re seeing with our ZS combination supports its potential to become the foundation of time-limited therapy, bringing us closer to a future where durable, treatment-free remission is possible. Together, these data reflect our ambition to define the next era of care in B-cell malignancies."

Updated CaDAnCe-101 data show durable responses with tacabrutideg in heavily pretreated R/R CLL/SLL and R/R WM (Oral Presentation: S152; June 14, 11:00 AM-12:15 PM CEST; Poster Presentation: PS2033; June 13, 2026, 6:45-7:45 PM CEST)
The oral presentation, which was selected for inclusion in the EHA (Free EHA Whitepaper) Press Program, will highlight data from 67 patients with R/R CLL/SLL treated with tacabrutideg across the different dose levels (50-500 mg), including patients with high-risk disease features (del(17p)/TP53 mutation, unmutated IGHV, complex karyotype, and BTK inhibitor resistance mutations). With a median study follow-up of 25.4 (range, 0.3-40.1) months, the analysis showed:

Overall response rate (ORR): 85.1%
Median time to first response (TTFR): 2.8 months (range, 2.0-19.4)
Median duration of response (DOR): 20.7 months (range, 0-27.6)
24-month progression-free survival (PFS) rate: 53.8% (95% CI, 38.8%-66.6%)
Safety: tacabrutideg was generally well tolerated in this heavily pretreated population with no treatment-related deaths and no new toxicities identified; patients with treatment response had rapid and sustained cytopenia improvement
In patients with R/R Waldenstrom macroglobulinemia (WM), tacabrutideg showed substantial responses in heavily pretreated patients, including those bearing BTK, CXCR4, and TP53 mutations, with major response rate (MRR) of 76.3% and very good partial response (VGPR) of 30.2% and a 15-month PFS rate of 70.4% (95% CI, 52.6-82.5) at a median PFS follow-up of 16.6 months.

Stephan Stilgenbauer, Professor of Medicine and Medical Director of the Comprehensive Cancer Center Ulm (CCCU), Head of the Early Clinical Trials Unit (ECTU), and Head of the Division of CLL Dept. of Internal Medicine III at Ulm University, said:
"Once patients with relapsed or refractory CLL progress after both BTK and BCL2 inhibitors, treatment options become extremely limited. In this study, tacabrutideg, which is designed to degrade BTK rather than inhibit it, achieved durable responses even in patients with high-risk clinical and biological characteristics, such as resistance mutations. These findings suggest a promising new approach for patients who currently have few effective therapies available."

First report of tacabrutideg in BTK inhibitor–naïve patients shows potential for improved efficacy in earlier treatment lines (Poster Presentation: PS1693; June 13, 2026, 6:45-7:45 PM CEST)
In the first clinical evaluation of tacabrutideg in patients who had not previously received a BTK inhibitor (N=54; CLL/SLL, n=29; mantle cell lymphoma [MCL], n=8; marginal zone lymphoma, n=10; Richter transformation, n=2; WM, n=5), tacabrutideg was well tolerated and showed promising and rapid antitumor activity. In 22 evaluable patients with CLL/SLL with median follow-up of 8.2 (range: 0.4-12.8) months, the study shows:

ORR: 86.4% Median TTFR: 2.8 (range, 2.7-5.6) months
At 6 months, none of the patients had progressed
Safety: tacabrutideg was generally well tolerated with no reported opportunistic infections, major hemorrhage or febrile neutropenia
Rapid, deep, and durable responses with ZS reinforce the potential to redefine time-limited treatment across CLL and MCL (Multiple Presentations)
Across multiple presentations at EHA (Free EHA Whitepaper) 2026, the all-oral ZS combination demonstrated rapid, deep, and durable responses across both treatment-naïve and relapsed/refractory settings. These data highlight the ability of ZS to drive high rates of undetectable minimal residual disease (uMRD) and sustained disease control regardless of risk factors reinforcing its potential to redefine expectations for fixed-duration, time-limited therapy in B-cell malignancies.

