On October 21, 2026 Thermo Fisher Scientific Inc. (NYSE: TMO), the world leader in serving science, reported its financial results for the third quarter ended September 26, 2026.

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Third Quarter Highlights

•Third quarter revenue grew 9% to $12.14 billion
•Third quarter GAAP diluted earnings per share (EPS) grew 9% to $4.64
•Third quarter adjusted EPS grew 15% to $6.68

"We are very pleased to deliver another excellent quarter, with outstanding financial performance on both the top and bottom line," said Marc N. Casper, chairman and chief executive officer of Thermo Fisher Scientific. "We’re advancing our proven growth strategy, which is resonating strongly with our customers, and our PPI Business System is enabling outstanding execution across the company."

Casper added, "Looking ahead, we’re well positioned to deliver an excellent 2026 as we continue to drive long-term value creation for all of our stakeholders and build an even brighter future for our company."

Growth Strategy and Capital Deployment

•Advanced our proven growth strategy, launching a range of high-impact, innovative new products during the quarter. Highlights include the Thermo Scientific Orbitrap Isora mass spectrometer, the first Orbitrap system designed for isotope ratio analysis, enabling faster, simplified workflows and providing deeper insights into the origin and composition of samples for environmental and life sciences research; the Thermo Scientific EMPAD G2 electron detector enabling faster, more detailed electron microscopy characterization of advanced materials to support the development of next-generation electronics, memory and energy technologies; the FDA-cleared EliA CTD 13 Screen in the U.S., a new autoimmune test for systemic connective tissue diseases, including lupus, helping laboratories streamline testing and providing clinicians with reliable information to inform patient care; and the Ion 560 Chip, the highest-throughput sequencing chip for the Ion GeneStudio S5 platform, providing nearly twice the sequencing capacity of the prior offering to enable laboratories to process more samples and meet growing genomic profiling needs in oncology research.

•Strengthened our industry-leading commercial engine and deepened our trusted partner status with customers. In partnership with Mayo Clinic, we launched Precure, a pioneering initiative that will combine data from more than one million patient samples with our differentiated proteomics ecosystem, including Orbitrap mass spectrometry and Olink technologies, to generate new insights into disease progression, enable earlier detection and advance precision medicine. In South Korea, we opened our first AI-Automation Innovation Center, bringing together our advanced analytical technologies, automation and AI to enable our customers to accelerate innovation and enhance R&D productivity. In our channel businesses, we also opened a highly automated distribution center in Kentucky, to enhance speed, flexibility and assurance of supply for our customers across North America.

•Continued to successfully execute our capital deployment strategy. During the quarter, we completed our previously announced divestiture of our microbiology business.

Financial Results

Revenue for the third quarter of 2026 grew 9% to $12.14 billion, versus $11.12 billion in the same quarter of 2025. Organic revenue growth was 6%.

GAAP Earnings Results

GAAP diluted EPS in the third quarter of 2026 was $4.64, 9% growth versus the third quarter of 2025. GAAP operating income for the third quarter of 2026 was $2.26 billion, 17% higher than the year-ago quarter. GAAP operating margin was 18.6%, compared with 17.4% in the third quarter of 2025.

Non-GAAP Earnings Results

Adjusted EPS for the third quarter of 2026 was $6.68, 15% growth versus the third quarter of 2025. Adjusted operating income for the third quarter of 2026 was $2.97 billion, 15% higher than the year-ago quarter. Adjusted operating margin was 24.5%, compared with 23.3% in the third quarter of 2025.

Annual Guidance for 2026

The company will provide updated 2026 financial guidance during its earnings conference call this morning at 7:00 a.m. Eastern Time.

(Press release, Thermo Fisher Scientific, OCT 21, 2026, View Source [SID1234673640])

On October 21, 2026 Merck (NYSE: MRK), known as MSD outside of the United States and Canada, reported the European Commission (EC) has approved KEYTRUDA (pembrolizumab), Merck’s anti-PD-1 therapy, in combination with Padcev (enfortumab vedotin-ejfv), as neoadjuvant treatment and then continued after radical cystectomy as adjuvant treatment for adults with resectable muscle-invasive bladder cancer (MIBC). This approval, which also covers KEYTRUDA SC [known as KEYTRUDA QLEXTM (pembrolizumab and berahyaluronidase alfa-pmph) in the U.S.], marks the first and only PD-1 inhibitor plus antibody-drug conjugate (ADC) regimen available for patients with MIBC regardless of cisplatin eligibility in the European Union (EU).

