On September 22, 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 a comparative analysis of lead candidate PRP against recently reported clinical datasets from Erasca, Inc.’s pan-RAS molecular glue ERAS-0015 in pancreatic ductal adenocarcinoma (PDAC).

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The analysis follows FDA approval of Revolution Medicines’ daraxonrasib in pretreated metastatic PDAC in August 2026 and FDA Fast Track designation for ERAS-0015 in metastatic pancreatic adenocarcinoma on August 24, 2026. Propanc believes these advances validate RAS as a tractable driver in PDAC while simultaneously highlighting the biology RAS inhibition leaves unaddressed — epithelial-mesenchymal transition (EMT), cancer stem cells (CSCs), fibrosis, and metastatic dissemination.

PRP, a proprietary fixed-ratio combination of the pancreatic proenzymes, trypsinogen and chymotrypsinogen (1:6), does not inhibit RAS. Instead, it promotes differentiation of malignant cells toward a more normal phenotype, reverses EMT, depletes CSCs, and remodels the fibrotic tumor microenvironment (TME). The Company believes this non-cytotoxic, differentiation-based approach is complementary to — not competitive with — RAS(ON) inhibitors and pan-RAS molecular glues, including ERAS-0015.

PRP Preclinical Profile in Advanced PDAC

In orthotopic and patient-derived xenograft (PDX) models of advanced PDAC, three-times-weekly intravenous PRP achieved:

Greater than 90%, mean, tumor-growth inhibition versus vehicle controls (p < 0.001).
Marked reduction in metastatic burden in the liver and peritoneum.
Significant remodeling of the tumor microenvironment, including decreased cancer-associated fibroblast activity, reduced fibrosis, and suppression of EMT markers.
Enhanced sensitivity of chemo-resistant PDAC cells to standard-of-care gemcitabine/nab-paclitaxel, supporting the potential for lower chemotherapy doses with improved efficacy.
Median overall survival extension of more than 2.5-fold in treated animals compared with controls.
These results complement previously reported >85% tumor-growth inhibition data and peer-reviewed findings on PRP’s effects on PDAC fibroblasts. Limited prior compassionate-use experience with related proenzyme formulations has shown signals of prolonged survival in advanced solid-tumor patients, with a favorable safety profile and no severe treatment-related adverse events.

PRP holds FDA Orphan Drug Designation for pancreatic cancer and is not restricted to a specific RAS genotype, supporting potential broad applicability across solid tumors and possible use in combination or sequential settings with RAS inhibitors or standard chemotherapy.

ERAS-0015 Clinical Snapshot in PDAC

According to Erasca’s public disclosures, ERAS-0015 is an oral pan-RAS molecular glue designed to inhibit RAS signaling, including signaling driven by mutant RAS. Preliminary Phase 1 monotherapy data from the U.S. AURORAS-1 trial and the China JYP0015M101 study have shown:

Unconfirmed overall response rates (uORR) of 40% at pharmacologically active doses of 16–32 mg once daily and 42% at recommended expansion doses of 24–32 mg in second-line KRAS G12X PDAC.
A July 2026 update reporting a 57% unconfirmed 8-week ORR at the 32 mg once-daily recommended expansion dose in second-line or later KRAS G12X PDAC. Responding patients remained on treatment as of May 25, 2026, data cutoff.
Generally favorable early tolerability, with mostly low-grade treatment-related adverse events, no dose-limiting toxicities at disclosed cutoffs, and 100% median relative dose intensity at 24 mg and 32 mg once daily.
FDA Fast Track designation for metastatic pancreatic adenocarcinoma (August 24, 2026), with Erasca outlining a planned Phase 3 PDAC trial and additional registration-oriented studies in lung cancer.
Propanc congratulates Erasca on Fast Track designation and on the early clinical activity observed with ERAS-0015. High response rates in RAS-mutant PDAC are an important advance for patients. The Company’s thesis is that converting those responses into deeper, more durable remissions will require a second layer of biology — reversing the mesenchymal, stem-like, fibrotic program that enables residual disease to persist, disseminate, and resist pathway blockade.

Comparative Snapshot

Sources: Company disclosures and peer-reviewed or conference reports as of September 2026. PRP efficacy cited is preclinical. ERAS-0015 and daraxonrasib data are from human clinical trials. Cross-modality numerical comparisons are directional only and are not head-to-head results.

Attribute PRP (PPCB) ERAS-0015 (ERAS) Daraxonrasib (RVMD)
Modality IV proenzyme combo (trypsinogen + chymotrypsinogen, 1:6) Oral pan-RAS molecular glue Oral RAS(ON) multi-selective inhibitor
Primary node Differentiation / EMT reversal / CSCs / TME Pan-RAS (KRAS G12X and related) Oncogenic RAS(ON) signaling
Evidence stage Preclinical PDAC + limited compassionate use; Phase 1b planned February 2027 Phase 1 dose-escalation / expansion; Fast Track; registration path outlined Phase 3 PDAC; FDA approved August 2026 for pretreated metastatic PDAC
PDAC activity >90% TGI; >2.5× median OS in models; metastasis and fibrosis reduced Ph1 2L KRAS G12X: uORR 40–42%; 57% uORR8wk at 32 mg RDE (2L+) Ph3 2L: mOS 13.2 vs 6.6–6.7 mo; mPFS 7.3 vs 3.5 mo; ORR ~33% vs ~12%
Genotype limit Not RAS-mutation restricted; FDA Orphan Drug Designation for pancreatic cancer RAS / KRAS G12X-enriched populations RAS-mutant tumors (multi-selective, not G12C-only)
Resistance biology addressed EMT, CSCs, CAFs, fibrosis, metastasis, chemo re-sensitization RAS output; combinations (e.g., anti-EGFR) being explored Oncogene-addicted proliferation; adaptive MAPK reactivation remains a known class issue

Why PRP May Complement ERAS-0015 and Other RAS Agents

RAS mutations drive approximately 90% of PDAC. Oral RAS inhibitors have now produced practice-changing clinical results. Propanc’s view is that turning RAS off is necessary but may not be sufficient.