In treatment-naïve CLL (Oral Presentation: S145; June 12, 2026; 5:15-6:30 PM CEST):

ORR: 100%, with complete responses in 59.5% of patients
Best uMRD4 rate: 98.8%
No patient that achieved uMRD4 reverted to uMRD positivity
Best uMRD in patients with TP53 mutation/del(17p): 92.9% across 2 dose levels
Median time from combination start to uMRD4: 4.5 months
At a median follow-up of 34.1 months, no disease progression events were observed at the recommended Phase 2 dose of 320mg, including patients who electively discontinued therapy
In R/R CLL (Poster Presentation: PS1697; June 13, 2026, 6:45-7:45 PM CEST), at the 320mg (RP2D) of sonrotoclax:

ORR: 100%, with complete responses in 52% of patients
Best uMRD4 rate: 85%
No patient that achieved uMRD4 reverted to uMRD positivity
36-month PFS: 95.5% (95% CI, 83.2%-98.9%) across all dose cohorts at a median follow-up of 40.6 months (range, 10.2-60.6 months)
In R/R MCL (Poster Presentation: PF933; June 12, 2026, 6:45-7:45 PM CEST), at the 320mg (RP2D) of sonrotoclax:

ORR: 82%, with complete responses in 59% of patients
Median duration of response (DOR): not reached
30-mo DOR: 78.3% (95% CI, 51.3.%-91.4%)
About Tacabrutideg (BGB-16673)
With first-in-class and best-in-class potential, tacabrutideg is a foundational, orally administered Bruton’s tyrosine kinase (BTK) degrader. Tacabrutideg is the most advanced BTK degrader in the clinic with 1,200+ patients dosed to date in an extensive global clinical development program. This program includes three randomized Phase 3 trials in R/R CLL, including the head-to-head Phase 3 trial versus pirtobrutinib, which began enrolling in Q4 2025. Originating from BeOne’s chimeric degradation activation compound (CDAC) platform, tacabrutideg is designed to promote the degradation, or breakdown, of both wildtype and mutant forms of BTK, including those that commonly result in resistance to BTK inhibitors in patients who experience progressive disease.

The U.S. Food and Drug Administration (FDA) granted Fast Track Designation to tacabrutideg for the treatment of adult patients with relapsed or refractory (R/R) chronic lymphocytic leukemia or small lymphocytic lymphoma (CLL/SLL), and adult patients with R/R mantle cell lymphoma (MCL). Additionally, the European Medicines Agency (EMA) granted tacabrutideg PRIority MEdicines (PRIME) designation for the treatment of patients with Waldenstrom’s macroglobulinemia (WM) previously treated with a BTK inhibitor.

About BEQALZI (sonrotoclax)
BEQALZI (bee-KAHL-zee; sonrotoclax) is a foundational, next-generation and potentially best-in-class B-cell lymphoma 2 (BCL2) inhibitor with a unique pharmacokinetic and pharmacodynamic profile. Preclinical and clinical studies in early drug development have shown that sonrotoclax is a highly potent and specific BCL2 inhibitor with a short half-life and no drug accumulation. Sonrotoclax has shown promising clinical activity across a range of B-cell malignancies, including chronic lymphocytic leukemia (CLL), and is in development as a monotherapy and in combination with other therapeutics, including zanubrutinib. To date, more than 2,500 patients have been enrolled across the broad sonrotoclax global development program.

BEQALZI is approved by the U.S. Food and Drug Administration (FDA) and China’s National Medical Products Administration for the treatment of adult patients with relapsed or refractory (R/R) mantle cell lymphoma (MCL), after at least two lines of systemic therapy, including a BTK inhibitor. It is also approved in China for adult patients with chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL) who have previously received at least one systemic therapy, including a BTK inhibitor.

