On March 4, 2026 Cellectar Biosciences, Inc. (NASDAQ: CLRB), a late-stage clinical biopharmaceutical company focused on the discovery and development of drugs for the treatment of cancer, reported financial results for the year ended December 31, 2025, and provided a corporate update.

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"2025 was a productive year for Cellectar, marked by disciplined execution across our pipeline and meaningful clinical, regulatory, and operational achievements," said James Caruso, president and CEO of Cellectar. "We advanced iopofosine I-131 toward its planned mid-2026 Conditional Marketing Authorization (CMA) submission in Europe, supported by a strong clinical dataset and productive dialogue with both the European and U.S. regulatory agencies. In parallel, we continued to shape the future of our radiotherapeutic platform with the initiation of our Phase 1b CLR 125 study in triple negative breast cancer and strengthened our supply chain and intellectual property estate."

"As we look ahead to 2026, our momentum is building. We expect important clinical readouts, continued regulatory progress, and expansion of our next-generation Phospholipid Drug Conjugate (PDC) programs. We remain focused on executing with excellence, communicating transparently, and delivering meaningful therapeutic advances for patients with difficult-to-treat cancers," added Mr. Caruso.

2025 and Recent Corporate Highlights

Iopofosine I 131, the Company’s Phospholipid Drug Conjugate (PDC) designed to provide targeted delivery of iodine-131 (radioisotope)
Following advice from the European Medicines Agency’s (EMA) Scientific Advice Working Party (SAWP), the Company plans to submit a CMA for iopofosine I 131 as a treatment for in Waldenström Macroglobulinemia (WM). The CMA submission will be supported by data from the CLOVER WaM study, including 12-month follow-up on all patients, updated overall and major response rates, progression-free survival, duration of response, and compelling subset analyses on post-BTKi patients.
Received Breakthrough Therapy Designation (BTD) from the U.S. Food and Drug Administration (FDA) for iopofosine I 131 in relapsed/refractory WM.
Received recommendation from the FDA to investigate iopofosine I 131 as a treatment option in post-BTKi indications as early as the second line, substantially expanding the available patients in the U.S. market.
CLR 121125 (CLR 125), an iodine-125 Auger-emitting program targeted for solid tumors
Initiated a Phase 1b study of CLR 125 in Triple Negative Breast Cancer (TNBC).
CLR 125 has been well tolerated in vivo with no signs of end-organ toxicity, including hematologic toxicity, and has also demonstrated reduction or inhibition of solid tumors in preclinical studies.
Enrollment is ongoing in the Phase 1b dose finding study of CLR 125, which will evaluate three doses of 32.75 mCi/m2/dose for up to 4 cycles, 62.5 mCi/m2/dose for up to 3 cycles and 95 mCi/m2/dose for up to 2 cycles in patients with relapsed TNBC.
The study’s primary endpoint is to determine a recommended Phase 2 dose and to evaluate safety, tolerability and initial response assessment (RECIST v1.1 and PFS).
Secured a supply agreement with Ionetix to provide commercial-scale supply of cGMP-grade Actinium-225 (Ac-225) and Astatine-211 (At-211) to support ongoing CLR 225 clinical development programs.
Corporate
Strengthened and expanded the Company’s global intellectual property estate with newly issued patents across Europe, Asia-Pacific, the Middle East and the Americas. The expanded IP coverage protects both iopofosine I 131 as well as the broader radiotherapeutic pipeline, including CLR 125.

2025 Financial Highlights

Cash and Cash Equivalents: As of December 31, 2025, the company had cash and cash equivalents of $13.2 million, compared to $23.3 million as of December 31, 2024. The company believes its cash balance as of December 31, 2025, is adequate to fund its basic budgeted operations into the third quarter of 2026.
Research and Development Expenses: R&D expenses for the year ended December 31, 2025, were approximately $11.5 million, compared to approximately $26.1 million for the year ended December 31, 2024. The decrease was primarily a result of reduced activity in our CLOVER WaM clinical study, as we were exclusively in patient follow-up during 2025. Additionally, manufacturing costs declined as we completed development of a fully redundant production and logistics pipeline.
General and Administrative Expenses: G&A expenses for the year ended December 31, 2025, were approximately $11.5 million, compared to approximately $25.6 million for the same period in 2024. The decrease was primarily a result of reduced pre-commercialization efforts and related personnel.
Other income and expense: Other income and expense, net, was approximately $1.2 million of income in 2025, as compared to approximately $7.3 million of income in the prior year. These amounts are almost exclusively a result of non-cash impacts from the cost to issue and in the valuation of certain warrants that are considered liabilities.
Net Loss: Net loss for the full year ending December 31, 2025, was $21.8 million or $8.35 per basic and diluted share, compared with $44.6 million or $36.52 per basic share and $41.89 per diluted share during 2024.