Cells that survive RAS blockade are frequently mesenchymal and stem-like. EMT is the program that allows carcinoma cells to leave the primary site, hide from therapy, and return. Fibrosis and cancer-associated fibroblasts further limit drug penetration and sustain a CSC reservoir through TGF-β signaling. None of those liabilities is the primary target of a "pan-RAS molecular glue".

PRP is designed to act downstream of the GTPase:

Proenzyme activation and PAR signaling. After intravenous administration, trypsinogen and chymotrypsinogen are activated and engage PAR-1 and PAR-2, which are frequently overexpressed on tumor cells. This cascade is associated with reduced TGF-β pathway output — a master inducer of EMT in late-stage cancer.
Restoration of an epithelial phenotype. PRP increases epithelial adhesion proteins such as E-cadherin and β-catenin and decreases EMT transcription factors. Cells become less motile, more adherent, and more differentiated.
Depletion of cancer stem cells. In pancreatic CSC models, PRP reduced ALDH-high cells and surface markers CD44, CD326, and CXCR4; suppressed primary and secondary sphere formation; and impaired tumor engraftment in vivo.
TME remodeling and chemo-sensitization. Decreased CAF activity and fibrosis can improve drug delivery. By pushing cells out of a mesenchymal, drug-tolerant state, PRP resensitized chemo-resistant PDAC cells to gemcitabine/nab-paclitaxel. The same logic applies to RAS inhibitors: a smaller mesenchymal reservoir should leave fewer cells capable of adaptive resistance.
"RAS inhibitors have rewritten what is possible in pancreatic and RAS-mutant lung cancer. That is a genuine inflection point for patients," said Mr. James Nathanielsz, Propanc’s Chief Executive Officer. "Our thesis is that turning RAS off is necessary but may not be sufficient. The cells that survive RAS blockade are often the mesenchymal, stem-like cells that PRP differentiate and disarm. If that biology holds in the clinic, PRP could help RAS-focused companies — including programs such as ERAS-0015 — convert high response rates into longer, cleaner remissions."

"EMT is the program that lets a carcinoma leave home, hide, and return," said Dr. Ralf Brandt, Propanc’s Research & Development Director. "PRP does not compete with daraxonrasib or ERAS-0015 at the GTPase. It reverses the downstream identity change those tumors used to resist almost every class of drug. That is why we see suppression of EMT markers, loss of CSC phenotypes, less fibrosis, fewer metastases, and more than a two-and-a-half-fold survival extension in PDAC models. Those are the exact liabilities a RAS inhibitor leaves on the table."

"Pancreatic cancer remains one of oncology’s greatest challenges, with five-year survival rates still near 13% and limited durable options for patients with metastatic disease," Mr. Nathanielsz added. "We are accelerating our Phase 1b First-in-Human study in advanced solid tumors, with pancreatic cancer as a key focus indication. PRP’s orphan designation, genotype-agnostic mechanism, and complementary profile versus emerging RAS agents give us strong conviction as we move toward the clinic."

Clinical Development Path

The Company is progressing GMP manufacturing, pharmacokinetics assay validation, and clinical partnerships in support of a planned Phase 1b First-in-Human study. The multicenter, open-label study is expected to enroll approximately 40 to 50 patients with advanced solid tumors, including pancreatic, ovarian, and other refractory cancers, with first patient dosing targeted for February 2027. A clinical trial application is expected in the coming months.

Propanc intends to evaluate PRP both as a single agent and, subject to emerging clinical data and partner interest, as a potential backbone in combination or sequential regimens with RAS-targeted therapies and standard chemotherapy.

(Press release, Propanc, SEP 22, 2026, View Source [SID1234671000])

On September 22, 2026 Takeda (TSE:4502/NYSE:TAK) reported that new data from its oncology pipeline and portfolio will be presented at the European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) Congress, taking place October 23-27, 2026, in Madrid, Spain. Key data will include a late-breaking abstract on arcotatug tavatecan (TAK-921; Innovent R&D code: IBI343*) and two presentations on TAK-928 (Innovent R&D code: IBI363*). Clinical and real-world analyses of ALUNBRIG (brigatinib) and FRUZAQLA (fruquintinib) will also be shared at the congress.

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"Takeda’s data at ESMO (Free ESMO Whitepaper) reflect our commitment to delivering rapid progress for patients living with some of the most prevalent and challenging cancers, including advanced gastric cancer and immunotherapy-resistant and previously untreated non-small cell lung cancer," said Phuong Khanh (P.K.) Morrow, M.D., Head of the Oncology Therapeutic Area Unit at Takeda. "Our mission is to advance new therapeutic approaches for patients who need more options or who remain underserved by current standards of care. Together, our late-stage oncology pipeline and portfolio of thoracic and gastrointestinal cancer medicines are helping address patients’ needs today while building possibilities for the future."

