On October 16, 2026 Aprea Therapeutics, Inc. (Nasdaq: APRE) ("Aprea", or the "Company"), a clinical-stage precision medicine oncology company focused on the discovery and development of targeted therapies for patients with biomarker-defined cancers, reported that it will host a virtual panel discussion, "The State of WEE1 Inhibition in Precision Oncology," on Tuesday, October 20, 2026, at 11 am ET.

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Disrupting the DNA damage response has become a compelling therapeutic strategy in oncology in recent years and WEE1 inhibitors are among the most promising drugs being developed within this class. Ahead of the European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) Congress 2026, this panel will cover the underlying biology of WEE1, the selectivity challenge that has shaped the class, and what to watch in the months ahead, across scientific, clinical, and market perspectives.

Moderated by Solomon Wilcots, NFL broadcaster and former player for the Cincinnati Bengals, the panel will feature the following participants:

Dr. Alex Spira, Director of the Thoracic and Phase I Program at the Virginia Cancer Specialists Research Institute, Chief Scientific Officer of NEXT Oncology and Clinical Assistant Professor at Johns Hopkins School of Medicine.
Kevin DeGeeter Managing Director in equity research at Ladenburg Thalmann & Co. Inc.
Dr. Eugene Kennedy, Chief Medical Advisor of Aprea Therapeutics, Inc.

To register, please visit View Source

Aprea’s lead program, APR-1051, is an oral, small-molecule WEE1 kinase inhibitor being evaluated in the ongoing Phase 1 ACESOT-1051 study in patients with biomarker-defined advanced solid tumors.

(Press release, Aprea, OCT 16, 2026, View Source [SID1234673528])

On October 16, 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 new preclinical research from an academic–industry collaboration from the Universities of Jaén and Granada, led by Dr. Maria Belén Toledo, has identified pancreatic proenzyme formulation, PRP, as a potential strategy for addressing chemotherapy resistance in pancreatic cancer.

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Chemotherapy-resistant tumor cells can acquire adaptive cellular states that allow them to survive treatment and maintain aggressive characteristics. The study investigated whether PRP could remodel these resistant states and increase their vulnerability to subsequent chemotherapy. It combined functional cellular analyses with transcriptome-wide (i.e. RNA molecules within the cell) profiling in pancreatic cancer models with acquired chemotherapy resistance.

"These findings are highly significant as we progress PRP to a world-first, Phase 1b, First-In-Human study for advanced cancer patients with solid tumors in Q1 2027, because we envision PRP as a welcome addition to the treatment process, as a long term, metronomic therapy that minimizes threat of recurrence, whilst enabling patients to respond to standard treatment options where tumor resistance has become a critical, life threatening factor," said Mr. James Nathanielsz, Propanc’s Chief Executive Officer. "Dr. Toledo’s findings shows that PRP’s targeted multiple effects reprograms pancreatic cancer cells through interconnected biological programs which alters chemoresistance, tumor cell plasticity and aggressive behavior. We are now in the unique position to investigate sequential combinatorial approaches that rely on inhibition of specific tumor pathways which are effective, but do not address tumor led resistance mechanisms."

A sequential strategy to remodel resistance

A defining feature of the experimental design was the treatment sequence. Chemoresistant (GR) cells were first exposed to PRP. Chemotherapy was then added to determine whether PRP pre-treatment had altered the resistant state and changed the subsequent response to chemotherapy.

GR CELLS → PRP PRE-TREATMENT → CHEMOTHERAPY → ASSESSMENT OF RESPONSE

According to Dr. Toledo, "This distinction is central to the study: PRP was used first as a resistance-modulating intervention, while chemotherapy was subsequently used as the challenge to test whether the cells had become more responsive and sensitive."

Reprogramming the resistant cellular state

PRP induced coordinated changes across interconnected biological processes associated with chemoresistance, tumor cell plasticity and aggressive behavior. At a high level, these included:

Tumor-cell plasticity and epithelial–mesenchymal transition (EMT)
Drug-response and metabolic processes
DNA replication and repair
Cellular stress and survival programs
Extracellular matrix organization
Apoptotic susceptibility
Importantly, PRP treatment alone produced changes consistent with partial restoration of features associated with chemotherapy sensitivity in resistant models. This supports the concept of PRP as a resistance-modulating intervention rather than simply a conventional cytotoxic agent.