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"Although cisplatin-based chemotherapy has been a standard treatment approach for many patients with muscle-invasive bladder cancer, recurrence remains a significant challenge," said Dr. Alfonso Gómez de Liaño, Hospital Universitario Insular de Gran Canaria, and KEYNOTE-B15 primary investigator. "Based on results from the KEYNOTE-B15 trial, today’s approval is a meaningful advance for patients with muscle-invasive bladder cancer in the European Union, extending this chemotherapy-free perioperative treatment option to patients regardless of cisplatin eligibility."

"Building on the previous approval of KEYTRUDA plus Padcev in the European Union less than six months ago, we’re pleased to bring this important treatment option to a broader patient population as the first PD-1 inhibitor plus antibody-drug conjugate regimen approved for people with muscle-invasive bladder cancer regardless of cisplatin eligibility," said Dr. Marjorie Green, senior vice president and head of oncology, global clinical development, Merck Research Laboratories. "This approval represents encouraging progress in bladder cancer care and underscores our commitment to addressing the needs of people who are living with this disease."

The EC approval is based on results from the Phase 3 KEYNOTE-B15 trial (also known as EV-304), which was conducted in collaboration with Pfizer and Astellas. In the study, KEYTRUDA plus Padcev, as perioperative treatment, demonstrated a statistically significant improvement in event-free survival (EFS), reducing the risk of EFS events (defined as disease progression, recurrence or death) by 47% (HR=0.53 [95% CI, 0.41-0.70]; p<0.0001; 87/405 [21%] versus 146/403 [36%]) in patients with MIBC who are eligible for cisplatin-based chemotherapy compared to neoadjuvant chemotherapy (gemcitabine and cisplatin) and surgery. KEYTRUDA plus Padcev also demonstrated a statistically significant improvement in overall survival (OS), reducing the risk of death by 35% (HR=0.65 [95% CI, 0.48-0.89]; p=0.0029; 69/405 [17%] versus 99/403 [25%]) in these patients when compared to neoadjuvant chemotherapy and surgery. The trial showed KEYTRUDA plus Padcev demonstrated a statistically significant improvement in pathologic complete response (pCR) rate compared to neoadjuvant chemotherapy (55.8% [95% CI: 50.8, 60.7] versus 32.5% [95% CI: 28.0, 37.3]; p<0.0001). The approval follows a positive recommendation issued by the European Medicines Agency’s Committee for Medicinal Products for Human Use in September 2026.

This approval authorizes marketing of this KEYTRUDA treatment regimen for this indication in all 27 EU member states, as well as Iceland, Liechtenstein and Norway. Timing for commercial availability of KEYTRUDA for this indication in individual EU countries will depend on multiple factors, including the completion of national reimbursement procedures.

In July 2026, KEYTRUDA in combination with Padcev was approved by the U.S. Food and Drug Administration (FDA) as neoadjuvant treatment and then continued after cystectomy as adjuvant treatment for the treatment of adult patients with MIBC based on the Phase 3 KEYNOTE-B15 trial. This also represented the first and only PD-1 inhibitor plus ADC regimen approved in the U.S. for adults with MIBC regardless of cisplatin eligibility.

