On March 4, 2026 MAIA Biotechnology, Inc., (NYSE American: MAIA) ("MAIA", the "Company"), a clinical-stage biopharmaceutical company developing targeted immunotherapies for cancer, reported the closing of its previously announced underwritten public offering of 20,000,000 shares of its common stock at a public offering price of $1.50 per share for aggregate gross proceeds of $30 million, prior to deducting underwriting discounts and other offering expenses. In addition, the Company has granted the underwriters a 30-day option to purchase up to an additional 3,000,000 shares of common stock at the public offering price per share, less the underwriting discounts to cover over-allotments, if any.

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The offering was structured as a straightforward common stock only investment with no warrant coverage and was led by healthcare-dedicated investors alongside existing shareholders.

Konik Capital Partners, LLC, a division of T.R. Winston & Company acted as the sole book-running manager for the offering.

MAIA intends to use the net proceeds from the offering to conduct clinical trials and for working capital and general corporate purposes.

The securities described above were offered and sold pursuant to a "shelf" registration statement on Form S-3 (File No. 333-273984), including a base prospectus, filed with the U.S. Securities and Exchange Commission (the "SEC") on August 15, 2023, and declared effective on August 23, 2023.

The offering was made only by means of a prospectus supplement and accompanying prospectus that form a part of the registration statement. A prospectus supplement describing the terms of the public offering has been filed with the SEC and forms a part of the effective registration statement.

Copies of the prospectus supplement and the accompanying prospectus relating to this offering may be obtained, on the SEC’s website at View Source or by contacting Konik Capital Partners LLC, a division of T.R. Winston & Company, at 7 World Trade Center, 46th Floor, New York, NY 10007, Attention: Capital Markets Team, Email: [email protected].

This press release shall not constitute an offer to sell or the solicitation of an offer to buy any of the securities described herein, nor shall there be any sale of these securities in any state or 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, MAIA Biotechnology, MAR 4, 2026, View Source [SID1234663271])

On March 4, 2026 Bayer reported annual reported annual report 2025.

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(Presentation, Bayer, MAR 4, 2026, View Source [SID1234663997])

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 4, 2026 Can-Fite BioPharma Ltd. (NYSE American: CANF) (TASE: CANF), a clinical-stage biotechnology company developing a pipeline of proprietary small molecule drugs for the treatment of cancer and inflammatory diseases, reported results from its Phase IIa open-label study evaluating namodenoson in patients with advanced pancreatic ductal adenocarcinoma (PDAC) who had progressed following prior systemic therapies.

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The study met its primary endpoint, which was safety, demonstrating that namodenoson was very well tolerated in this heavily pretreated patient population. No new safety signals were identified, and the safety profile was consistent with the known clinical experience of namodenoson in other oncological diseases.

The study enrolled 20 patients with advanced PDAC who had received one or more prior lines of therapy. Patients represented a high-risk population, including individuals with varying performance status and advanced metastatic disease.

Secondary endpoints included overall survival (OS) and progression-free survival (PFS). Survival follow-up remains ongoing, with 1/3 of patients currently alive at the time of data cut-off. As follow-up continues, survival outcomes are expected to further mature and will be announced during upcoming scientific meetings.

"The favorable safety profile observed in this difficult-to-treat population supports continued clinical evaluation of namodenoson," Prof. Salomon Stemmer, a renowned oncologist and key opinion leader at the Davidoff Center, Rabin Medical Center, Israel. "We are continuing to monitor survival outcomes as data mature."

Namodenoson is a highly selective A3 adenosine receptor (A3AR) agonist, which has shown a compelling safety profile and demonstrated anti-tumor activity in preclinical pancreatic cancer models. The drug is also being evaluated in clinical trials for advanced liver cancer.

Namodenoson has received Orphan Drug Designation from the U.S. Food and Drug Administration (FDA) for the treatment of pancreatic cancer.

(Press release, Can-Fite BioPharma, MAR 4, 2026, View Source [SID1234663256])

On March 4, 2026 NeOnc Technologies Holdings, Inc. (Nasdaq: NTHI) ("NeOnc" or the "Company"), a multi-Phase 2 clinical-stage biopharmaceutical company developing novel therapies for central nervous system (CNS) cancers, reported data from the dose-escalation portion of its Phase 1/2 clinical trial for NEO212, the Company’s novel oral bio-conjugated therapy and will host a conference call to discuss the data today at 9:00am ET.

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NeOnc has formally notified the FDA that the Phase 1 dose-escalation portion of the NEO212-01 Phase 1/2 clinical trial has reached Maximum Tolerated Dose (MTD) at Cohort 5 (810 mg, Days 1–5, 28-day cycle) following a second Dose-Limiting Toxicity. In accordance with protocol-defined stopping rules, dose escalation has been halted, no further patients will be enrolled at 810 mg, and the Recommended Phase 2 Dose (RP2D) has been set at 610 mg (Cohort 4). For the Phase 2a metastasis cohort, the starting dose will be 400 mg (Cohort 3).