About BRUKINSA (zanubrutinib)
BRUKINSA is an orally available, small molecule inhibitor of Bruton’s tyrosine kinase (BTK) designed to deliver complete and sustained inhibition of the BTK protein by optimizing bioavailability, half-life, and selectivity. With differentiated pharmacokinetics compared with other approved BTK inhibitors, BRUKINSA has been demonstrated to inhibit the proliferation of malignant B cells within a number of disease-relevant tissues.

With the broadest label globally, BRUKINSA is the foundational BTK inhibitor and is the only BTK inhibitor to demonstrate superiority to another BTK inhibitor in a Phase 3 study. It is also the only BTK inhibitor to provide the flexibility of once or twice daily dosing.

The global BRUKINSA clinical development program includes more than 8,000 patients enrolled in over 30 countries and regions across more than 45 trials. BRUKINSA is approved in 80 markets in at least one indication, and more than 290,000 patients have been treated globally.

Select Important Safety Information for BEQALZITM (sonrotoclax)
Serious and sometimes fatal adverse reactions have occurred with BEQALZI, including tumor lysis syndrome (TLS), serious infections, neutropenia, and embryo-fetal toxicity. BEQALZI is contraindicated with strong CYP3A inhibitors at initiation and during the ramp-up phase due to the potential for an increased risk of tumor lysis syndrome.

In the safety population (N=115), tumor lysis syndrome occurred in 7% of patients who followed the recommended dose ramp-up. Serious infections occurred in 14% of patients, and Grade 3 or 4 infections occurred in 17% (fatal: 2.6%), with pneumonia (10%) being the most common Grade 3 or greater infection. Grade 3 or 4 decreases in neutrophils occurred in 18% of patients (Grade 4: 6%), and febrile neutropenia occurred in 1.7% of all patients. The most common adverse reactions (≥15%) were pneumonia (16%) and fatigue (16%). The most common Grade 3–4 laboratory abnormalities (≥15%) were decreases in lymphocytes (29%) and neutrophils (18%).

Please see full Prescribing Information.

Select Important Safety Information for BRUKINSA
Serious adverse reactions, including fatal events, have occurred with BRUKINSA, including hemorrhage, infections, cytopenias, second primary malignancies, cardiac arrhythmias, and hepatotoxicity (including drug-induced liver injury).

In the pooled safety population (N=1729), the most common adverse reactions (≥30%), including laboratory abnormalities, in patients who received BRUKINSA were neutrophil count decreased (51%), platelet count decreased (41%), upper respiratory tract infection (38%), hemorrhage (32%), and musculoskeletal pain (31%).

Please see full U.S. Prescribing Information including U.S. Patient Information.

The information provided in this press release is intended for a global audience. Product indications vary by region.

(Press release, BeOne Medicines, JUN 12, 2026, View Source [SID1234666609])

On June 12, 2026 Cogent Biosciences, Inc. (Nasdaq: COGT), a biotechnology company focused on developing precision therapies for genetically defined diseases, reported preclinical data from its novel, potential best-in-class JAK2 V617F mutant-selective inhibitor in a poster presentation at the 2026 European Hematology Association (EHA) (Free EHA Whitepaper) Congress taking place in Stockholm, Sweden, June 11-14, 2026.

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"We’re encouraged by the preclinical data from our next-generation JAK2 program being presented at EHA (Free EHA Whitepaper) today," said Andrew Robbins, Cogent’s President and Chief Executive Officer. "This highly selective, potent inhibitor of JAK2 V617F has the potential to address the underlying mutational driver of disease while mitigating off-target hematological effects. We are rapidly advancing this program and remain on track to submit our Investigational New Drug application in 2026."