About KEYNOTE-B15

KEYNOTE-B15, also known as EV-304, is an open-label, randomized, multicenter, active-control Phase 3 trial (ClinicalTrials.gov, NCT04700124) evaluating perioperative KEYTRUDA in combination with Padcev and surgery (radical cystectomy [RC] and pelvic lymph node dissection [PLND]) versus neoadjuvant chemotherapy (gemcitabine plus cisplatin) and surgery in patients with previously untreated MIBC who are eligible for cisplatin-based chemotherapy. The trial enrolled 808 patients who were randomized 1:1 to receive either:

Neoadjuvant KEYTRUDA 200 mg intravenously on Day 1 and Padcev 1.25 mg/kg intravenously on Days 1 and 8 of each 21-day cycle for four cycles prior to surgery, followed by adjuvant KEYTRUDA 200 mg on Day 1 of each 21-day cycle for 13 cycles and adjuvant Padcev 1.25 mg/kg on Days 1 and 8 of each 21-day cycle for five cycles (n=405), or;
Neoadjuvant gemcitabine 1000 mg/m 2 on Days 1 and 8 and cisplatin 70 mg/m 2 on Day 1 of each 21-day cycle for four cycles prior to surgery, followed by observation (n=403).
The major efficacy outcome measure was EFS as assessed by blinded independent central review (BICR), defined as the time from randomization to the first occurrence of the following events: disease progression preventing curative surgery, failure to undergo surgery for participants with muscle invasive residual disease, incomplete surgical resection, local or distant recurrence after surgery or death. Additional efficacy outcome measures were OS and pCR rate as assessed by blinded independent pathology review.

About bladder cancer

Bladder cancer is the eighth most common cancer worldwide, diagnosed in more than 635,000 patients each year globally. In Europe, it is estimated there were approximately 208,291 patients diagnosed with bladder cancer and more than 67,000 deaths from the disease in 2024. According to some clinical practice guidelines, about 25% of newly diagnosed bladder cancer cases are MIBC. The standard of care for patients with MIBC is neoadjuvant cisplatin-based chemotherapy followed by surgery, which is shown to prolong survival. However, nearly half of patients who undergo this standard treatment experience recurrence. Additionally, up to half of patients with MIBC are not eligible to receive cisplatin and face limited treatment options, typically undergoing surgery alone.

(Press release, Merck & Co, OCT 21, 2026, View Source [SID1234673639])

On October 21, 2026 ImmunityBio, Inc. (NASDAQ: IBRX), an immunotherapy company, reported completion of the database lock for Cohort A of QUILT-2.005 (NCT02138734), its randomized, controlled, registrational trial evaluating ANKTIVA (nogapendekin alfa inbakicept-pmln) in combination with Bacillus Calmette-Guérin (BCG) versus BCG alone in patients with BCG-naïve NMIBC. The chemotherapy-free combination is delivered directly into the bladder.

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The database lock follows the completion of the data review, verification, and reconciliation of all 366 randomized patients, allowing the final efficacy analysis to proceed. The trial is designed to determine whether adding ANKTIVA to standard BCG therapy improves CR rates compared with BCG alone.

An interim analysis requested by the U.S. Food and Drug Administration (FDA) demonstrated statistically significant longer duration of complete response with ANKTIVA plus BCG compared to BCG alone. With the database lock complete for all patients enrolled, the final analysis is now underway and will assess the trial’s primary endpoint and key secondary endpoints, including the duration of response, in accordance with the prespecified statistical analysis plan.

ImmunityBio anticipates reporting topline results in November 2026 and remains on track to submit an sBLA to the FDA in the fourth quarter of 2026 for ANKTIVA plus BCG in patients with BCG-naïve NMIBC.

Cohort A completed enrollment in February 2026, with 366 patients randomized to receive ANKTIVA plus BCG versus BCG alone. In March 2026, following a protocol-specified interim review of the data from 183 evaluable patients, the Independent Data Monitoring Committee (IDMC) determined that the enrolled population provided sufficient statistical power to detect the prespecified clinically meaningful difference between treatment arms, with no additional enrollment required.

"QUILT-2.005 was designed to investigate whether, ANKTIVA, an IL-15 receptor agonist, could build upon the trained immunity induced by BCG by activating natural killer (NK) cells and CD8+ cytotoxic T cells with upregulating memory T cells to enhance therapeutic effectiveness earlier in the bladder cancer treatment journey," 1,2 said Patrick Soon-Shiong, M.D., Founder, Executive Chairman and Global Chief Medical and Scientific Officer of ImmunityBio. "With the database lock now complete in this randomized trial of 366 patients, we are entering a critical phase of validating the important role an IL-15 superagonist plays in the next evolution of immunotherapy. It has been established that chemotherapeutic approaches for the treatment of bladder cancer result in a reduction of NK and T cells, lymphocytes that are important for durable responses. The final analysis of this study will determine whether adding ANKTIVA to BCG improves complete response rates and the durability of those responses when compared with BCG alone, potentially resulting in the first intravesical, chemotherapy-free treatment approach for patients with BCG-naïve NMIBC. We look forward to sharing the findings once the analysis is complete."