Late-breaking data from the Phase 3 G-HOPE-001 study (NCT06238843) of arcotatug tavatecan being conducted in Japan and China in patients with previously treated advanced gastric or gastroesophageal junction adenocarcinoma (G/GEJA) will be presented during the ESMO (Free ESMO Whitepaper) proffered paper session on October 23, 13:30-15:00 CEST (Abstract LBA77). Arcotatug tavatecan is an investigational Claudin 18.2-targeted antibody-drug conjugate (ADC) with an exatecan payload and an Fc-silenced backbone designed to reduce Fc-mediated toxicities. Pending evaluation of final study results, data from G-HOPE-001 could support a potential regulatory filing for this indication in Japan.

Additionally, new findings for TAK-928 plus bevacizumab in immunotherapy-resistant non-small cell lung cancer (NSCLC) and TAK-928 plus chemotherapy in first-line NSCLC will be featured in two presentations. TAK-928 is a potential first-in-class PD-1/alpha-biased IL-2 bispecific fusion protein. Based on data showing promising efficacy and manageable safety in NSCLC to date, Takeda is conducting the global Phase 3 MarsLight-11 study (NCT07217301) evaluating TAK-928 vs. docetaxel in patients with squamous NSCLC whose disease has progressed on or after chemotherapy and immunotherapy. Enrollment is ongoing at trial sites globally, including in the U.S. In addition, Takeda will expand the MarsLight-11 study to include a new sub-trial for patients with non-squamous NSCLC.

Takeda is committed to developing oncology medicines in three strategic areas of focus: hematologic, thoracic and gastrointestinal cancers. Further presentations at ESMO (Free ESMO Whitepaper) 2026 will highlight clinical and real-world analyses spanning Takeda’s approved medicines across thoracic and gastrointestinal cancers, including:

Real-world interim results on treatment patterns and outcomes with ALUNBRIG as a first-line treatment for adults with anaplastic lymphoma kinase positive (ALK+) NSCLC to be presented as an e-poster
Updated results from a global FRUZAQLA Expanded Access Program for patients with previously treated metastatic colorectal cancer (mCRC) to be presented as a poster
Arcotatug tavatecan and TAK-928 are investigational compounds that have not been approved for use by the U.S. FDA or any other regulatory authorities.

*Innovent refers to arcotatug tavatecan (TAK-921) and TAK-928 as IBI343 and IBI363, respectively. Takeda entered into a license and collaboration agreement with Innovent. Under the agreement, Takeda holds the rights to develop, manufacture and commercialize arcotatug tavatecan worldwide outside of greater China. For TAK-928, Takeda will lead global co-development and U.S. co-commercialization and has exclusive commercialization rights outside the U.S. and Greater China.

ALUNBRIG (brigatinib) IMPORTANT SAFETY INFORMATION
INDICATION
ALUNBRIG is a kinase inhibitor indicated for the treatment of adult patients with anaplastic lymphoma kinase (ALK)-positive metastatic non-small cell lung cancer (NSCLC) as detected by an FDA-approved test.

WARNINGS AND PRECAUTIONS
Interstitial Lung Disease (ILD)/Pneumonitis
Severe, life-threatening, and fatal pulmonary adverse reactions consistent with interstitial lung disease (ILD)/pneumonitis have occurred with ALUNBRIG. In ALTA 1L, ILD/pneumonitis occurred in 5.1% of patients receiving ALUNBRIG. ILD/pneumonitis occurred within 8 days of initiation of ALUNBRIG in 2.9% of patients, with Grade 3 to 4 reactions occurring in 2.2% of patients. In the ALTA study, at the approved dose (90→180 mg), ILD/pneumonitis occurred in 9.1% of patients. Monitor for new or worsening respiratory symptoms (dyspnea, cough, etc.), particularly during the first week of initiating ALUNBRIG. Withhold ALUNBRIG in any patient with new or worsening respiratory symptoms, and promptly evaluate for ILD/pneumonitis or other causes of respiratory symptoms (e.g., pulmonary embolism, tumor progression, and infectious pneumonia). For Grade 1 or 2 ILD/pneumonitis, either dose reduce or permanently discontinue ALUNBRIG. Permanently discontinue ALUNBRIG for Grade 3 or 4 ILD/pneumonitis or recurrence of Grade 1 or 2 ILD/pneumonitis.

Hypertension
In ALTA 1L, hypertension was reported in 32% of patients receiving ALUNBRIG; 13% of patients experienced Grade 3 hypertension. Control blood pressure prior to treatment with ALUNBRIG. Monitor blood pressure and withhold ALUNBRIG for Grade 3 hypertension despite optimal antihypertensive therapy. Consider permanent discontinuation of treatment with ALUNBRIG for Grade 4 hypertension or recurrence of Grade 3 hypertension. Use caution when administering ALUNBRIG in combination with antihypertensive agents that cause bradycardia.

Bradycardia
In ALTA 1L, heart rates less than 50 beats per minute (bpm) occurred in 8.1% of patients receiving ALUNBRIG; one patient (0.7%) experienced Grade 3 bradycardia. Monitor heart rate and blood pressure during treatment with ALUNBRIG. For symptomatic bradycardia, withhold ALUNBRIG and review concomitant medications for those known to cause bradycardia; dose reduce concomitant medication or ALUNBRIG as appropriate. Discontinue ALUNBRIG for life-threatening bradycardia if no contributing concomitant medication is identified.

Visual Disturbance
In ALTA 1L, Grade 1 or 2 adverse reactions leading to visual disturbance, including blurred vision, photophobia, photopsia, and reduced visual acuity, were reported in 7.4% of patients receiving ALUNBRIG. In the ALTA study, at the approved dose (90→180 mg), Grade 3 macular edema and cataract occurred in one patient each. Advise patients to report any visual symptoms. Withhold ALUNBRIG and obtain an ophthalmologic evaluation in patients with new or worsening visual symptoms of Grade 2 or greater severity; upon recovery, dose reduce as appropriate. Permanently discontinue treatment with ALUNBRIG for Grade 4 visual disturbances.