Notably, although Phase 1 was mainly designed to assess safety, tolerability, and identify the MTD, promising signs of clinical efficacy appeared during this phase of the study. These efficacy signs—including indications of lasting disease control in heavily pretreated patients with recurrent GBM and brain metastases—were observed within the dose-escalation groups.

The emergence of measurable anti-tumor activity in Phase 1 offers early clinical confirmation of NEO212’s therapeutic potential and supports the Company’s progress into the Phase 2 segment of the trial.

"These early efficacy signals, observed even within a dose-escalation safety study, provide meaningful clinical validation of NEO212’s therapeutic potential," said Amir Heshmatpour, Chairman and CEO of NTHI. "With RP2D now established, we believe NeOnc is entering Phase 2 with positive clinical momentum and a clear development pathway."

The transition into Phase 2 will focus on further assessing efficacy at the RP2D in specific expansion cohorts, aiming to generate strong clinical data to support potential accelerated development pathways in recurrent CNS cancers.

Importantly, this represents the first clinical readout of NeOnc’s bioconjugated temozolomide (TMZ) platform in an oral formulation, demonstrating NeOnc’s drug-engineering capabilities beyond its established intranasal delivery platform. The data validate the Company’s ability to optimize CNS penetration and therapeutic exposure across both intranasal and oral modalities. NeOnc intends to request a Type B (End-of-Phase 1) FDA meeting to review safety, PK/PD, preliminary efficacy, RP2D justification, Phase 2 design modifications, and a potential Accelerated Approval pathway. Supporting regulatory materials, including MedWatch Form FDA 3500A and Form FDA 1571, have been submitted via eCTD, ensuring regulatory transparency and alignment as the program transitions into Phase 2 development.

Mr. Heshmatpour, continued:

"This clinical data readout represents a meaningful advancement relative to the historical standard of care in brain cancer, temozolomide (TMZ), originally developed by Merck (NYSE: MRK). Importantly, we have successfully engineered and clinically evaluated a bio-conjugated oral formulation of TMZ, NEO212, and have established the Recommended Phase 2 Dose (RP2D). Achieving dose confirmation is a critical milestone that substantially de-risks the program and positions us for the next stage of development.

We believe NEO212 has the potential to meaningfully improve upon conventional TMZ by enhancing therapeutic performance while maintaining the practicality of oral administration. With this milestone achieved, we are preparing to engage the U.S. Food and Drug Administration to align on the design of what we anticipate will be a pivotal, registrational Phase 2 study, subject to FDA feedback and approval.

If successful, this program could redefine the treatment paradigm for glioblastoma, astrocytoma, and other aggressive CNS malignancies."

NEO212 is specifically designed to overcome a key biological limitation of TMZ: MGMT-mediated resistance. Preclinical studies have shown that NEO212 effectively inactivates and promotes the degradation of O6-methylguanine-DNA methyltransferase (MGMT), a crucial DNA repair enzyme that causes TMZ resistance. Standard TMZ treatment does not significantly lower MGMT levels and remains vulnerable to MGMT-driven DNA repair in brain tumors. This mechanistic difference may be especially important for TMZ-resistant and MGMT-high recurrent glioblastoma patients, offering a strong biological reason to advance NEO212 into Phase 2 development in the post-TMZ setting.

Mr. Heshmatpour added:

"This marks our first clinical readout of a bio-conjugated oral oncology asset and validates the broader scientific foundation of our platform. Supported by approximately ten issued patents and patent applications across the NEO212 and NEO100 programs, we believe our intellectual property portfolio provides meaningful long-term strategic protection.

Our immediate priority is regulatory engagement and disciplined execution toward a pivotal registrational pathway. We remain focused on advancing differentiated CNS therapies that can create durable clinical value for patients and sustainable long-term value for shareholders."

Founder, Dr. Thomas Chen, Vice-Chairman and Chief Medical Officer noted that, "The determination of the RP2D at 610 mg is a scientifically significant achievement. It confirms that our bio-conjugation technology allows for high-dose delivery of therapeutic agents with a manageable toxicity profile. We are now positioned to explore the efficacy of this optimized dose in our upcoming Phase 2 expansion."

Dr. Henry Friedman of Duke University emphasized the importance of this milestone, stating, "Establishing a safe and tolerable dose is the foundation of any successful oncology program. The identification of the RP2D for NEO212 allows NeOnc to proceed with confidence into efficacy studies for a patient population in desperate need of new oral therapies."

NEO212 is NeOnc’s first oral chemical conjugated chemotherapy drug, uniquely combining Temozolomide (TMZ), the current standard of care for glioblastoma and other brain cancers (marketed as Temodar), with NEO100 (a proprietary form of perillyl alcohol (POH), which is owned and patented by NeOnc). This proprietary conjugation is designed to overcome the limitations of TMZ, including resistance and limited efficacy, by enhancing blood-brain barrier penetration and antitumor activity.

Conference Call Details:

Date: March 4, 2026
Time: 6:00 a.m. PT / 9:00 a.m. ET
Webcast: A live webcast can be accessed at: View Source or by visiting View Source

(Press release, Neonc, MAR 4, 2026, View Source [SID1234663272])