"Achieving database lock brings us another step closer to our planned sBLA submission and our goal of expanding chemotherapy-free treatment options for patients with NMIBC," said Richard Adcock, President and Chief Executive Officer of ImmunityBio. "This progress reflects the coordinated efforts of our clinical development team, investigators, and site personnel across 110 U.S. and global clinical sites. We are especially grateful to the patients whose participation has made this important research possible."

About the QUILT-2.005 Study

QUILT-2.005 (NCT02138734) is a randomized, controlled registrational trial comparing the intravesical chemotherapy-free combination of ANKTIVA (nogapendekin alfa inbakicept-pmln) with BCG versus BCG alone in patients with BCG-naïve NMIBC. BCG-naïve patients are those receiving BCG-based therapy for the first time, representing an earlier stage of treatment than the BCG-unresponsive population for which ANKTIVA is currently approved. Enrollment of Cohort A was completed in February 2026 with 366 randomized patients. Following a protocol-specified interim review in March 2026, the IDMC determined that no additional enrollment was required to maintain the study’s prespecified statistical power. Full details can be found on clinicaltrials.gov.

About ANKTIVA (nogapendekin alfa inbakicept-pmln)

The interleukin-15 (IL-15) cytokine plays a crucial role in the immune system by affecting the development, maintenance, and function of key immune cells, NK and CD8+ killer T cells, that are involved in killing cancer cells. By activating NK cells, ANKTIVA overcomes the tumor escape phase of clones resistant to T cells and restores memory T cell activity with resultant prolonged duration of complete response. ANKTIVA is a first-in-class IL-15 receptor agonist IgG1 fusion complex, consisting of an IL-15 mutant (IL-15N72D) fused with an IL-15 receptor alpha, which binds with high affinity to IL-15 receptors on NK, CD4+, and CD8+ T cells. This fusion complex of ANKTIVA mimics the natural biological properties of the membrane-bound IL-15 receptor alpha, delivering IL-15 independent of dendritic cells and driving the activation and proliferation of NK cells with the generation of memory killer T cells that have retained immune memory against these tumor clones.

IMPORTANT SAFETY INFORMATION

INDICATION AND USAGE: ANKTIVA is an interleukin-15 (IL-15) receptor agonist indicated in combination with Bacillus Calmette-Guérin (BCG) for the treatment of adult patients with BCG-unresponsive non-muscle invasive bladder cancer (NMIBC).

WARNINGS AND PRECAUTIONS: Risk of Metastatic Bladder Cancer with Delayed Cystectomy. Delaying cystectomy can lead to the development of muscle-invasive or metastatic bladder cancer, which can be lethal. If patients with BCG-unresponsive NMIBC have evidence of high-grade disease after a second induction course of ANKTIVA with BCG, reconsider cystectomy.

DOSAGE AND ADMINISTRATION: For Intravesical Use Only. Do not administer by subcutaneous or intravenous routes.

USE IN SPECIFIC POPULATIONS: Pregnancy: May cause fetal harm. Advise females of reproductive potential of the potential risk to a fetus and to use effective contraception.

ADVERSE REACTIONS: The most common (≥15%) adverse reactions, including laboratory test abnormalities, are increased creatinine, dysuria, hematuria, urinary frequency, micturition urgency, urinary tract infection, increased potassium, musculoskeletal pain, chills, and pyrexia. For more information, please see the Prescribing Information for ANKTIVA at Anktiva.com.