JAK2 V617F is the most prevalent molecular abnormality in BCR-ABL-negative myeloproliferative neoplasms (MPNs), occurring in approximately 95% of patients with polycythemia vera and 50% of patients with primary myelofibrosis or essential thrombocythemia. The poster highlights CGT1145, a potent inhibitor of the JAK2 V617F mutation with >100x selectivity over JAK2 WT and the JAK1/3 isoforms, along with high oral bioavailability and low clearance across species. CGT1145 has the potential to eradicate JAK2 V617F myeloproliferative neoplasm propagating cells and induce molecular remission with improved hematologic tolerability.

Cogent’s EHA (Free EHA Whitepaper) posters and presentation will be available on the company’s website at: View Source

(Press release, Cogent Biosciences, JUN 12, 2026, View Source [SID1234666608])

On June 12, 2026 Cogent Biosciences, Inc. (Nasdaq: COGT), a biotechnology company focused on developing precision therapies for genetically defined diseases, reported detailed and updated clinical results from the registration-directed APEX clinical trial of bezuclastinib in patients with advanced systemic mastocytosis (AdvSM) demonstrating clinically meaningful results as measured by consensus criteria used to assess patient response. The company also shared a more detailed review of the pathobiology data in AdvSM patients from the APEX trial, reinforcing the rapid and deep clinical benefit bezuclastinib has demonstrated in these patients. The data will be presented at the 2026 European Hematology Association (EHA) (Free EHA Whitepaper) Congress taking place in Stockholm, Sweden, June 11-14, 2026.

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"We are excited to share updated and detailed results from the APEX trial in AdvSM patients, building upon previously announced results from bezuclastinib in the SUMMIT trial in NonAdvSM patients," said Andrew Robbins, Cogent’s President and Chief Executive Officer. "The results shown across these two trials demonstrate that a selective, potent KIT D816V inhibitor like bezuclastinib will have tremendous opportunity to become the new standard of care and change the lives of patients living with systemic mastocytosis. We are on track to complete the APEX NDA submission in the very near future and plan to launch bezuclastinib later this year in both systemic mastocytosis and GIST following FDA approval."

As of the updated data cutoff of March 31, 2026 in Part 2 of the APEX trial, 81 AdvSM patients were treated with 150 mg of bezuclastinib, including 57 patients with SM-AHN, 11 patients with ASM and 13 patients with MCL. The primary endpoint of response per mIWG-MRT-ECNM was assessed on 68 evaluable patients and showed 65% ORR (CR+CRh+PR+CI), including 57% of patients who achieved CR, CRh or PR as best response.

Additional highlights include:

Key secondary endpoint of response per pure pathological response (PPR) criteria was assessed on 81 patients which showed an 81% ORR (CR+CRh+PR).
Bezuclastinib demonstrated reversal of bone marrow pathobiology including rapid and deep reductions in aberrant CD25 and CD30 expression, normalization of mast cell morphology, normalization of bone marrow cellularity, and improvement in myelofibrosis.
Bezuclastinib demonstrated durable clinical activity and prolonged PFS with a 12-month PFS rate of 79% and a 12-month OS rate of 87%. Median duration of PFS and OS were immature at the time of the data cutoff.
Bezuclastinib achieved clear and clinically significant reductions in objective disease markers for these AdvSM patients:
Outcome measure Bezuclastinib
Proportion with ≥50% reduction in serum tryptase (n=80) 89 %
Proportion with ≥50% reduction in bone marrow mast cells or clearance of aggregates (n=80) 89 %
Proportion with ≥50% reduction in KIT D816V variant allele frequency (n=43) 91 %

"The results from the APEX trial demonstrate clear evidence of bezuclastinib’s rapid and deep clinical activity in patients with advanced systemic mastocytosis," said Daniel J. DeAngelo, M.D., Ph.D., Chief of the Division of Leukemia at the Dana-Farber Cancer Institute and Professor of Medicine, Harvard Medical School. "Coupled with an impressive safety and tolerability profile minimizing off-target toxicities that allows for long-term therapeutic dosing, bezuclastinib will become an important treatment option for patients with advanced SM."