Conference Call & Webcast Details
Cellectar management will host a conference call and webcast today, March 4, 2026, at 8:30 AM Eastern Time to discuss these results and answer questions. Stockholders and other interested parties may participate in the conference call by dialing 1-800-717-1738. A live webcast of the conference call can be accessed in the "Events & Presentations" section of Cellectar’s website at www.cellectar.com. A recording of the webcast will be available and archived on the Company’s website for approximately 90 days.

(Press release, Cellectar Biosciences, MAR 4, 2026, View Source [SID1234663242])

On March 4, 2026 AIM ImmunoTech Inc. (NYSE American: AIM) – AIM ImmunoTech Inc. ("AIM" or the "Company"), an immuno-pharma company focused on the research and development of its lead product, Ampligen (rintatolimod), for the treatment of late-stage pancreatic cancer – a lethal and unmet global health problem – reported the preliminary results of its previously announced rights offering (the "Rights Offering") which expired at 5:00 p.m., Eastern Time, on March 3, 2026. The Company estimates that the Rights Offering will result in total subscriptions of approximately $1.8 million. The results of the Rights Offering are preliminary and subject to change pending finalization and verification by the Company and its subscription agent, Broadridge Corporate Issuer Solutions, LLC.

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Each right entitled the holder to purchase one unit ("Unit"), at a subscription price of $1,000 per Unit, consisting of one share of the Company’s Series G Convertible Preferred Stock (the "Preferred Stock"), and 2,000 Class G Common Stock Purchase Warrants to purchase the Company’s Common Stock (the "Warrants").

The Company anticipates the closing of the Rights Offering will occur on or about March 6, 2026, subject to satisfaction or waiver of all conditions to closing. Upon the closing, the subscription agent will distribute, by way of direct registration in book-entry form or through the facilities of DTC, as applicable, shares of the Preferred Stock and Warrants to holders of rights who have validly exercised their rights and paid the subscription price in full. No physical stock or warrant certificates will be issued to such holders.

Maxim Group LLC acted as dealer-manager for the Rights Offering. Questions about the Rights Offering or requests for copies of the final prospectus may be directed to Maxim Group LLC at 300 Park Avenue, New York, NY 10022, Attention: Syndicate Department, or via email at [email protected] or telephone at (212) 895-3745.

The Company’s registration statement on Form S-1 (Registration No. 333-292085) was declared effective by the Securities and Exchange Commission ("SEC") on February 10, 2026. The prospectus relating to and describing the terms of the Rights Offering has been filed with the SEC as a part of the registration statement and is available on the SEC’s website at View Source

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

(Press release, AIM ImmunoTech, MAR 4, 2026, View Source [SID1234663241])

On March 4, 2026 Denovicon Therapeutics, Inc. reported the discovery of DNT-1569, a small molecule inhibitor of poly(ADP-ribose) polymerase 7 (PARP7) designed as a potential oral immunomodulatory therapy for solid tumors. To the best of our knowledge, no small molecule immuno-oncology drug has reached the market — the entire immunotherapy revolution to date relies on biologics. DNT-1569 is designed to change that. The compound demonstrates potent PARP7 inhibition with approximately 2,000-fold selectivity over PARP1 and 2,500-fold selectivity over PARP2 — a selectivity profile that distinguishes it from all known PARP7 inhibitors, including the clinical compound RBN-2397 (atamparib).

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Why PARP7 — and Why Selectivity Matters
After nearly 25 years in drug discovery — including 17 years at Johnson & Johnson, where I co-led seven clinical candidates — one pattern stands out: good mechanisms fail when the molecules carrying them aren’t clean enough to dose properly.

PARP7 is a compelling immuno-oncology target. Inhibiting PARP7 restores type I interferon signaling in tumor cells, activating the innate immune system and potentially converting immunologically "cold" tumors — the ones that don’t respond to checkpoint inhibitors like Keytruda — into "hot" tumors that the immune system can recognize and attack. PARP7 is dysregulated across multiple solid tumor types, including lung, breast, ovarian, head and neck, pancreatic, and colorectal cancers.

The clinical precedent exists. Ribon Therapeutics’ RBN-2397 entered Phase 1 trials and demonstrated preliminary antitumor activity, establishing proof of concept that PARP7 inhibition produces clinical benefit. But RBN-2397 is not a selective PARP7 inhibitor — it potently inhibits PARP1 and PARP2 as well, which creates the same hematological toxicities seen with traditional PARP inhibitors. This likely resulted in tox-limited dosing and, consequently, the achievable efficacy.

The mechanism is validated. The selectivity problem was not.

