On August 13, 2026 Abeona Therapeutics Inc. (Nasdaq: ABEO) reported financial results for the second quarter of 2026 and provided an update on commercial execution for ZEVASKYN (prademagene zamikeracel).

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Commercial Update

Steady launch-year growth for ZEVASKYN. Commercial execution continued to strengthen during the second quarter of 2026 with five patients treated with ZEVASKYN. In the third quarter of 2026 to-date, three patients have completed treatments. Since launch, 12 patient treatments have been completed. Revenue was not recognized for two patients due to low manufacturing yield or not meeting lot release specifications.

Expanded qualified treatment center (QTC) network and increased patient onboarding. Abeona continues to expand the ZEVASKYN QTC network, and the number of QTCs that have treated patients with ZEVASKYN has increased. Key recent milestones include:

NewYork-Presbyterian/Columbia University Irving Medical Center and Children’s Hospital of Philadelphia (CHOP) were activated as QTCs during the second quarter of 2026.
CHOP and University of Texas Medical Branch (UTMB) have commenced collection of patient biopsies, and CHOP has treated its first patient with ZEVASKYN.
In the third quarter of 2026, Abeona announced the activation of Cincinnati Children’s as the newest ZEVASKYN QTC. Cincinnati Children’s is one of the largest epidermolysis bullosa treatment centers in the U.S.
Secured CMS New Technology Add-On Payment (NTAP) status for ZEVASKYN. Effective October 1, 2026, ZEVASKYN will have NTAP status under the fiscal year 2027 Hospital Inpatient Prospective Payment System Final Rule from the Centers for Medicare & Medicaid Services (CMS). NTAP provides a pathway for eligible hospitals to receive a supplemental payment from CMS, in addition to the base diagnosis-related group (DRG) payment, when treating Medicare beneficiaries with ZEVASKYN. This designation is expected to support hospital adoption and help facilitate access for Medicare patients, who represent approximately 10 percent of RDEB patients.

Continued engagement raising RDEB community awareness. The Company presented 5-year long-term follow-up data after ZEVASKYN application from the VIITAL Phase 3 clinical study and a case report from the longest follow-up of 12 years from the Phase 1/2a study. Presentations were made at key medical congresses, including the Society for Investigative Dermatology (SID) and Society for Pediatric Dermatology (SPD) annual meetings, as well as the debra Care Conference, to drive physician awareness, patient identification, and enable patient referral to the expanding QTC network.

"Our confidence in ZEVASKYN’s substantial opportunity is reinforced by our launch progress and experience to date as we engage with a growing number of patients and expand our QTC network," said Vish Seshadri, Ph.D., Chief Executive Officer of Abeona Therapeutics. "As early real-world experience with ZEVASKYN matures across activated sites, we expect to drive broader adoption and long-term growth."

Second Quarter 2026 Financial Results

Net ZEVASKYN revenue for the quarter ended June 30, 2026 increased 31% quarter-over-quarter to $11.4 million, compared to $8.7 million in the first quarter of 2026. While five patients were treated with ZEVASKYN during the second quarter of 2026, revenue was recognized for four treatments as one batch yielded fewer than the threshold number of sheets for revenue recognition.

Research and development (R&D) expenses were $5.0 million for the second quarter of 2026 compared to $9.6 million in the first quarter of 2026, which included the one-time, up-front cost of $7.0 million for in-licensing ABO-701.

Selling, general and administrative expenses were $15.8 million for the second quarter of 2026, compared to $19.5 million for the first quarter of 2026. The decrease primarily reflects fewer engineering runs and less manufacturing training costs in the second quarter of 2026.

Net loss was $(20.2) million, or $(0.35) per basic and diluted common share, for the quarter ended June 30, 2026. Net loss for the first quarter of 2026 was $(17.1) million, or $(0.30) per basic and diluted common share.

Cash, cash equivalents and short-term investments totaled $146.8 million as of June 30, 2026, compared to $191.4 million as of December 31, 2025.

Conference Call Details

The Company will host a conference call and webcast on August 13, 2026, at 8:30 a.m. ET to discuss its financial results and corporate progress. To access the call, dial 888-506-0062 (U.S. toll-free) or 973-528-0011 (international) and Entry Code: 245916 five minutes prior to the start of the call. A live, listen-only webcast can be accessed on the Investors & Media section of Abeona’s website at View Source An archived webcast replay will be available for 30 days following the call.