Testing whether resistance can be overcome

Following PRP pre-treatment, chemotherapy was introduced to determine whether the resistant phenotype had been functionally weakened. The sequential PRP → chemotherapy strategy produced the strongest functional response in the study, supporting the hypothesis that remodeling the resistant state before chemotherapy can increase therapeutic vulnerability. The study evaluated complementary phenotypes including cellular growth, clonogenic capacity, migration, invasion and cell-death susceptibility.

A multimodal mechanism

Transcriptomic analyses revealed that PRP does not appear to act through a single resistance mechanism. Instead, the response involved coordinated remodeling of interconnected biological programs. The nature and magnitude of these changes differed between tumor models (WT and GR), highlighting the heterogeneity of chemotherapy resistance. Together, the data supports a systems-level interpretation in which PRP weakens adaptive programs sustaining the resistant state, creating a cellular context that is more vulnerable to subsequent chemotherapy.

Summary of Preclinical Findings

Observations Results
Restoring Chemotherapy Sensitivity & Reducing Proliferation
PRP monotherapy reduced cancer cell proliferation by 50% in wild-type (WT) and 54% in chemoresistant (GR) cells
Long-term clonogenic survival (colony formation capacity over 21 days) was suppressed by 59% in WT and 39% in GR cells following PRP pre-treatment
Suppressing Metastatic Behavior (Migration and Invasion)
In 72-hour wound-healing migration assays, PRP monotherapy limited cell migration to 21% wound closure in WT and 57% in GR cells (compared to 100% closure in untreated controls)
Matrigel invasion assays demonstrated that PRP monotherapy reduced invasive capacity by 81% in WT and 47% in GR cells
Reversing Epithelial-Mesenchymal Transition (EMT) & Plasticity
PRP treatment induced strong epithelial differentiation, significantly upregulating key epithelial markers E-cadherin (up to 5.29-fold in WT and 4.86-fold in GR cells) and EPCAM (up to 4.39-fold in WT)
Concurrently, PRP downregulated key mesenchymal drivers including Vimentin (reduced to ~0.31–0.32-fold of control) and Snail (reduced to 0.28–0.62-fold)
Inhibiting Canonical TGF-β/SMAD Signaling
Quantitative RT-qPCR showed significant downregulation of SMAD2, SMAD3, and TGFBR1 gene expression (reduced to 0.23–0.42-fold in GR cells)
Protein-level immunofluorescence analysis confirmed that PRP monotherapy reduced nuclear translocation of SMAD2/3 by 81% in WT and 78% in GR cells
Inducing Apoptosis and Suppressing Oncogenic Stemness Drivers
PRP shifted cells toward a pro-apoptotic state, increasing BAX expression (2.49-fold in WT and 2.74-fold in GR) while decreasing anti-apoptotic BCL2 (0.49-fold)
PRP upregulated cell cycle and stress response regulators CDKN1A (p21) (3.90 to 4.10-fold), ATM (2.88 to 3.34-fold), and TP53 (3.29 to 3.64-fold)
Key drivers of aggressiveness and cancer stemness, MYC and SOX2, were suppressed down to 0.11-fold and 0.22-fold in chemoresistant cells, respectively
Enhanced Synergistic Effect with TGF-β Inhibition (PRP + TGF-β inhibitor)
Combining PRP with a TGF-β inhibitor further amplified therapeutic response in chemoresistant cells, achieving 80% invasion inhibition, an 8.24-fold increase in E-cadherin, a 93% reduction in nuclear SMAD2/3 translocation, and a 4.42-fold induction of BAX

Future development

These findings provide a preclinical rationale for further investigation of PRP as a resistance-modulating strategy, including its potential use as a standalone intervention to remodel resistant tumor cells and as a sequential approach preceding chemotherapy.

Validation in clinically relevant models will be undertaken to determine whether this resistance-remodeling effect can translate into a therapeutic benefit, ultimately, in patients.

CHEMORESISTANCE → RESISTANCE REMODELLING → THERAPEUTIC VULNERABILITY

(Press release, Propanc, OCT 16, 2026, View Source [SID1234673527])

On October 16, 2026 Actinium Pharmaceuticals, Inc. (NYSE American: ATNM) (Actinium or the Company), a pioneer in differentiated targeted radiotherapies with the potential to transform cancer treatment, reported three presentations, including an oral presentation and two e-posters, highlighting preclinical data supporting ATNM-400’s broad potential at the 39th Annual Congress of the European Association of Nuclear Medicine (EANM), October 17–21, 2026, in Vienna, Austria.