Creatine Phosphokinase (CPK) Elevation
In ALTA 1L, creatine phosphokinase (CPK) elevation occurred in 81% of patients who received ALUNBRIG. The incidence of Grade 3 or 4 CPK elevation was 24%. Dose reduction for CPK elevation occurred in 15% of patients. Advise patients to report any unexplained muscle pain, tenderness, or weakness. Monitor CPK levels during ALUNBRIG treatment. Withhold ALUNBRIG for Grade 3 or 4 CPK elevation with Grade 2 or higher muscle pain or weakness. Upon resolution or recovery to Grade 1 CPK elevation or baseline, resume ALUNBRIG at the same dose or at a reduced dose.

Pancreatic Enzyme Elevation
In ALTA 1L, amylase elevation occurred in 52% of patients and Grade 3 or 4 amylase elevation occurred in 6.8% of patients who received ALUNBRIG. Lipase elevations occurred in 59% of patients and Grade 3 or 4 lipase elevation occurred in 17% of patients. Monitor lipase and amylase during treatment with ALUNBRIG. Withhold ALUNBRIG for Grade 3 or 4 pancreatic enzyme elevation. Upon resolution or recovery to Grade 1 or baseline, resume ALUNBRIG at the same dose or at a reduced dose.

Hepatotoxicity
In ALTA 1L, aspartate aminotransferase (AST) elevations occurred in 72% of patients and Grade 3 or 4 AST elevations occurred in 4.5% of patients who received ALUNBRIG. Alanine aminotransferase (ALT) elevations occurred in 52% of patients and Grade 3 or 4 ALT elevations occurred in 5.2% of patients. One patient (0.7%) had a serious adverse reaction of hepatocellular injury. Monitor AST, ALT and total bilirubin during treatment with ALUNBRIG, especially during the first 3 months. Withhold ALUNBRIG for Grade 3 or 4 hepatic enzyme elevation with bilirubin less than or equal to 2 × ULN. Upon resolution or recovery to Grade 1 or less (less than or equal to 3 × ULN) or to baseline, resume ALUNBRIG at a next lower dose. Permanently discontinue ALUNBRIG for Grade 2 to 4 hepatic enzyme elevation with concurrent total bilirubin elevation greater than 2 times the ULN in the absence of cholestasis or hemolysis.

Hyperglycemia
In ALTA 1L, 56% of patients who received ALUNBRIG experienced new or worsening hyperglycemia. Grade 3 hyperglycemia, based on laboratory assessment of serum fasting glucose levels, occurred in 7.5% of patients. In the ALTA study, 2 of 20 (10%) patients with diabetes or glucose intolerance at baseline required initiation of insulin while receiving ALUNBRIG. Assess fasting serum glucose prior to initiation of ALUNBRIG and monitor periodically thereafter. Initiate or optimize anti-hyperglycemic medications as needed. If adequate hyperglycemic control cannot be achieved with optimal medical management, withhold ALUNBRIG until adequate hyperglycemic control is achieved and consider reducing the dose of ALUNBRIG.

Photosensitivity
In ALTA 1L, 3.7% of patients who received ALUNBRIG experienced photosensitivity, with 0.7% of patients experiencing Grade 3 to 4 reactions. Advise patients to limit sun exposure while taking ALUNBRIG, and for at least 5 days after discontinuation of treatment. Advise patients, when outdoors, to wear protective clothing and use a broad-spectrum sunscreen (SPF ≥30) to help protect against sunburn. Based on the severity, withhold ALUNBRIG, then resume at the same dose, or reduce the dose, or permanently discontinue.

Embryo-Fetal Toxicity
Based on its mechanism of action and findings in animals, ALUNBRIG can cause fetal harm when administered to pregnant women. There are no clinical data on the use of ALUNBRIG in pregnant women. Advise women of the potential risk to a fetus.

ADVERSE REACTIONS
The most common adverse reactions (≥25%) with ALUNBRIG were diarrhea, fatigue, nausea, rash, cough, myalgia, headache, hypertension, vomiting, and dyspnea.

DRUG INTERACTIONS
CYP3A Inhibitors: Avoid coadministration of ALUNBRIG with strong or moderate CYP3A inhibitors. If coadministration of a strong or moderate CYP3A inhibitor is unavoidable, reduce the dose of ALUNBRIG.

CYP3A Inducers: Avoid coadministration of ALUNBRIG with strong or moderate CYP3A inducers. If coadministration of a moderate CYP3A inducer is unavoidable, increase the dose of ALUNBRIG.

USE IN SPECIFIC POPULATIONS
Females and Males of Reproductive Potential
Verify pregnancy status in females of reproductive potential prior to initiating ALUNBRIG. Advise females of reproductive potential to use effective contraception during treatment with ALUNBRIG and for at least 4 months after the final dose. Advise males with female partners of reproductive potential to use effective contraception during treatment with ALUNBRIG and for at least 3 months after the final dose. ALUNBRIG may cause reduced fertility in males.

Lactation: Advise patients not to breastfeed.

Hepatic Impairment: Reduce the dose of ALUNBRIG for patients with severe hepatic impairment.

Renal Impairment: Reduce the dose of ALUNBRIG for patients with severe renal impairment.

To report SUSPECTED ADVERSE REACTIONS, contact Takeda Pharmaceuticals U.S.A., Inc. at 1-844-217-6468 or the FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.

Please see full Prescribing Information.