(Press release, Abeona Therapeutics, AUG 13, 2026, View Source [SID1234670058])

On August 12, 2026, TScan Therapeutics, Inc. (the "Company") reportd to have received notice from Amgen Inc. ("Amgen") of its election to terminate, in its entirety, the Research Collaboration and License Agreement, dated as of May 8, 2023, by and between the Company and Amgen (the "Collaboration Agreement") pursuant to Amgen’s right under the Collaboration Agreement to terminate the agreement in its entirety upon 90 days’ prior written notice. Under the terms of the Collaboration Agreement, the termination will be effective 90 days following delivery of the notice, or November 10, 2026. No early termination penalty is payable by the Company in connection with the termination.

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Under the Collaboration Agreement, the Company and Amgen collaborated to use the Company’s proprietary target discovery platform to identify antigens recognized by T-cells in patients with Crohn’s disease. The Collaboration Agreement granted Amgen an exclusive, worldwide, sublicensable license to develop and commercialize product candidates created and developed during the collaboration. The Collaboration Agreement provided for a non-refundable, upfront payment of $30.0 million to the Company, which was received in 2023, success-based milestone payments of over $500 million in the aggregate, and tiered single-digit royalty payments on net sales of products developed from the collaboration.

Upon receipt of written notice, the Company is obligated to use commercially reasonable efforts to promptly and efficiently wind down its activities under the then-current research plan. Upon the effective date of termination, the licenses granted under the Collaboration Agreement will terminate in accordance with its terms. Following termination, the Company does not expect to receive future milestone or royalty payments under the Collaboration Agreement unless Amgen, its affiliates or sublicensees continue to exploit product candidates, in which case applicable milestone and royalty obligations will survive in accordance with the terms of the Collaboration Agreement.

The foregoing description of the Collaboration Agreement does not purport to be complete and is qualified in its entirety by reference to the full text of the Collaboration Agreement, a copy of which is filed as Exhibit 10.1 to the Company’s Quarterly Report on Form 10-Q for the quarterly period ended June 30, 2023, filed with the Securities and Exchange Commission on August 10, 2023, and incorporated by reference herein.

(Filing, 8-K, TScan Therapeutics, AUG 12, 2026, View Source [SID1234670209])

On August 12, 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, reproted a scientific comparison of its lead candidate PRP with the RAS-targeted approaches of Revolution Medicines, Inc. and Erasca, Inc. The Company articulates why PRP’s unique mechanism—promoting cancer cell differentiation, reversing epithelial-mesenchymal transition (EMT), and targeting cancer stem cells via pancreatic proenzymes—positions it as a potential long-term therapy of choice, particularly for aggressive, treatment-resistant cancers such as pancreatic ductal adenocarcinoma (PDAC).

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"As we enter a world first clinical study for the use of our lead asset, PRP, as a novel way to combat PDAC but also aggressive, less differentiated tumor types often associated with a poor patient prognosis, we felt it was an important opportunity to highlight that we are entering a transformative phase for these killer diseases which is unprecedented," said Mr. James Nathanielsz, Propanc’s Chief Executive Officer. "Recent advances by Revolution Medicines and Erasca Inc. are tremendously exciting, but further improvements can be made with complementary treatment modalities such as PRP that target the way cancer cells become malignant, invasive and spread. PRP is a novel therapy that targets these dangerous cells but leaves healthy cells intact. Therefore, it is not cytotoxic. It does not involve an inhibitory approach which often leads to drug resistance, but proteolysis (protein breakdown) is the basis for enforcing cancer cells to express certain pathways that induce differentiation so that they return to a normal state and die naturally. We expect to file a clinical trial application for the Phase 1b clinical study in advanced cancer patients in Q4 this year and are confident of replicating the successful peer reviewed, published results obtained in preclinical models and clinical observations from terminal patients treated at much lower doses for up to 18 months in a previous compassionate use study. We look forward to generating meaningful data demonstrating PRP as a long-term treatment option for metastatic cancer from solid tumors."

Propanc’s Science: Proenzyme-Driven Differentiation and Metastasis Suppression

PRP is a proprietary fixed-ratio combination of pancreatic proenzymes trypsinogen and chymotrypsinogen, administered once weekly by intravenous injection. Unlike cytotoxic agents or pathway inhibitors that directly kill dividing cells or block signaling, PRP activates upon administration to induce differentiation of malignant cells toward a more normal phenotype (cellular characteristics).