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The presentations feature ATNM-400, the Company’s first-in-class Actinium-225 (²²⁵Ac) radiotherapy, in non-small cell lung cancer (NSCLC), colorectal cancer, and ovarian cancer models. Together, the studies demonstrate preclinical antitumor activity as monotherapy and enhanced activity in combination with standard-of-care agents, supporting both approaches to development across solid tumors. These findings further expand the preclinical evidence supporting ATNM-400’s potential across multiple cancer indications, complementing its ongoing clinical development in metastatic castration-resistant prostate cancer (mCRPC).

In NSCLC, ATNM-400 demonstrated antitumor activity as monotherapy and enhanced activity in combination with KRAS or ALK inhibitors, including in resistant models. These findings extend earlier EGFR-mutant results and support mutation-agnostic development both as a standalone therapy and in combination with established treatments.

In colorectal cancer, ATNM-400 demonstrated monotherapy activity in SW620 xenografts and enhanced activity when combined with bevacizumab plus oxaliplatin in HCT15 xenografts, a model with moderate target expression and limited response to the standard-of-care combination. These findings support both monotherapy development and combinations aimed at improving outcomes in poorly responsive disease.

In ovarian cancer, ATNM-400 monotherapy produced durable antitumor activity, including in bevacizumab-refractory tumors. These findings support its potential as a standalone treatment in recurrent disease, with further evaluation of ATNM-400 alone and in combination with standard-of-care therapies extending this development strategy.

"These findings build a compelling preclinical foundation for ATNM-400’s pan-cancer potential and our vision to expand targeted radiotherapy across major solid tumor indications," said Sandesh Seth, Actinium’s Chairman and CEO. "The high prevalence of ATNM-400’s target in NSCLC, coupled with activity in KRAS- and ALK-driven models that builds on our earlier EGFR-mutant findings, supports the potential to reach a broad lung cancer population regardless of oncogenic mutation. Encouraging results in colorectal and treatment-resistant ovarian cancer models further extend this opportunity into areas of significant unmet need. Together, these data support our strategy to develop ATNM-400 as both a standalone therapy and a combination partner for established treatments, with the potential to address multiple large patient populations."

ATNM-400 EANM 2026 Presentation Details

Abstract Title: ATNM-400 Elicits Durable Anti-tumor Responses in KRAS- and ALK-Driven NSCLC Models in a Mutation-Agnostic Manner
Abstract Number: EPS-149
Presentation Type: Oral presentation
Session: 1109 — Translational Imaging and Therapy
Session Date & Time: Monday, October 19, 2026, 4:45–6:15 p.m. CEST | Vienna, Austria
Location: Hall G2

Abstract Title: ATNM-400, a First-in-Class Actinium-225 Radioconjugate Improves Response to Standard-of-Care Therapeutics in Colorectal Cancer Models
Abstract Number: EP-0163
Presentation Type: e-Poster

Abstract Title: ATNM-400, a First-in-Class Actinium-225 Radioconjugate Triggers Durable Antitumor Responses in Ovarian Cancer Models
Abstract Number: EP-0176
Presentation Type: e-Poster

(Press release, Actinium Pharmaceuticals, OCT 16, 2026, View Source [SID1234673526])

On October 16, 2026 Microbiotica, a clinical-stage biopharma company developing a pipeline of orally-dosed, precision microbiome medicines, reported the first close of a £36 million ($48 million) Series C financing.

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The financing was led by British Business Bank, with participation from Tencent, IP Group, Cambridge Innovation Capital, Flerie Invest, and Seventure Partners. All existing Series B investors participated in the financing.

Proceeds will support the advancement of MB310 into Phase 2 clinical development in ulcerative colitis, following positive results from the COMPOSER-1 Phase 1b study, which met its primary and secondary endpoints and demonstrated statistically significant improvements in clinical remission versus placebo. MB310 also showed disease modifying potential through improvements in histological measures and markers of intestinal epithelial barrier integrity. The randomised, double-blind, placebo controlled Phase 2 study will seek to confirm these highly encouraging early results.