FRUZAQLA (fruquintinib) IMPORTANT SAFETY INFORMATION
INDICATION
FRUZAQLA is indicated for the treatment of adult patients with metastatic colorectal cancer (mCRC) who have been previously treated with fluoropyrimidine-, oxaliplatin-, and irinotecan-based chemotherapy, an anti-VEGF therapy and, if RAS wild-type and medically appropriate, an anti-EGFR therapy.

WARNINGS AND PRECAUTIONS
Hypertension occurred in 49% of 911 patients with mCRC treated with FRUZAQLA, including Grade 3-4 events in 19%, and hypertensive crisis in three patients (0.3%). Do not initiate FRUZAQLA unless blood pressure is adequately controlled. Monitor blood pressure weekly for the first month and at least monthly thereafter as clinically indicated. Initiate or adjust anti-hypertensive therapy as appropriate. Withhold, reduce dose, or permanently discontinue FRUZAQLA based on severity of hypertension.
Hemorrhagic Events including serious, fatal events can occur with FRUZAQLA. In 911 patients with mCRC treated with FRUZAQLA, 6% of patients experienced gastrointestinal hemorrhage, including 1% with a Grade ≥3 event and 2 patients with fatal hemorrhages. Permanently discontinue FRUZAQLA in patients with severe or life-threatening hemorrhage. Monitor the International Normalized Ratio (INR) levels in patients receiving anticoagulants.
Infections. FRUZAQLA can increase the risk of infections, including fatal infections. In 911 patients with mCRC treated with FRUZAQLA, the most common infections were urinary tract infections (6.8%), upper respiratory tract infections (3.2%) and pneumonia (2.5%); fatal infections included pneumonia (0.4%), sepsis (0.2%), bacterial infection (0.1%), lower respiratory tract infection (0.1%), and septic shock (0.1%). Withhold FRUZAQLA for Grade 3 or 4 infections, or worsening infection of any grade. Resume FRUZAQLA at the same dose when the infection has resolved.
Gastrointestinal Perforation occurred in patients treated with FRUZAQLA. In 911 patients with mCRC treated with FRUZAQLA, 1.3% experienced a Grade ≥3 gastrointestinal perforation, including one fatal event. Permanently discontinue FRUZAQLA in patients who develop gastrointestinal perforation or fistula.
Hepatotoxicity. FRUZAQLA can cause liver injury. In 911 patients with mCRC treated with FRUZAQLA, 48% experienced increased ALT or AST, including Grade ≥3 events in 5%, and fatal events in 0.2% of patients. Monitor liver function tests (ALT, AST, and bilirubin) before initiation and periodically throughout treatment with FRUZAQLA. Temporarily hold and then reduce or permanently discontinue FRUZAQLA depending on the severity and persistence of hepatotoxicity as manifested by elevated liver function tests.
Proteinuria. FRUZAQLA can cause proteinuria. In 911 patients with mCRC treated with FRUZAQLA, 36% experienced proteinuria and 2.5% of patients experienced Grade ≥3 events. Monitor for proteinuria before initiation and periodically throughout treatment with FRUZAQLA. For proteinuria ≥2g/24 hours, withhold FRUZAQLA until improvement to ≤Grade 1 proteinuria and resume FRUZAQLA at a reduced dose. Discontinue FRUZAQLA in patients who develop nephrotic syndrome.
Palmar-Plantar Erythrodysesthesia (PPE) occurred in 35% of 911 patients treated with FRUZAQLA, including 8% with Grade 3 events. Based on severity of PPE, withhold FRUZAQLA and then resume at the same or reduced dose.
Posterior Reversible Encephalopathy Syndrome (PRES), a syndrome of subcortical vasogenic edema diagnosed by characteristic finding on MRI, occurred in one of 911 patients treated with FRUZAQLA. Perform an evaluation for PRES in any patient presenting with seizures, headache, visual disturbances, confusion, or altered mental function. Discontinue FRUZAQLA in patients who develop PRES.
Impaired Wound Healing. In 911 patients with mCRC treated with FRUZAQLA, 1 patient experienced a Grade 2 event of wound dehiscence. Do not administer FRUZAQLA for at least 2 weeks prior to major surgery. Do not administer FRUZAQLA for at least 2 weeks after major surgery and until adequate wound healing. The safety of resumption of FRUZAQLA after resolution of wound healing complications has not been established.
Arterial Thromboembolic Events. In 911 patients with mCRC treated with FRUZAQLA, 0.8% of patients experienced an arterial thromboembolic event. Initiation of FRUZAQLA in patients with a recent history of thromboembolic events should be carefully considered. In patients who develop arterial thromboembolism, discontinue FRUZAQLA.
Allergic Reactions to FD&C Yellow No. 5 (Tartrazine) and No. 6 (Sunset Yellow FCF). FRUZAQLA 1 mg capsules contain FD&C Yellow No. 5 (tartrazine), which may cause allergic-type reactions (including bronchial asthma) in certain susceptible persons. FRUZAQLA 1 mg contains FD&C Yellow No. 6 (sunset yellow FCF), which may cause allergic reactions.
Embryo-Fetal Toxicity. Based on findings in animal studies and its mechanism of action, FRUZAQLA can cause fetal harm when administered to pregnant women. Advise pregnant women of the potential risk to a fetus.
ADVERSE REACTIONS
The most common adverse reactions (incidence ≥20%) following treatment with FRUZAQLA included hypertension, palmar-plantar erythrodysesthesia (hand-foot skin reactions), proteinuria, dysphonia, abdominal pain, diarrhea, and asthenia.

DRUG INTERACTIONS

Avoid concomitant administration of FRUZAQLA with strong or moderate CYP3A inducers.