Pathobiology Data

Cogent will also present new data highlighting the impact bezuclastinib has at a cellular level in patients with AdvSM. In the APEX study, bezuclastinib demonstrated robust improvement in disease pathology, with effects observed as early as eight weeks, including high PPR rates, improvement (including normalization) in bone marrow mast cell distribution, improvement in broader bone marrow characteristics and a majority of patients achieving normalization of serum tryptase. In addition, approximately one-third of patients treated with bezuclastinib achieved undetectable levels of KIT D816V VAF, signifying modification of the underlying AdvSM disease with bezuclastinib treatment.

APEX Safety and Tolerability

As of the data cutoff, bezuclastinib continued to be well-tolerated, with infrequent need for dose reduction or discontinuation for treatment-related adverse events (TRAEs). The most frequent TRAEs reported on bezuclastinib treatment were hair color change (31%), neutropenia (31%), altered taste (28%), thrombocytopenia (25%), and ALT/AST elevations (21%). The majority of transaminase elevations were of low grade, asymptomatic and reversible. Of the two patients who experienced Grade 3 transaminase elevation, one discontinued treatment and one remains on therapy following dose reduction.

The EHA (Free EHA Whitepaper) posters and presentation will be available on the Cogent website at: View Source

Bezuclastinib – Expanded Access Program

Working with the FDA, Cogent has established active Expanded Access Programs (EAPs) for U.S. patients SM or GIST who meet disease-specific criteria and could benefit from treatment with bezuclastinib or the combination of bezuclastinib and sunitinib. For more information please visit: View Source

(Press release, Cogent Biosciences, JUN 12, 2026, View Source [SID1234666607])

On June 12, 2026 Merck (NYSE: MRK), known as MSD outside of the United States and Canada, reported the U.S. Food and Drug Administration (FDA) approved KEYTRUDA (pembrolizumab) and KEYTRUDA QLEXTM (pembrolizumab and berahyaluronidase alfa-pmph), Merck’s anti-PD-1 therapies, each in combination with WELIREG (belzutifan), Merck’s first-in-class, oral hypoxia-inducible factor-2 alpha (HIF-2α) inhibitor, for the adjuvant treatment of adult patients with renal cell carcinoma with a clear cell component (ccRCC) at intermediate-high or high risk of recurrence following nephrectomy, or following nephrectomy and resection of metastatic lesions. These approvals represent the first approval for WELIREG in earlier-stage ccRCC and the first approvals for PD-1 and HIF-2α inhibitor combination regimens.

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The approvals are based on results from the pivotal Phase 3 LITESPARK-022 trial. LITESPARK-022 enrolled 1,841 patients and demonstrated that KEYTRUDA in combination with WELIREG significantly improved disease-free survival (DFS), the trial’s primary endpoint, reducing the risk of disease recurrence, metastasis or death by 28% (HR=0.72 [95% CI 0.59-0.87]; p=0.0003) for patients with ccRCC at intermediate-high or high risk of recurrence following nephrectomy, or following nephrectomy and resection of metastatic lesions compared to KEYTRUDA plus placebo. The estimated 24-month DFS rate was 81% (95% CI 0.78-0.83) with KEYTRUDA plus WELIREG compared to 74% (95% CI 0.71-0.77) with KEYTRUDA plus placebo. Median DFS was not reached in either arm. Overall survival (OS) results were not yet mature at this interim analysis. The effectiveness of KEYTRUDA QLEX for its approved indications has been established based upon evidence from the adequate and well-controlled studies conducted with KEYTRUDA and additional data from MK-3475A-D77 comparing the pharmacokinetic, efficacy, and safety profiles of KEYTRUDA QLEX and KEYTRUDA.