Key effects include:

Reversal of EMT, reducing invasive and stem-like properties of cancer cells.
Suppression of metastasis, angiogenesis, and tumor microenvironment support (including effects on cancer-associated fibroblasts).
Enhanced cell adhesion and promotion of natural cell death pathways.
Favorable preclinical activity: >90%, mean tumor growth inhibition in orthotopic and patient-derived xenograft (PDX) models of advanced PDAC, marked reduction in metastatic burden (liver and peritoneum), and >2.5-fold extension of median overall survival versus controls (p < 0.001). PRP has also shown potential to resensitize chemo-resistant PDAC cells to standard agents such as gemcitabine/nab-paclitaxel at lower doses.
PRP holds FDA Orphan Drug Designation for pancreatic cancer. Limited prior compassionate-use experience with related proenzyme formulations showed signals of prolonged survival in advanced solid-tumor patients without severe treatment-related adverse events. The Company is advancing toward a Phase 1b first-in-human study in up to 40 – 45 patients with advanced solid tumors (focus on PDAC and other high-unmet-need indications), with GMP manufacturing and clinical partnerships progressing in 2026.

Revolution Medicines (RVMD): RAS(ON) Tri-Complex Inhibitors

RVMD develops a portfolio of RAS(ON) inhibitors that target the active, GTP-bound state of mutant (and in some cases wild-type) RAS proteins via a cyclophilin A tri-complex mechanism. Lead assets include daraxonrasib (RMC-6236), a multi-selective RAS(ON) inhibitor; allele-selective inhibitors such as zoldonrasib (RMC-9805, G12D-selective) and others targeting G12C and G12V; and emerging catalytic RAS(ON) approaches designed to stimulate GTP hydrolysis.

These agents block RAS-effector interactions, suppress downstream MAPK and other signaling, and have demonstrated robust preclinical and clinical activity, including statistically significant overall survival and progression-free survival benefits versus chemotherapy in previously treated metastatic PDAC (e.g., Phase 3 RASolute 302 data for daraxonrasib). They address a major oncogenic driver present in ~90%+ of PDAC, substantial fractions of NSCLC and colorectal cancer, and other RAS-addicted tumors. Limitations can include pathway reactivation/resistance mechanisms, on-target effects on wild-type RAS in normal tissues, and the need for continuous pathway suppression

Erasca (ERAS): RAS/MAPK Pathway Clamping and Direct RAS Targeting

Erasca focuses on the RAS/MAPK pathway with a modality-agnostic strategy. Key approaches include MAPKlamp (upstream SHP2 and downstream ERK inhibition to "clamp" signaling), direct RAS targeting via pan-RAS molecular glues such as ERAS-0015 (which forms a ternary complex with cyclophilin A and active RAS to block effector engagement), pan-KRAS inhibitors, and agents addressing escape routes (e.g., EGFR).

ERAS-0015 has shown early clinical signals of antitumor activity in RAS-mutant solid tumors, including encouraging unconfirmed response rates in KRAS G12X NSCLC and PDAC cohorts, with pharmacodynamic evidence of target engagement (ctDNA reductions). The pipeline aims for broad coverage of RAS/MAPK alterations and resistance mechanisms. Like other targeted pathway inhibitors, challenges include incomplete pathway shutdown, adaptive resistance, and managing toxicity from multi-node inhibition.

Comparison and Contrast

Aspect Propanc (PRP) RVMD (RAS(ON) inhibitors) Erasca (MAPKlamp / pan-RAS glues)
Primary Target Cancer stem cells, EMT, differentiation Active RAS(ON) proteins RAS/MAPK nodes (SHP2, ERK, RAS itself)
Mechanism Proenzyme-induced phenotypic reprogramming; metastasis suppression Steric blockade of RAS-effector binding via tri-complex Pathway clamping or molecular glue inhibition of RAS signaling
Breadth Solid tumors broadly (stem-like/metastatic phenotype); not mutation-specific RAS-mutant cancers (multi- or allele-selective) RAS/MAPK-altered cancers
Toxicity Profile Favorable in limited human experience; non-cytotoxic Manageable but on-target pathway effects Generally well-tolerated in early data; multi-node considerations
Resistance Risk Targets upstream biology of aggressiveness rather than single pathway Pathway reactivation / bypass possible Escape routes actively addressed but still pathway-dependent
Administration Once weekly IV Oral (daily) Oral
Stage Preclinical/translational → Phase 1b FIH planned Late-stage clinical / NDA pathway for some assets Early-to-mid clinical

RVMD and Erasca represent important advances in directly targeting the long, "undruggable" RAS oncogene and its downstream pathway—addressing a core driver of many solid tumors. Their science is highly complementary to conventional chemotherapy and emerging combinations. However, both remain fundamentally pathway-centric: they suppress oncogenic signaling but do not inherently reverse the stem-like, mesenchymal, metastatic phenotype that drives recurrence and treatment failure, especially in PDAC and other aggressive cancers.