DNT-1569: Solving the Selectivity Problem
DNT-1569 was designed to be the PARP7 inhibitor that RBN-2397 was not — one that inhibits the intended target without carrying off-target PARP1/2 liabilities.

Biochemical Profile:

DNT-1569 (Denovicon) RBN-2397 (Ribon)
PARP7 4 nM 3 nM
PARP1 8,000 nM 37 nM
PARP2 10,000 nM 17 nM
PARP1 Selectivity ~2,000× ~12×
PARP2 Selectivity ~2,500× ~6×
Scaffold Novelty Tanimoto = 0.14 vs. RBN-2397 —
Virtual Design Time < 2 days Years (traditional)
DNT-1569 matches RBN-2397’s PARP7 potency while pushing PARP1 and PARP2 activity into the micromolar range. This selectivity profile is designed to enable full therapeutic dosing of PARP7 without the PARP1/2-driven toxicities that likely constrained RBN-2397’s clinical performance.

Importantly, DNT-1569 sits on a novel chemical scaffold — a Tanimoto similarity of 0.14 relative to RBN-2397 confirms that this is not an analogue or derivative of existing PARP7 chemistry. The compound emerged from an entirely different design process, not from iterating on a known scaffold.

How We Got Here
DNT-1569 was designed using Denovicon’s computational drug discovery platform, which uses physics-based machine learning to design molecules with druglike properties built in from the start — not optimized after the fact.

Rather than starting with target affinity and then spending years trying to engineer in druglike properties — the traditional break-fix cycle that accounts for the majority of preclinical program failures — our approach optimizes across ADMET, pharmacokinetic, toxicity, and affinity properties from the outset. Every design decision maps to real chemical features that medicinal chemists can interrogate — no black boxes.

The entire virtual design phase for DNT-1569 was completed in under two days. The program from inception to the selectivity data reported here took under one year.

Since the DNT-1569 program, Denovicon’s platform has evolved into a quantum physics-driven generative AI architecture that extends these capabilities to trillion-molecule chemical spaces, enabling simultaneous multi-objective optimization in a single computational step. The core principle remains the same: build druglikeness in by design. The scale and speed at which we can now do it has fundamentally changed.

Clinical Implications
The immuno-oncology landscape is dominated by biologics — checkpoint inhibitors, CAR-T therapies, bispecific antibodies — all of which require infusion, cold chain logistics, specialized administration, and carry substantial cost. To the best of our knowledge, there is no marketed small molecule immuno-oncology drug. DNT-1569 is designed to address that gap: an oral small molecule that modulates the immune system’s ability to recognize and attack tumors.

A truly selective small molecule PARP7 inhibitor opens two therapeutic paths.

Monotherapy: If PARP7 inhibition alone is sufficient to drive antitumor immunity in selected patient populations — as early evidence in squamous cell lung cancer and head and neck cancers suggests — a selective oral PARP7 inhibitor could offer meaningful clinical benefit without the toxicity burden of pan-PARP inhibition. As a small molecule, it reaches compartments that antibodies cannot — including the central nervous system — and can be manufactured and distributed at a fraction of the cost of biologics.

Combination therapy: The greater opportunity may lie in combining a selective PARP7 inhibitor with existing immune checkpoint inhibitors. Approximately 70% of cancer patients do not respond to checkpoint inhibitors alone, largely because their tumors are immunologically cold. A selective PARP7 inhibitor that activates the type I interferon pathway — turning cold tumors hot — could serve as an oral immunomodulatory backbone for checkpoint inhibitor combinations. Critically, this combination is viable only if the PARP7 inhibitor does not add significant toxicity to the regimen. DNT-1569’s selectivity profile is designed to make that combination feasible.

An oral, well-tolerated small molecule immunomodulator would represent a new therapeutic modality — one with implications not just for efficacy, but for global patient access.

What Comes Next
Immune biomarker assays for DNT-1569 are underway. These data will provide the first readout on whether the selectivity advantage observed in biochemical assays translates to the expected immunomodulatory activity in cellular systems. Denovicon is actively engaging pharmaceutical partners for proof-of-concept collaborations around the PARP7 program and the broader quantum physics-driven generative AI platform.

(Press release, Denovicon Therapeutics, MAR 4, 2026, View Source [SID1234663214])

On March 3, 2026 Persevere Therapeutics, Inc. ("Persevere"), a Delaware-incorporated, clinical-stage oncology biotechnology company, reported its official launch following a period of stealth operations. The company is emerging with a Phase 1b/2a-ready clinical asset and the first close of its Seed financing.

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As part of its launch, Persevere has acquired the clinical-stage program and related assets for misetionamide (GP-2250) from Geistlich Pharma AG. Misetionamide is a novel, first-in-class dual inhibitor of c-MYC and NFκB with clinical activity in a Phase 1 trial.