(Press release, ImmunityBio, OCT 21, 2026, View Source [SID1234673638])

On October 21, 2026 HUTCHMED (China) Limited ("HUTCHMED" or the "Company") (Nasdaq/AIM:HCM; HKEX:13) reported that further to its announcement on September 3, 2026 and following the completion of customary closing conditions including antitrust regulatory reviews, the exclusive development and license agreement between HUTCHMED Limited (a subsidiary of the Company) and a subsidiary of GSK plc ("GSK") has closed. The agreement grants the GSK subsidiary worldwide rights excluding Mainland China, Hong Kong, Macau and Taiwan to develop and commercialize HMPL-A830.

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This first-in-class Antibody-Targeted Therapy Conjugate ("ATTC") drug candidate comprises a highly selective and potent Kirsten rat sarcoma ("KRAS") small molecule inhibitor payload conjugated to an anti-epidermal growth factor receptor ("EGFR") antibody. Colorectal, pancreatic and lung cancers have the highest incidence of patients with KRAS-altered tumors, who often lack safe and durable KRAS therapy. HMPL-A830 is designed to address this need by delivering a KRAS inhibitor directly to EGFR-expressing tumors, while simultaneously blocking EGFR and KRAS signaling to enhance efficacy, durability, and tolerability. The Phase Ia part of a global clinical trial of HMPL-A830 in patients with unresectable, advanced or metastatic solid tumors in China and the US was initiated in September 2026 (clinicaltrials.gov identifier NCT07718581).

Under the terms of the agreement, HUTCHMED Limited is responsible for the global Phase I development program. The GSK subsidiary will be responsible for all subsequent clinical development and commercialization activities in its territory. Following the closing of the exclusive license agreement, HUTCHMED Limited expects to receive US$110 million upfront payment shortly, and may receive additional development, regulatory and commercial milestone payments of up to a total of US$1.185 billion, as well as tiered royalties on annual net sales.

About HUTCHMED ATTCs

HUTCHMED’s ATTCs represent a next-generation approach to precision oncology, combining monoclonal antibodies with proprietary small-molecule inhibitor payload platforms to deliver dual mechanisms of action. Unlike traditional cytotoxin-based antibody-drug conjugates, ATTCs combine targeted therapies to achieve synergistic anti-tumor activity and durable responses in preclinical models, outperforming standalone antibody or small-molecule inhibitor components in both efficacy and safety.

Built on over 20 years of targeted therapy expertise, the ATTC platforms enable development of drug candidates across diverse cancer types. By leveraging antibody-guided delivery and tumor-specific payload release, ATTCs improve accessibility to tumors and reduce off-tumor toxicity. This may overcome the on-target, off-tumor toxicity limitations of systemically-delivered small molecule inhibitors, which in turn could ensure safer long-term use and support combinations with chemotherapy and immunotherapy in earlier-line treatments.

About KRAS

Rat sarcoma ("RAS") mutations represent one of the most prevalent and well-established drivers in human oncology, driving the progression and aggressive pathology of multiple solid tumors. KRAS, the most dominant RAS isoform, is mutated in approximately 44% of colorectal cancer ("CRC"), 34% of lung adenocarcinoma and up to 89% of pancreatic ductal adenocarcinoma ("PDAC") patients.1 KRAS regulates key downstream pathways, including RAS/MAPK and PI3K/AKT/mTOR, to drive cell differentiation, proliferation, and survival.

While recent targeted therapies have validated KRAS as a viable therapeutic target, significant clinical gaps persist, particularly for patients with non-G12C mutations. Most patients eventually experience disease progression driven by acquired resistance, largely fueled by upstream receptor tyrosine kinase upregulation and secondary KRAS alterations. Beyond mutation coverage, systemic delivery of pan-KRAS and pan-RAS inhibitors is associated with on-target toxicities, such as dermatological toxicity reflecting RAS pathway inhibition in normal tissue. These present challenges for dosing, long-term tolerability, and combination with cytotoxic chemotherapy or immunotherapy backbones that constitute frontline standard-of-care.

About EGFR

EGFR is a widely expressed receptor tyrosine kinase and established driver of tumor cell proliferation, survival, and disease progression across multiple solid tumors, including CRC, PDAC, and non-small cell lung cancer ("NSCLC"). Signaling through EGFR activates the downstream RAS/MAPK and PI3K/AKT/mTOR pathways, positioning the receptor immediately upstream of KRAS. EGFR has also emerged as a key mediator of resistance to KRAS-targeted therapies, particularly in CRC, where adaptive feedback and increased upstream EGFR signaling reactivate the MAPK pathway and limit the depth and durability of KRAS inhibition. Together, these provide a strong rationale for the dual targeting of EGFR and KRAS, not only in CRC but also additional indications such as PDAC and NSCLC.