USE IN SPECIFIC POPULATIONS

Lactation: Advise women not to breastfeed during treatment with FRUZAQLA and for 2 weeks after the last dose.
Females and Males of Reproductive Potential
Pregnancy Testing: Verify pregnancy status of females of reproductive potential prior to initiating FRUZAQLA.
Contraception: Females of childbearing potential and males with female partners of childbearing potential should use effective contraception during treatment and for 2 weeks after the last dose of FRUZAQLA.
Infertility: Advise females of reproductive potential that FRUZAQLA may cause post-implantation loss.

(Press release, Takeda, SEP 22, 2026, View Source;utm_term=&utm_content=1033477&utm_id=9b2de23c-1b8d-432e-89da-925d65f93d07&sfmc_activityid=01bf63e4-57d1-4bca-96c8-9dad86fbb8f4&utm_medium=email&utm_campaign=PressReleases_EN_Automated_Gray_700px_Email1&sfmc_journey_id=9b2de23c-1b8d-432e-89da-925d65f93d07&sfmc_journey_name=rPse_seRelsa_eNEL_naJ_uonrye2_20_4rPdo&sfmc_activity_id=01bf63e4-57d1-4bca-96c8-9dad86fbb8f4&sfmc_activity_name=rPseRsleaees_sNEA_tumotadeG_ar_y07p0_xmEia1l&sfmc_asset_id=1033477&sfmc_channel=email [SID1234670999])

On September 22, 2026 Compass Therapeutics, Inc. (Nasdaq: CMPX), a clinical-stage, oncology-focused biopharmaceutical company developing proprietary antibody-based therapeutics to treat multiple human diseases, reported that the U.S. Food and Drug Administration (FDA) recommended that Compass conduct a trial demonstrating a survival benefit before proceeding with a Biologics License Application (BLA) submission for tovecimig in patients with previously treated, advanced biliary tract cancer (BTC).

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BTC is an aggressive, life-threatening cancer with poor survival outcomes, and effective options remain limited for patients who have received prior treatment, underscoring the urgent need for new approaches.

As previously disclosed, in the positive Phase 2/3 COMPANION-002 study, tovecimig plus paclitaxel demonstrated a statistically significant improvement in the primary endpoint of objective response rate (ORR) of 18.0% vs. 5.3% with paclitaxel alone (p=0.0228) and a highly significant improvement in progression-free survival (PFS) in patients with BTC who had received prior treatment. Median PFS was 4.7 vs. 2.6 months with a hazard ratio of 0.44 (p<0.0001), representing a compelling 56% reduction in the risk of disease progression. Overall survival (OS) analyses were confounded by both high crossover and notably prolonged survival in crossover patients randomized to the control arm then treated with tovecimig and, therefore, did not meet statistical significance. The safety profile was generally consistent with previously reported data from prior tovecimig studies.

"While this is not the response we expected, we respect the FDA’s feedback and our priority is to work with the Agency to determine the best path forward to support our planned BLA submission and address this pressing unmet need," said Thomas Schuetz, M.D., Ph.D., Chief Executive Officer of Compass. "We remain confident that the COMPANION-002 findings, including the statistically significant improvements in PFS and ORR combined with subset analyses on survival, demonstrate clinically meaningful activity in patients with previously treated, advanced BTC."

About Tovecimig
Tovecimig is an investigational DLL4 x VEGF-A bispecific antibody designed to block two angiogenic pathways simultaneously, representing a first-in-class approach to disrupting tumor angiogenesis. In COMPANION-002, tovecimig was evaluated in combination with paclitaxel in patients with previously treated, advanced biliary tract cancer. Tovecimig has received Fast Track and Orphan Drug Designation from the U.S. Food and Drug Administration.

(Press release, Compass Therapeutics, SEP 22, 2026, View Source [SID1234670998])

On September 22, 2026 IMUNON, Inc. (Nasdaq: IMNN), a clinical-stage biotechnology company developing DNA-mediated immunotherapies, reported that the Independent Data Monitoring Committee (IDMC) overseeing its ongoing Phase 2 minimal residual disease (MRD) translational study of IMNN-001 has reviewed all safety data to date and recommended that the study continue without modification after identifying no new safety signals and confirming comparable safety across both treatment arms.

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The IDMC is comprised of independent medical experts in gynecologic cancers. The Phase 2 MRD study is a randomized, controlled translational study assessing minimal residual disease following treatment with standard-of-care chemotherapy and bevacizumab, with or without IMNN-001, in women with newly diagnosed advanced ovarian cancer. The multi-site study is being conducted in collaboration with Break Through Cancer and is led by investigators at The University of Texas MD Anderson Cancer Center.

"The IDMC’s recommendation to continue our Phase 2 MRD study without modification provides important independent validation of the favorable safety profile we have consistently observed across our clinical development program," said Stacy Lindborg, Ph.D., President and Chief Executive Officer of IMUNON. "Across our completed and ongoing clinical studies, we have observed no cytokine release syndrome, no systemic toxicities and no serious immune-related adverse events—an important distinction for an IL-12-based immunotherapy. Combined with the encouraging biological and clinical activity reported from this study in July, these findings further strengthen our confidence as we continue advancing our pivotal Phase 3 OVATION 3 trial."

Consistent with this experience, the latest IDMC review identified no new safety concerns in the ongoing pivotal Phase 3 OVATION 3 trial. The MRD study has also achieved two important safety objectives by demonstrating the safety and tolerability of IMNN-001 both in combination with bevacizumab and in the maintenance setting.