The WELIREG prescribing information contains a boxed warning that exposure to WELIREG during pregnancy can cause embryo-fetal harm. Verify pregnancy status prior to the initiation of WELIREG. Advise patients of these risks and the need for effective non-hormonal contraception. WELIREG can render some hormonal contraceptives ineffective. WELIREG can cause severe anemia that can require blood transfusion. Monitor for anemia before initiation of, and periodically throughout, treatment with WELIREG. WELIREG can cause severe hypoxia that may require discontinuation, supplemental oxygen or hospitalization. Monitor oxygen saturation before initiation of, and periodically throughout, treatment with WELIREG. For more information, see "Selected Safety Information" below.

KEYTRUDA QLEX is contraindicated in patients with known hypersensitivity to berahyaluronidase alfa, hyaluronidase or to any of its excipients. KEYTRUDA and KEYTRUDA QLEX are associated with the following Warnings and Precautions: severe and fatal immune-mediated adverse reactions in any or multiple organs, which can occur during or after treatment, including pneumonitis, colitis, hepatitis, endocrinopathies, nephritis, dermatologic reactions, solid organ transplant rejection, other transplant (including corneal graft) rejection; severe and life-threatening infusion or injection-related reactions; fatal and other serious complications in patients who receive allogeneic hematopoietic stem cell transplantation before or after beginning treatment; embryo-fetal toxicity; and increased mortality in patients with multiple myeloma when KEYTRUDA or KEYTRUDA QLEX is added to a thalidomide analogue plus dexamethasone, which is not recommended outside of controlled trials. Immune-mediated adverse reactions listed here may not include all such possible severe or fatal reactions. For more information, see "Selected Safety Information" below.

"Patients with earlier-stage renal cell carcinoma at high risk of recurrence after surgery may see their cancer return, frequently as metastatic disease," said Dr. Toni K. Choueiri, director, Lank Center for Genitourinary Oncology, Dana-Farber Cancer Institute and Jerome and Nancy Kohlberg professor of medicine, Harvard Medical School. "The results of the LITESPARK-022 trial demonstrated the ability of pembrolizumab in combination with belzutifan to reduce the risk of disease recurrence, metastasis, or death by 28%, which represents an important new option for these patients to help keep their clear cell renal cell carcinoma from coming back."

"Reflecting on my own experience as a clinical oncologist, I know the significant impact that improved disease-free survival can have on the lives of patients," said Dr. M. Catherine Pietanza, vice president, global clinical development, Merck Research Laboratories. "These approvals demonstrate Merck’s commitment to pursuing innovative treatment options that may help these patients experience longer periods without disease."

"The FDA approval of the novel KEYTRUDA and WELIREG combination is exciting news for the kidney cancer community," said Bryan Lewis, CEO and co-founder, KidneyCan. "This progress reflects an important step in addressing the needs of patients with earlier-stage renal cell carcinoma."

Study design and additional data from LITESPARK-022

LITESPARK-022 is a multicenter, randomized, double-blind Phase 3 trial (ClinicalTrials.gov, NCT05239728) evaluating WELIREG in combination with KEYTRUDA compared to placebo plus KEYTRUDA for the adjuvant treatment of ccRCC post nephrectomy. Eligible patients had intermediate-high or high risk of recurrence of RCC, or M1 no evidence of disease (NED). Patients must have undergone a partial or radical nephrectomy, and if indicated, metastasectomy within two years of nephrectomy, within ≥4 weeks prior to the time of screening. Patients were excluded from the trial if they had received prior systemic therapy for advanced RCC. The trial enrolled 1,841 patients who were randomized (1:1) to receive either:

WELIREG (120 mg orally once daily) plus KEYTRUDA (400 mg intravenously [IV] every six weeks) for up to 9 cycles (54 weeks) until disease recurrence or unacceptable toxicity (n=921), or;
KEYTRUDA (400 mg IV every six weeks) plus oral placebo for up to 9 cycles (54 weeks) until disease recurrence or unacceptable toxicity (n=920).
The major efficacy outcome measure was investigator-assessed DFS and an additional outcome measure was OS.