Propanc’s PRP operates at a different biological layer. By promoting differentiation and reversing EMT, it aims to reduce the reservoir of cancer stem cells responsible for resistance, dormancy, and dissemination. Preclinical data showing high tumor growth inhibition, metastatic burden reduction, survival extension, and potential chemo-sensitization support the hypothesis that PRP could serve as a backbone or sequential therapy—potentially enhancing durability when combined with RAS pathway inhibitors or used in maintenance settings where chronic, low-toxicity treatment is desirable.

Why PRP Could Prove the Therapy of Choice

For patients with advanced or high-risk solid tumors – particularly those with limited options after progression on chemotherapy or targeted agents – PRP’s profile offers several potential advantages:

Non-cytotoxic, a differentiation-based approach that may spare normal tissues while addressing the root drivers of metastasis and recurrence.
Broad applicability across solid tumors (80–90% of cancers) without requiring specific RAS mutations.
Favorable tolerability supporting long-term or intermittent use, critical for preventing relapse.
Synergy potential with existing standards of care and emerging RAS inhibitors (chemo-sensitization data already observed).
Orphan designation and focused development in PDAC, an indication with profound unmet need where both RVMD and Erasca are also active.
Propanc believes that while RAS(ON) and RAS/MAPK-targeted agents will transform outcomes for many patients by hitting the oncogenic switch, therapies that reprogram the malignant phenotype itself may ultimately deliver more durable control and improved quality of life. As PRP advances into the clinic, the Company looks forward to generating human data that will further clarify its role—potentially as a foundational, long-term option in the evolving treatment landscape for metastatic solid tumors.

(Press release, Propanc, AUG 12, 2026, View Source [SID1234670036])

On August 12, 2026 Freenome, Inc. (Nasdaq: FRNM), an early cancer detection company developing blood-based screening tests, reported that the U.S. Food and Drug Administration (FDA) has granted Breakthrough Device Designation to SimpleScreen Lung, the company’s investigational lung cancer screening test.

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The designation applies to the proposed use of SimpleScreen Lung in adults ages 50 to 80 who have at least a 20 pack-year smoking history and are not currently participating in guideline-recommended lung cancer screening. The test, which would be ordered by a healthcare provider, is designed to detect early signals of lung cancer in a blood sample from a standard blood draw.

The FDA Breakthrough Devices Program is intended to accelerate the development and review of medical devices that provide more effective treatment or diagnosis of life-threatening or irreversibly debilitating diseases and meet other criteria. The program offers Freenome the opportunity for interactive communication and prioritized review during the premarket submission process.

Lung cancer is the leading cause of cancer death in the United States,1 yet the screening gap remains substantial. According to the Centers for Disease Control and Prevention, only about 18% of U.S. adults for whom lung cancer screening is recommended have been screened. Today, low-dose computed tomography (LDCT) is the only guideline-recommended screening for lung cancer. Common barriers to LDCT adoption include strict eligibility criteria, lack of awareness, social stigma around smoking, fear of a cancer diagnosis, concern of repetitive radiation exposure, and logistical and financial obstacles.

By offering a non-invasive blood test, Freenome aims to help patients and providers overcome some of those obstacles and make lung cancer screening easier and more accessible.

"The Breakthrough Device Designation from the FDA recognizes the substantial unmet need for lung cancer screening and accelerates our path to bring SimpleScreen Lung to patients," said Aaron Elliott, Ph.D., CEO of Freenome. "By identifying high-risk individuals who would benefit from LDCT, we believe our test will complement the current standard of care and improve detection rates. We continue to advance the clinical work necessary to submit SimpleScreen Lung for FDA review."

The development of SimpleScreen Lung builds upon Freenome’s base-level methylation and next-generation sequencing platform, which is the technology underlying the FDA approval last month of the SimpleScreen CRC colorectal cancer screening test. SimpleScreen Lung incorporates multiomics through methylation and proteomics technologies with an AI/ML-powered classifier to determine whether a lung cancer signal has been detected. Under the proposed indication, a positive result means the test detected a signal that may suggest lung cancer and should be followed by LDCT imaging. A negative result means the test did not detect a lung cancer-associated signal, but it does not guarantee the absence of lung cancer. Healthcare providers should determine appropriate follow-up for each individual.

Freenome reported initial development data for the investigational SimpleScreen Lung test at the 2026 AACR (Free AACR Whitepaper) Annual Meeting.2 Freenome is continuing clinical evaluation of the test, including through its prospective PROACT LUNG study (NCT06122077).