In July 2026, the Company reported encouraging preliminary data from the MRD study, which is designed both to evaluate clinical activity and to better understand how IMNN-001 remodels the tumor immune microenvironment following frontline treatment. Among patients who reached the study’s primary assessment at second-look laparoscopy, treatment with IMNN-001 was associated with:

A lower rate of MRD positivity compared with the control arm (44% versus 67%);
Higher clearance of circulating tumor DNA (ctDNA) (87.5% versus 62.5%); and
A higher proportion of patients achieving "no evidence of disease" following frontline therapy (100% versus 56%).
While preliminary and based on a limited number of patients, these findings provide encouraging evidence that IMNN-001 may drive deeper anti-tumor responses while maintaining the highly favorable safety profile consistently observed across the Company’s clinical development program. These clinical findings are supported by translational analyses that demonstrated robust IL-12 expression within macrophages, activation of downstream cytokines including interferon-gamma, and evidence of both macrophage and T-cell activation, consistent with remodeling the tumor immune microenvironment from an immunologically "cold" state to one that is immunologically active, or "hot."

About the Translational Phase 2 MRD Study

The Phase 2 MRD study (NCT05739981) is evaluating IMNN-001 in combination with standard-of-care neoadjuvant and adjuvant chemotherapy plus bevacizumab in women with newly diagnosed advanced ovarian cancer, conducted through the Break Through Cancer Targeting Minimal Residual Disease in Ovarian Cancer TeamLab. Patients in the experimental arm receive IMNN-001, administered intraperitoneally, in combination with N/ACT plus bevacizumab, followed by interval cytoreductive surgery and additional cycles of adjuvant chemotherapy plus IMNN-001. Patients then undergo second-look laparoscopy (SLL) to assess for minimal residual disease, followed by maintenance therapy assigned according to homologous recombination deficiency (HRD) status. The primary endpoint of the study is MRD-positive rate at SLL; the secondary endpoint is progression-free survival (PFS). The study also includes serial translational analyses of tumor tissue, circulating tumor DNA (ctDNA), microbiome, and intraperitoneal fluid, to further characterize IMNN-001’s impact on the tumor immune microenvironment.

About IMNN-001 Immunotherapy

Designed using IMUNON’s proprietary TheraPlas platform technology, IMNN-001 is an IL-12 DNA plasmid vector encased in a nanoparticle delivery system that enables cell transfection followed by persistent, local secretion of the IL-12 protein. IL-12 is one of the most active cytokines for the induction of potent anticancer immunity, acting through the induction of T-lymphocyte and natural killer cell proliferation. IMUNON previously reported positive safety and encouraging Phase 1 results with IMNN-001 administered as monotherapy or as combination therapy in patients with advanced peritoneally metastasized primary or recurrent ovarian cancer, and completed a Phase 1b dose-escalation trial (the OVATION 1 Study) of IMNN-001 in combination with carboplatin and paclitaxel neoadjuvantly in patients with newly diagnosed ovarian cancer. IMUNON previously reported positive results from the completed Phase 2 OVATION 2 Study, which assessed IMNN-001 (100 mg/m2 administered intraperitoneally weekly) plus neoadjuvant and adjuvant chemotherapy (N/ACT) of paclitaxel and carboplatin compared to standard-of-care N/ACT alone in 112 patients with newly diagnosed advanced ovarian cancer.

About Epithelial Ovarian Cancer

Epithelial ovarian cancer is the sixth deadliest malignancy among women in the U.S. There are approximately 20,000 new cases of ovarian cancer every year and approximately 70% are diagnosed in advanced stage III/IV. Epithelial ovarian cancer is characterized by dissemination of tumors in the peritoneal cavity with a high risk of recurrence (75%, stage III/IV) after surgery and chemotherapy. Since the five-year survival rates of patients with stage III/IV disease at diagnosis are poor (41% and 20%, respectively), there remains a need for a therapy that not only reduces the recurrence rate but also improves overall survival. The peritoneal cavity of advanced ovarian cancer patients contains the primary tumor environment and is an attractive target for a regional approach to immune modulation.

(Press release, IMUNON, SEP 22, 2026, View Source [SID1234670997])

On September 22, 2026 Lantern Pharma Inc. (NASDAQ: LTRN), an AI‑driven precision oncology company transforming the cost, pace, and timeline of oncology drug discovery and development, reported that the United States Patent and Trademark Office (USPTO) has issued a Notice of Allowance for U.S. Patent Application No. 18/500,032, titled "Method for Treating Blood Cancers," with claims directed to the use of the company’s drug candidate LP‑284 to treat patients with mantle cell lymphoma (MCL), double‑hit lymphoma (DHL), and other blood cancers.

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The allowed claims cover methods of treating a subject diagnosed with blood cancer by administering an effective amount of LP‑284, when the cancer is mantle cell lymphoma or double‑hit lymphoma. Additional allowed claims cover the co‑administration of LP‑284 with a second anti‑cancer agent selected from: DNA damaging agents, glucocorticoids, immunomodulatory drugs (IMiDs), BCL2 inhibitors, Bruton’s tyrosine kinase (BTK) inhibitors, spironolactone, PARP inhibitors, and proteasome inhibitors. Additional claims also cover routes of administration including intravenous and intraperitoneal delivery. A Notice of Allowance is issued after the USPTO determines that prosecution on the merits of a patent application has concluded, and the patent grants upon payment of the required issuance fee.