MB310 targets a significant unmet need in ulcerative colitis

Ulcerative colitis is the most common form of inflammatory bowel disease and is a major debilitating disease that affects up to 5 million people globally. Despite available treatments, many patients do not achieve or maintain remission, highlighting the need for new therapeutic approaches. MB310 is a once-daily oral capsule comprised of a consortium of eight specific live gut commensal bacterial strains. Its differentiated mechanism of action promotes gut epithelial barrier repair and delivers anti-inflammatory effects, directly addressing the key drivers of disease which, together with its favourable safety profile, makes it ideally placed to be combined with existing ulcerative colitis products.

Carmine Circelli, Senior Investment Director, Life Sciences at the British Business Bank, commented: "We believe Microbiotica is emerging as a world leader in the development of microbiome therapeutics. Its Phase 1b study in ulcerative colitis produced statistically significant clinical remission, best in disease potential with no safety issues. This funding allows the Company to move MB310 forward into a Phase 2 trial which, if it confirms the promise seen in Phase 1b, has the potential to be a major breakthrough in the treatment of ulcerative colitis. By investing in companies like Microbiotica, we help the UK’s most promising life sciences companies to convert research into treatments while also building the UK’s thriving life sciences market."

A unique genomics-driven microbiome platform

Spun out of the Wellcome Sanger Institute in 2016, Microbiotica has a unique genomics-driven microbiome platform which combines a diverse microbiome culture collection, a proprietary human Reference Genome Database, advanced bioinformatics, and machine learning tools. When this platform is applied to clinical trial datasets, it can precisely identify bacteria associated with favourable clinical trial outcomes in specific patient populations. This clinical-data led approach informs the selection of bacterial strains for therapeutic development with the potential to improve the likelihood of clinical success.

The Company has established partnerships with MSD, Cancer Research UK, Genentech, The University of Adelaide and Cambridge University Hospitals NHS Foundation Trust.

The platform is also supporting the development of Microbiotica’s broader pipeline. The Company is advancing MB097, its precision microbiome asset for patients with advanced melanoma. Emerging clinical data from the ongoing Phase 1b MELODY-1 study has demonstrated encouraging results when MB097 is administered in combination with KEYTRUDA (pembrolizumab), MSD’s anti-PD-1 therapy.

Dr Sam Williams, Venture Partner at IP Group, said: "We have been very impressed by Microbiotica’s progress since we first invested in the Company, from translating pioneering microbiome science from the Wellcome Sanger Institute into a powerful genomics-driven microbiome platform that has generated promising efficacy in two Phase 1b clinical trials. There is an important opportunity to advance Microbiotica’s precision microbiome approach into a larger clinical study, and we are pleased to continue supporting the Company as it enters this next phase of development."

Tim Sharpington, Chief Executive Officer of Microbiotica, added: "This financing marks an important next stage for Microbiotica and reflects the significant progress we have made in translating our powerful genomics-driven microbiome platform into clinical-stage products, alongside developing a scalable and cost-effective manufacturing process. The strong Phase 1b results for MB310, together with the positive clinical data from our immuno-oncology programme, provide important validation of our approach. We are thankful for the support received from our investors and are now focused on taking MB310 into Phase 2 clinical development, where we have an opportunity to further establish MB310 as a breakthrough treatment option for people living with ulcerative colitis."

(Press release, Microbiotica, OCT 16, 2026, View Source [SID1234673525])

On October 16, 2026 Johnson & Johnson, a worldwide leader in multiple myeloma, reported that the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) recommends the approval of an indication extension of TALVEY (talquetamab). The recommendation is for talquetamab plus daratumumab with or without pomalidomide for the treatment of adults with relapsed or refractory multiple myeloma (RRMM), who have received at least one prior therapy.

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Combination of talquetamab plus daratumumab offers a novel target approach to RRMM treatment, with potential to spare healthy immune cells
Talquetamab targets a protein called GPRC5D, which is found on multiple myeloma cells (as well as some healthy cells in the body).2 GPRC5D expression is independent of other targets, including BCMA, and is absent or expressed at low levels on normal B-cells.2 Talquetamab works by targeting myeloma cells while largely sparing healthy B-cells.2 With daratumumab priming the immune system for enhanced talquetamab activity, the combination benefits from complementary mechanisms of action, reinforcing the potential effectiveness of this approach in multiple myeloma.2, 3, 4

Expert and company perspectives support talquetamab use earlier in the treatment pathway
"MonumenTAL-3 demonstrated significant improvements in progression-free survival, overall survival, response rates and depth of response with the combination of talquetamab and daratumumab," said Ester in ’t Groen, EMEA Therapeutic Area Head, Haematology, Johnson & Johnson. "For patients facing their first relapse, this combination has the potential to provide deep responses and keep their disease under control for longer at a critical point in their treatment journey. This CHMP recommendation reflects the continued evolution of the talquetamab programme in multiple myeloma, and further strengthens the potential of talquetamab-based therapies as early as second line, building on our commitment to generate data that can help inform treatment choices based on patients’ prior therapies and disease characteristics."