(Press release, HUTCHMED, OCT 21, 2026, View Source [SID1234673637])

On October 21, 2026 Genprex, Inc. ("Genprex" or the "Company") (NASDAQ: GNPX), a clinical-stage biotechnology company developing gene therapies designed to restore tumor-suppressor function in cancer and insulin-producing function in diabetes, reported new peer-reviewed research in mice identifying an important role for the TUSC2 tumor suppressor gene in maintaining cellular processes associated with healthy brain aging and supporting broader understanding of how disruption of normal biological function may contribute to disease.

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The study, entitled "Mitochondrial calcium sensor TUSC2 protects the aging hippocampus from proteostasis collapse in a sex-specific manner," was published in Mechanisms of Ageing and Development by researchers at Meharry Medical College. TUSC2 is the therapeutic gene used in Genprex’s investigational REQORSA gene therapy, which is being developed for the treatment of cancer.

The research found that loss of TUSC2 in mice was associated with substantial disruption of mitochondrial function, of protein homeostasis and of pathways involved in neuronal communication within the hippocampus, a region of the brain essential for learning and memory. These effects were markedly more pronounced in male mice than in females, suggesting important sex-specific differences in the biological response to TUSC2 deficiency.

Importantly, the researchers also analyzed existing human gene-expression datasets and found that TUSC2 expression declined significantly with age in 11 of 13 examined brain regions, with additional reductions observed in Alzheimer’s disease datasets. Levels of TUSC2 protein in the hippocampus, as in the rest of the brain, decrease as humans age. Comparisons between the mouse findings and human hippocampal aging datasets identified overlapping molecular changes, supporting further investigation of TUSC2’s role in brain aging.

While the research did not evaluate REQORSA as a treatment for aging or neurodegenerative disease, the findings expand scientific understanding of the biological functions of TUSC2, the gene underlying Genprex’s lead oncology program.

"This research adds to our understanding of the diverse biological functions of TUSC2, the tumor suppressor gene at the center of our REQORSA oncology program," said Mark Berger, Chief Medical Officer of Genprex. "The findings highlight the important role TUSC2 plays in mitochondrial function, cellular stress responses, and protein homeostasis, while revealing intriguing differences between males and females. Importantly, the parallels identified between the preclinical findings and human brain aging data further reinforce the biological significance of TUSC2 beyond its established role in cancer. While these findings are exploratory, they contribute to a growing body of research into the broader functions of this important gene."

The research utilized an engineered mouse TUSC2 knockout (KO) model to investigate how the loss of TUSC2 accelerates molecular changes associated with hippocampal aging, before the onset of overt neurodegeneration. The findings establish the TUSC2 KO model as a valuable tool for investigating early stages of mitochondrial dysfunction, impaired protein homeostasis, and age-related changes in brain function.

Key study highlights:

Sex-Specific Resilience: The study identified marked differences in mitochondrial stress resilience between male and female mice. While TUSC2 loss in males disrupted mitochondrial, protein homeostasis and synaptic pathways, females exhibited adaptive cellular stress responses, suggesting greater resilience to TUSC2 deficiency.
Protein Homeostasis: TUSC2 deficiency was associated with impaired protein quality-control pathways and a significant increase in protein aggregate size in the male hippocampus, supporting a role for TUSC2 in maintaining cellular protein homeostasis.
Synaptic Pathway Maintenance: The researchers identified substantial disruption of pathways involved in neuronal communication and synaptic function including differences between gene expression and corresponding protein levels, suggesting that TUSC2 contributes to the maintenance of normal synaptic processes.
These findings further support the importance of understanding how biological functions are disrupted in aging and how restoring TUSC2 may open new avenues for therapeutic intervention in age-related cognitive disorders.

(Press release, Genprex, OCT 21, 2026, View Source [SID1234673636])