(Press release, Freenome, AUG 12, 2026, View Source [SID1234670035])

On August 12, 2026 Acrivon Therapeutics, Inc. ("Acrivon" or "Acrivon Therapeutics") (Nasdaq: ACRV), a clinical stage biotechnology company discovering and developing precision medicines utilizing its proprietary Generative Phosphoproteomics AP3 (Acrivon Predictive Precision Proteomics) platform deployed for rational drug design and predictive clinical development, reported financial results for the second quarter ended June 30, 2026 and reviewed recent business highlights.

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"As we look ahead to the second half of 2026, we remain excited about the continued rapid clinical advancement of our precision medicine pipeline," said Peter Blume-Jensen, M.D., Ph.D., chief executive officer, president and co-founder of Acrivon. "For ACR-368, this includes the prespecified interim analysis of the registrational-intent, all-comer, serous endometrial cancer arms of the Phase 2b study. For ACR-2316, we have recently entered the randomized dose expansion stage in our Phase 1/2 study, supported by a favorable, differentiated safety profile and durable single-agent activity, including in heavily pretreated lung cancer subjects. Several subjects from the dose escalation phase now remain on treatment for more than one year."

Recent Highlights

ACR-368

Dosing continues in both all-comer serous EC arms (Arm 4 single agent and Arm 3 with ultra-low dose gemcitabine sensitization) in the registrational-intent Phase 2b study, across both US and European clinical sites.
Two presentations at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting highlighted data showing the underlying molecular mechanisms for potent synergies between ACR-368 and immune checkpoint inhibitors (ICIs) or Topoisomerase 1 (Topo 1) inhibitors identified by AP3. These findings support the potential for clinical combination studies with antibody-drug conjugates (ADCs) or ICIs.
ACR-2316

ACR-2316 advanced into the randomized dose expansion stage of the Phase 1/2 study, supported by observed favorable safety profile and durable antitumor activity. The expansion phase is evaluating 120 mg and 160 mg doses, administered orally, once-daily (QD) utilizing a 3d on / 4d off weekly administration schedule.
Dose expansion phase will assess safety and activity in subjects with AP3-identified, molecularly-defined lung, endometrial, cervical, and esophago-gastric junction cancers.
Data presented at the AACR (Free AACR Whitepaper) Annual Meeting uncovered the molecular underpinnings driving strong synergy and resulting in complete tumor regression with durable immune memory upon treatment with ACR-2316 and ICI, providing a mechanistic rationale for potential combinations with ICIs.
Oral podium and poster presentations at the AACR (Free AACR Whitepaper) Drug Discovery and Development conference demonstrated how AP3 guided the design of ACR-2316 for optimal intracellular pathway effects, including sustained activation of CDK1, CDK2, and importantly also of PLK1, and quenching of the dominant resistance mechanisms to drive potent pro-apoptotic tumor cell death.
CDK11 Inhibitor Program

Internally-discovered development candidate from company’s AP3-driven cell cycle program and several equally promising back-up lead compounds showing complete regression in preclinical in vivo AML models being advanced in Investigational New Drug (IND)-enabling studies.
Anticipated Upcoming Milestones

ACR-368 Ongoing Registrational Intent Phase 2b Study

A prespecified simultaneous interim analysis and data update from both all-comer (biopsy-independent) serous EC arms of the ACR-368 Phase 2b study in second half of 2026
Initiate Phase 3 confirmatory trial for ACR-368 in first half of 2027
Based on interim data read-out, complete enrollment of the registrational intent all-comer (biopsy-independent) serous EC Arm 3 or Arm 4 by fourth quarter of 2026
Broader Pipeline

Submit IND filing to the FDA for CDK11 inhibitor development candidate in first half of 2027
Initiate additional AP3-driven drug discovery programs in 2026
Second Quarter 2026 Financial Results

Net loss for the quarter ended June 30, 2026 was $18.0 million compared to a net loss of $21.0 million for the same period in 2025.

Research and development expenses were $13.8 million for the quarter ended June 30, 2026 compared to $16.2 million for the same period in 2025. The difference is primarily driven by two milestones achieved for ACR-368 in 2025 which did not recur in 2026, as well as timing of the progression of other programs.

General and administrative expenses were $4.8 million for the quarter ended June 30, 2026, compared to $6.5 million for the same period in 2025. The difference was primarily due to a decrease in employee-related expenses, including stock-based compensation.

As of June 30, 2026, the company had cash, cash equivalents and investments of $90.0 million, which is expected to fund operating expenses and capital expenditure requirements into the fourth quarter of 2027.

(Press release, Acrivon Therapeutics, AUG 12, 2026, View Source [SID1234670034])