The safety of WELIREG in combination with KEYTRUDA was evaluated in LITESPARK-022. A total of 915 patients received WELIREG in combination with KEYTRUDA and a total of 913 patients received oral placebo in combination with KEYTRUDA. The median duration of exposure to WELIREG was 12.4 months (range 1 day to 20.1 months). The median duration of exposure to KEYTRUDA in the treatment arm was 11.1 months (range: 1 day to 16.1 months).

Serious adverse reactions occurred in 30% of patients who received WELIREG in combination with KEYTRUDA. The most frequently reported serious adverse reactions (≥1%) were pneumonia (2%), hypoxia (1.9%), pneumonitis (1.6%), arrhythmia (1.5%), diarrhea (1.1%), and acute kidney injury (1.1%). Fatal adverse reactions occurred in 1.1% of patients who received WELIREG in combination with KEYTRUDA, including sepsis (0.1%).

WELIREG was permanently discontinued due to adverse reactions in 27% of patients. Adverse reactions which resulted in permanent discontinuation of WELIREG in ≥1% of patients included anemia (4%), fatigue (2.2%), rash (2%), increased alanine aminotransferase (ALT) (1.7%), hypoxia (1.6%), diarrhea (1.4%), pneumonitis (1.3%), increased aspartate aminotransferase (AST) (1.1%), and hepatic function abnormal (1%).

KEYTRUDA was permanently discontinued due to adverse reactions in 23% of patients. Adverse reactions which resulted in permanent discontinuation of KEYTRUDA in ≥1% of patients included increased ALT (4.5%), increased AST (3%), pneumonitis (2.4%), diarrhea (2.4%), and rash (1.5%).

Dosage interruptions of WELIREG due to an adverse reaction occurred in 52% of patients. Of the patients who received WELIREG in combination with KEYTRUDA, 30% were ≥65 years old and 5% were ≥75 years old. Dose interruptions of WELIREG occurred in 57% of patients ≥65 years of age and in 49% of younger patients. Adverse reactions which required dosage interruption of WELIREG in ≥2% of patients included anemia (25%), fatigue (3.7%), increased ALT (3.5%), diarrhea (3.4%), increased AST (3.4%), COVID-19 (2.6%), hypoxia (2.5%), pyrexia (2.5%), musculoskeletal pain (2.1%), and rash (2.1%).

Dose interruptions of KEYTRUDA due to an adverse reaction occurred in 29% of patients. Adverse reactions which required dosage interruption of KEYTRUDA in ≥2% of patients included anemia (3.2%), diarrhea (3%), increased ALT (3%), and increased AST (2.5%).

Dose reductions of WELIREG due to an adverse reaction occurred in 34% of patients. Dose reductions of WELIREG occurred in 39% of patients ≥65 years of age and in 32% of younger patients. Adverse reactions which required dose reduction in ≥3% of patients included anemia (17%), hypoxia (3.5%), increased ALT (3.2%), and fatigue (3.1%).

The most common (≥25%) adverse reactions, including laboratory abnormalities, in patients who received WELIREG in combination with KEYTRUDA were decreased hemoglobin (95%), increased ALT (57%), fatigue (49%), increased AST (46%), decreased lymphocytes (38%), and increased alkaline phosphatase (29%).

About renal cell carcinoma

Renal cell carcinoma (RCC) is the most common type of kidney cancer, with about nine out of 10 kidney cancer diagnoses being RCC. In 2022, there were about 435,000 new cases of kidney cancer diagnosed and approximately 156,000 deaths from the disease worldwide. In the U.S., it is estimated there will be more than 80,000 new cases of kidney cancer diagnosed and more than 15,000 deaths from the disease in 2026. Renal cell carcinoma is about twice as common in men as in women. Cases of RCC might be discovered incidentally during imaging tests for other reasons. Clear cell renal cell carcinoma, which accounts for 70% of RCC diagnoses, is the most common subtype.

(Press release, Merck & Co, JUN 12, 2026, View Source [SID1234666606])