By John Vandermosten, CFA
NASDAQ:HURA
READ THE FULL HURA RESEARCH REPORT
ASH Presentation
TuHURA (NASDAQ:HURA) addressed the American Society of Hematology (ASH) Annual Meeting and Exposition with a presentation and poster on Sunday, December 7th in Orlando, Florida. Updated results from the delta opioid receptor (DOR) program were provided. The content highlighted DOR expression on myeloid-derived suppressor cells (MDSCs) and the effects of DOR inhibition on tumor-associated macrophages (TAMs).
The oral presentation was entitled Delta Opioid Receptor (DOR) Expression on Myeloid-Derived Suppressor Cells (MDSCs) Represents a Novel Target to Overcome Resistance to Immune Checkpoint Inhibitors (ICIs). The newly appointed Vice President Immunology at TuHURA, Dr. Michael Turner, presented the data validating DOR expression on MDSCs. The data further showed that the pharmacological antagonism of the DOR reduced the suppressive activity of MDSCs. The study showed that antagonism of the DOR with a specific inhibitor modulated a variety of direct and indirect MDSC-mediated immunosuppressive factors and reversed T cell suppression. These features suggest that the DOR may be a novel target to reprogram MDSC-induced immunosuppression in the tumor microenvironment (TME).
The poster presentation was entitled Delta Opioid Receptor (DOR): A Novel Target for Reprogramming Tumor-Associated Macrophage (TAM) Immunosuppressive Phenotype to Overcome Acquired Resistance and Enhance the Effectiveness of Cancer Immunotherapies. It was presented by Dr. Krit Ritthipichai, TuHURA’s Director of Immunology. The poster presented data showing that DOR is highly expressed on tumor-infiltrating myeloid cells, particularly TAMs. The poster concluded that the TME induces DOR upregulation relative to peripheral macrophages and that targeting the DOR may be a strategy to address several vulnerabilities. These include reprogramming suppressive TAMs and MDSCs, alleviating T-cell dysfunction, and potentially overcoming resistance to checkpoint blockade and other immunotherapies.
Data from this work show that the DOR is expressed on Tregs and further controls the expression of FOXP3, a critical immunosuppressive gene. In parallel with work conducted by Nobel Prize winners Mary E. Brunkow, Fred Ramsdell, and Shimon Sakaguchi and their groundbreaking discoveries on peripheral immune tolerance, TuHURA’s work is important because it shows that the tumor microenvironment can be tuned to be either more or less immunosuppressive by agonizing or antagonizing the DOR. This is especially important for TuHURA’s anticipated antibody drug conjugate (ADC) that will combine a DOR inhibitor with anti-VISTA, the combination of which is expected to increase the activity of T cells immune action against cancer cells.
After reviewing laboratory work identifying the expression of the DOR on various cells, the poster offered several conclusions:
- DOR is highly expressed in tumor-infiltrating myeloid cells, particularly TAMs, indicating that the tumor microenvironment induces DOR upregulation relative to peripheral macrophages;
- M1 macrophages consistently exhibited the highest DOR expression, whereas M2 macrophages, which are key drivers of immunosuppression showed the lowest, revealing a polarization-dependent regulation of DOR;
- Macrophage polarization states were validated by their characteristic immunophenotypes, functional activities, and cytokine secretion profiles, supporting the biological relevance of DOR expression patterns;
- Pharmacological inhibition of DOR effectively reversed M2 macrophage–mediated suppression of T-cell proliferation, demonstrating a functional role for DOR in driving immunosuppressive signaling;
- Targeting DOR provides a promising strategy to reprogram suppressive TAMs and MDSCs, alleviate T-cell dysfunction, and potentially overcome resistance to checkpoint blockade and other immunotherapies.
Financing and Corporate Update
TuHURA announced a registered direct offering on December 9th that is expected to raise $15.6 million through the issuance of 9,462,423 shares of common stock and warrants. The purchase price for the equity shares is set at $1.65 and the exercise price for the warrants is $1.95. Warrants can be exercised six months after issue. The closing of the transaction is scheduled to occur in three tranches. The first was on December 10th with the issuance of 5,219,999 shares and matching number of warrants. The second is expected to occur before January 30th, 2026, issuing 3,030,303 shares and warrants and the third is targeted on or before February 27th, 2026 with the issuance of 1,212,121 shares and warrants. As a proportion of the total, the first, second and third transactions will raise 55%, 32% and 13% of the targeted $15.6 million gross proceeds.
Following the financing announcement, TuHURA held a corporate update call on December 11th. The call noted that two IFx-2.0 trials are ongoing and data from the trials in Merkel Cell Carcinoma (MCC) are expected to be presented at the American Society of Clinical Oncology (ASCO) conference in 2026. Dr. Bianco also touched on the details of the anti-VISTA candidate TBS-2025 which is slated to be the subject of a Phase II trial in patients with NPM1 mutated acute myeloid leukemia (AML) with a menin inhibitor against menin inhibitor monotherapy. The CEO also highlighted the selection of the DOR presentations at ASH, which reflected growing interest in the oncology community with the immune suppressive environment around tumors. The 2025 Nobel Prize in Medicine was awarded for work done on immune tolerance and FOXP3 gene mutations. This may be a growing area of interest for established biopharma companies who may make investments in related candidates. Milestones for 2026 were reiterated and can be found later in this report.
REM-001 Photodynamic Therapy
TuHURA inherited REM-001 as part of the reverse merger with Kintara Therapeutics. As part of the merger transaction, Kintara shareholders were offered a contingent value right (CVR) that would grant shares if REM-001 achieved predetermined milestones. On December 15th, 2025, TuHURA announced that the contingent value right (CVR) would be released to Kintara shareholders after achieving the milestones.
The REM-001 candidate is a photodynamic therapy (PDT) for the treatment of cutaneous metastatic breast cancer (CMBC). It uses light-sensitive compounds, or photosensitizers, that, when exposed to specific wavelengths of light, act as a catalyst to produce a form of reactive oxygen that induces local tumor cell death. The REM-001 therapy consists of three parts: the laser light source, the light delivery device and the drug REM-001. REM-001 is first administered by intravenous infusion and allowed to disperse within the body and be taken up by the tumors. Tumors are then illuminated using the light delivery device, which is attached to the laser light source, so that the accumulated REM-001 can be activated for the desired clinical effect.
Under Kintara, the REM-001 program was suspended pending additional funding. In mid-2023, the program received a grant from the National Institutes of Health which led to the initiation of treatment in four patients in November 2024 and the study is now complete. In connection with the Kintara merger, TuHURA agreed to payment of CVRs based on achieving multiple milestones related to the trial. TuHURA has completed enrollment of ten CMBC patients in the REM-001 trial and has achieved the primary endpoint. The endpoint is the demonstration of safety with signs of clinical efficacy following eight weeks of follow-up. Now that the milestone has been achieved, Kintara shareholders are entitled to receive 1,539,958 shares of common stock. The shares are expected to be distributed to the CVR holders before year end 2025. Further details of the arrangement are provided in corporate filings and in the CVR Agreement. We do not expect TuHURA to continue development with REM-001.
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