"This Notice of Allowance marks an important step in building a durable, layered intellectual-property portfolio around LP‑284," said Panna Sharma, President and Chief Executive Officer of Lantern Pharma. "The anticipated patent claims cover the use of LP‑284 as a monotherapy and in combination with other therapeutic agent classes for mantle cell lymphoma and double-hit lymphoma, two aggressive B-cell lymphomas with significant unmet needs globally. Together with our composition-of-matter patent estate, this patent is expected to provide LP‑284 protection into 2042 and strengthen the program’s long-term commercial potential. Advancing LP‑284 from AI-generated insights through our RADR platform to a first-in-human clinical trial in less than three years demonstrates the potential of our precision approach to efficient, data-driven drug development for novel therapies."

Strengthening a Global LP‑284 Patent Estate

The newly allowed method‑of‑treatment patent builds on Lantern’s existing LP‑284 composition‑of‑matter estate, which provides protection into 2039 across major medicine markets, including the United States, European Union, Japan, China, India, Mexico, Korea, and Australia. Lantern received its first U.S. composition‑of‑matter Notice of Allowance for LP‑284 in April 2023, followed by a Certificate of Patent from the Japan Patent Office in June 2024 and a European Patent Office allowance in July 2025. Once issued, the "Method for Treating Blood Cancers" patent is expected to extend Lantern’s LP‑284 protection into 2042, adding a distinct layer of method‑of‑use protection on top of the underlying composition‑of‑matter rights.

Lantern intends to continue prosecuting additional patent applications directed to further indications, combination regimens, and formulations of LP‑284 to further strengthen its intellectual property portfolio.

LP‑284 — An AI‑Optimized, Next‑Generation Acylfulvene for Aggressive B‑Cell Cancers

LP‑284 is an investigational, next‑generation acylfulvene and the stereoisomer (enantiomer) of Lantern’s drug candidate LP‑184. It was optimized using Lantern’s proprietary RADR artificial intelligence platform, which identified its synthetically lethal mechanism targeting cancer cells with DNA damage repair (DDR) deficiencies. Unlike LP‑184, whose activity depends on the enzyme PTGR1, LP‑284’s cytotoxic activity is independent of PTGR1 expression, making it well suited to hematologic malignancies. LP‑284 induces DNA lesions that are primarily repaired by the transcription‑coupled nucleotide excision repair (TC‑NER) pathway, and its activity is retained in tumors deficient in ATM — a gene inactivated in an estimated 40%–50% of MCL patients — as well as regardless of TP53 mutation status or lymphoma surface antigen expression.

In preclinical studies, LP‑284 has demonstrated nanomolar potency across a panel of B‑cell non‑Hodgkin’s lymphoma models, with the highest potency observed in MCL cell lines, including lines resistant to standard‑of‑care agents. In data presented at the 2022 Society of Hematologic Oncology (SOHO) Annual Meeting, LP‑284 showed its lowest IC50 of 88 nM in the bortezomib‑resistant MINO MCL cell line and 193 nM in the ibrutinib/venetoclax‑resistant MAVER‑1 line, demonstrating activity even in models resistant to ibrutinib, bortezomib, venetoclax, and zanubrutinib. LP‑284 has also shown preclinical synergy with rituximab in high‑grade B‑cell lymphoma models, and combination with spironolactone enhanced sensitivity to LP‑284 by 2.4‑fold in a multiple myeloma cell line.

LP‑284 holds three FDA Orphan Drug Designations: for mantle cell lymphoma (granted January 2023), for high‑grade B‑cell lymphoma with MYC and BCL2 rearrangements (granted November 2023), and for soft tissue sarcomas (granted January 2026). These represent three of the six total Orphan Drug Designations granted across Lantern’s clinical pipeline.

Clinical Program

LP‑284 is currently being evaluated in an ongoing Phase 1a dose‑escalation clinical trial (NCT06132503) in patients with relapsed or refractory B‑cell non‑Hodgkin’s lymphomas and solid tumors. In 2025, Lantern reported that a heavily pretreated 41‑year‑old patient with aggressive Grade 3 non‑germinal center B‑cell diffuse large B‑cell lymphoma (DLBCL) — who had failed three prior state‑of‑the‑art treatment regimens, including CAR‑T cell therapy and a CD3xCD20 bispecific antibody — achieved a confirmed complete metabolic response after just two 28‑day cycles of LP‑284. To date, LP‑284 has been well tolerated, with primarily Grade 1–2 adverse events reported.

Market Opportunity and Unmet Need

MCL and DHL are aggressive B‑cell lymphomas characterized by high relapse rates and poor prognoses. Nearly all MCL patients acquire resistance to and relapse from standard‑of‑care therapies, and patients with double‑hit lymphoma face particularly poor outcomes following relapse. Lantern estimates that LP‑284 targets a global market estimated at $4 billion annually for blood cancers, driven by the rising incidence of non‑Hodgkin’s lymphoma globally, and has potential to address an estimated market that could improve outcomes for 40,000 to 80,000 blood cancer patients annually.

About LP‑284

LP‑284 is an investigational next‑generation acylfulvene designed to exploit synthetic lethal interactions in cancer cells with DNA damage repair deficiencies. Developed through Lantern’s RADR AI platform, LP‑284 induces DNA lesions primarily repaired by transcription‑coupled nucleotide excision repair (TC‑NER), creating a distinct anti‑tumor profile. The compound’s efficacy remains unaffected by TP53 mutation or lymphoma surface antigen expression, and preclinical studies demonstrate synergistic activity with rituximab and the ability to overcome ibrutinib resistance. LP‑284 is currently in Phase 1 evaluation (NCT06132503) and has received multiple FDA Orphan Drug Designations, including for mantle cell lymphoma, high‑grade B‑cell lymphomas, and soft tissue sarcomas.

(Press release, Lantern Pharma, SEP 22, 2026, View Source [SID1234670996])