"At Johnson & Johnson, our strategy is grounded in pursuing differentiated immunotherapy approaches earlier in the disease course to address diverse patient characteristics and the evolving complexity of multiple myeloma," said Yusri Elsayed, M.D., M.H.Sc., Ph.D., Global Therapeutic Area Head, Oncology, Johnson & Johnson. "This off-the-shelf, immunotherapy-based combination leverages the power of our portfolio by bringing together talquetamab with the well-established therapy of daratumumab. By simultaneously targeting GPRC5D and CD38, our goal is to deliver deeper and longer lasting responses for patients."

Talquetamab combination has delivered significant clinical benefits from second line
The MonumenTAL-3 study evaluated talquetamab plus daratumumab (Tal-D) or Tal-D and pomalidomide (Tal-DP) compared to daratumumab plus pomalidomide and dexamethasone (DPd) in patients with RRMM who have received at least one prior line of therapy.5 At a median follow-up of two years (24.6 months), results showed significant improvement in progression-free survival (PFS) for Tal-DP (hazard ratio [HR], 0.28; 95% confidence interval [CI], 0.20-0.40; p<0.0001) and Tal-D (HR, 0.33; 95% CI, 0.24-0.46; p<0.0001).2 At 24 months, Tal-DP showed a PFS rate of 81.3% and Tal-D showed a PFS rate of 77.6%.2 All participants (N=864) were previously exposed to lenalidomide and a proteasome inhibitor and received at least one prior line of therapy.2 Most patients enrolled were refractory to lenalidomide (85.1%) and their last line of therapy (93.4%), and some were exposed to an anti-CD38 antibody (11.8%).1

Statistically significant improvements compared to DPd were observed across key secondary endpoints of overall response rate (ORR), complete response or better (≥CR) and minimal residual disease (MRD)-negative ≥CR (10-5, next-generation sequencing [NGS]) for Tal-DP and Tal-D.2 ORRs (88.2%, 88.5%, 77.6%), ≥CR rates (71.1%, 68.9%, 34.5%) and MRD-negative ≥CR rates (52.3%, 46.3%, 15.9%) were significantly higher for Tal-DP and Tal-D vs DPd, respectively, after two years median follow-up.2 Clinically meaningful improvement in overall survival (OS) was shown with Tal-DP (HR, 0.47; 95% CI, 0.30-0.73; p=0.0006) and Tal-D (HR, 0.51; 95% CI, 0.33-0.78; p=0.0015) vs DPd.2 At 24 months, Tal-DP delivered an OS rate of 89.2% and Tal-D delivered an OS rate of 87.9%.2

Safety profiles consistent with the known safety profiles of each monotherapy
The overall safety profiles for the talquetamab plus daratumumab treatment arms were consistent with the known safety profiles of each monotherapy.2 Overall, rates of Grade 3/4 treatment-emergent adverse events (TEAEs) were comparable across treatment arms (94.9% with Tal-DP, 74.8% with Tal-D and 91.5% with DPd).1 Infections occurred at rates of 87.3% (Tal-DP), 84.3% (Tal-D) and 83.0% (DPd).2 Tal-D had the lowest rate of Grade 3/4 infections (29.2%), followed by Tal-DP (37.7%) and DPd (42.2%).2 There were some instances of Grade 5 adverse events (AEs) across the entire population of the study; the Tal-DP arm saw the fewest (1.8%), followed by Tal-D (4.0%) and DPd (4.6%), with approximately 0.7% (Tal-DP), 1.5% (Tal-D) and 1.8% (DPd) due to infections.1

Treatment discontinuations due to AEs occurred in 10.5% of Tal-DP, 8.0% of Tal-D and 6.7% of DPd patients.2 At data cutoff; 70.3% (Tal-DP), 69.7% (Tal-D) and 47.3% (DPd) of patients remained on study treatment.2