Persevere has closed on a first tranche of a Seed round and is actively engaging prospective investors for the remaining allocation. The company is prepared to share equity round terms with qualified investors.

The Seed financing proceeds will be used to complete a Phase 1b/2a proof-of-concept clinical trial evaluating misetionamide in patients with platinum-resistant ovarian cancer (PROC), an area of significant unmet medical need.

"We named the company Persevere as an enduring reminder that we must ‘Never Give Up’ on behalf of cancer patients, who persevere every day," said Greg Bosch, Founder and CEO. "Persevere Therapeutics’ mission is the unwavering pursuit of improved clinical outcomes for cancer patients with our novel therapeutic, misetionamide."

Persevere benefits from the solid foundation already established by the significant effort and investment to-date in the development of misetionamide. These advancements include a broad preclinical program and the completion of a successful Phase 1 clinical trial where 56 cancer patients were treated. Persevere’s investors have a unique opportunity to leverage this prior investment as the company now advances the program into its next stage of clinical development. In addition to the multi-center Phase 1 which demonstrated excellent safety and encouraging efficacy profile of misetionamide, significant milestones have already been achieved including all CMC, toxicology and regulatory hurdles with two open INDs as well as 16 scientific publications and an extensive patent estate.

"Platinum resistant ovarian cancer remains one of the most challenging and underserved areas in gynecologic oncology, leaving patients with limited effective options and a poor prognosis," noted Dr. Robert Coleman, MD, gynecologic oncologist with Texas Oncology and Chief Medical Officer at Vaniam Group. "Persevere’s misetionamide offers a much-needed therapeutic innovation, not only as a differentiated alternative to the growing number of antibody drug conjugates [ADCs] in development, but also as a potential option for patients whose disease has been exposed to, and/or progressed on prior ADC therapy."

(Press release, Persevere Therapeutics, MAR 3, 2026, View Source [SID1234663276])

On March 3, 2026 T-knife Therapeutics, Inc., a biopharmaceutical company developing next-generation T cell therapies to fight cancer, reported the authorization of its Clinical Trial Application (CTA) to begin the Phase 1 ATLAS trial of TK-6302 in Europe. TK-6302 is a multi-armored PRAME-targeted T cell therapy specifically engineered to overcome the challenges associated with treating solid tumor cancers. The ATLAS trial, which is poised to begin this year, is an adaptive, first-in-human, open-label, Phase 1 trial of TK-6302 in patients with advanced PRAME-positive solid tumors.

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"We are proud to achieve this important milestone, which enables the initiation of the Phase 1 ATLAS clinical trial and our transition to becoming a clinical-stage company," stated Thomas M. Soloway, President and Chief Executive Officer of T-knife. "TK-6302 is a highly differentiated therapy, engineered for greater potency against PRAME, a clinically validated target with attractive commercial potential. PRAME is highly prevalent across multiple high unmet-need solid tumor indications, including squamous non-small cell lung, ovarian, endometrial, skin, and triple-negative breast cancers. Today’s announcement reflects the dedication, expertise, and urgency our team brings to transforming innovative science into life-changing therapies."

Peggy Sotiropoulou, Ph.D., Chief Scientific Officer of T-knife, added, "The CTA was supported by a comprehensive and compelling preclinical data package demonstrating TK-6302’s best-in-class anti-tumor efficacy. By bolstering T-cell fitness and persistence while overcoming challenging tumor mediated immune barriers, TK-6302 has the potential to deliver meaningful clinical benefit, including deep, durable responses across a range of solid tumor cancers. Bringing a first-of-its-kind multi-armored, CRISPR gene-edited T cell therapy into the clinic underscores our commitment to pushing scientific boundaries in the service of delivering transformative therapies to patients."

About TK-6302
TK-6302 is a PRAME-targeted T cell therapy that has been "supercharged" by the inclusion of multiple armoring innovations: a high affinity PRAME targeting receptor to enhance cytotoxicity; a costimulatory CD8 coreceptor to engage CD4 T cells and enhance T cell fitness and persistence; and a FAS-based checkpoint converter designed to boost engraftment and promote T cell survival in the hostile tumor micro-environment. Preclinical data with TK-6302 demonstrated sustained serial killing and cytokine secretion in a model mirroring the inhibitory ligand expression in PRAME-expressing tumors. In a complex 3-dimensional (3D) spheroid tumor model, TK-6302 eliminated multiple rounds of tumors and demonstrated superior anti-tumor activity compared to controls. TK-6302 is manufactured with a non-viral gene editing process for improved T cell receptor expression, and it has been successfully manufactured at-scale using the clinical process.

(Press release, T-Knife, MAR 3, 2026, View Source [SID1234663274])