About the MonumentTAL-3 Study
The MonumenTAL-3 (NCT05455320) study is an ongoing Phase 3 study of talquetamab in combination with daratumumab subcutaneous (SC) with or without pomalidomide compared to daratumumab SC combined with pomalidomide and dexamethasone in patients with relapsed or refractory multiple myeloma (RRMM) who have received at least one prior line of therapy.5 The primary endpoint is progression-free survival (PFS) and secondary endpoints include overall response rate (ORR), complete response or better (≥CR), minimal residual disease (MRD)-negative ≥CR (10-5 by next-generation sequencing), overall survival (OS) and safety.5 The MonumenTAL-3 study is a part of the MonumenTAL clinical programme, which includes exploring the potential of talquetamab as a combination regimen.5

About Talquetamab
Talquetamab received conditional marketing authorisation (CMA) from the European Commission (EC) in August 2023, as monotherapy for the treatment of adult patients with RRMM who have received at least three prior therapies, including an immunomodulatory agent, a proteasome inhibitor, and an anti-CD38 antibody and have demonstrated disease progression on the last therapy.6 The U.S. FDA also granted talquetamab approval in August 2023, for the treatment of adult patients with RRMM who have received at least four prior lines of therapy, including a proteasome inhibitor, an immunomodulatory agent, and an anti-CD38 antibody.7

Talquetamab is a bispecific T-cell engaging antibody that binds to CD3 on T-cells, and GPRC5D, a novel target which is highly expressed on the surface of multiple myeloma cells, with minimal to no expression detected on B-cells or B-cell precursors.6 To date, more than 11,000 patients have been treated with talquetamab worldwide8

For a full list of adverse events and information on dosage and administration, contraindications and other precautions when using talquetamab, please refer to the Summary of Product Characteristics. In line with the European Medicine Agency’s regulations for new medicines and those given conditional approval, talquetamab is subject to additional monitoring.

▼ In line with EMA regulations for new medicines and those given conditional approval, talquetamab is subject to additional monitoring.6

About Daratumumab and Daratumumab SC
Johnson & Johnson is committed to exploring the potential of daratumumab for patients with multiple myeloma across the spectrum of the disease.

In August 2012, Janssen Biotech, Inc., a Johnson & Johnson company, and Genmab A/S entered a worldwide agreement, which granted Johnson & Johnson an exclusive licence to develop, manufacture and commercialise daratumumab. Since launch, daratumumab has become a foundational therapy in the treatment of multiple myeloma, having been used in the treatment of more than 830,000 patients worldwide.9 Daratumumab was the first CD38-directed antibody approved to be given subcutaneously to treat patients with multiple myeloma.10,11 Daratumumab SC was also the first oncology injectable approved for administration by patients living with multiple myeloma or their caregivers from the fifth dose, if determined to be appropriate by their healthcare professional and following proper training.11,12 Daratumumab SC is co-formulated with recombinant human hyaluronidase PH20 (rHuPH20), Halozyme’s ENHANZE drug delivery technology.11

CD38 is a surface protein that is present in high numbers on multiple myeloma cells, regardless of the stage of disease.11,[xii] Daratumumab binds to CD38 and inhibits tumour cell growth causing myeloma cell death.11 Daratumumab may also have an effect on normal cells.11 Data across ten Phase 3 clinical trials, in both the frontline and relapsed settings across all newly diagnosed multiple myeloma patients, have shown that daratumumab-based regimens resulted in significant improvement in progression-free survival and/or overall survival.14, 15, 16, 17, 18, 19, 20, 21, 22, 23

For further information on daratumumab, please see the Summary of Product Characteristics at:
View Source

About Multiple Myeloma
Multiple myeloma is a complex blood cancer that affects a type of white blood cell called plasma cells, which are found in the bone marrow.24, 25 In multiple myeloma, these malignant plasma cells continue to proliferate, accumulating in the body and crowding out normal blood cells, as well as often causing bone destruction and other serious complications.26, 27 In the European Union, it is estimated that more than 35,000 people were diagnosed with multiple myeloma in 2024, and more than 21,900 patients died.28 Patients living with multiple myeloma experience relapses which become more frequent with each line of therapy, while remissions become progressively shorter.29, 30, 31Whilst some patients with multiple myeloma initially have no symptoms, others can have common signs and symptoms of the disease, which can include bone fracture or pain, low red blood cell counts, fatigue, high calcium levels, infections, or kidney damage.

(Press release, Johnson & Johnson, OCT 16, 2026, View Source [SID1234673524])