On April 22, 2026 Actinium Pharmaceuticals, Inc. (NYSE AMERICAN: ATNM) (Actinium or the Company), a pioneer in the development of targeted radiotherapies, reported data at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting supporting transcriptional reprogramming as a central mechanism driving the mutation-agnostic anti-leukemic activity of Actimab-A (lintuzumab-Ac225) in acute myeloid leukemia (AML).

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

Preclinical translational data demonstrated that lintuzumab-Ac225 delivers potent cytotoxic activity across AML models harboring common mutations, including FLT3, NPM1, KMT2A, and TP53, as well as in primary patient samples. Importantly, combining Actimab-A with standard-of-care therapies – the menin inhibitor revumenib, the FLT3 inhibitor gilteritinib, and the hypomethylating agent azacitidine – resulted in enhanced leukemic cell killing in vivo across all tested models, independent of mutation status. These results support a combination-driven clinical strategy aimed at improving depth and durability of response. The findings provide the mechanistic foundation for Actimab-A’s observed clinical activity and, together with the manageable safety profile demonstrated across prior Actimab-A trials in more than 150 AML patients, reinforce its suitability as a combination backbone across multiple treatment settings.

Actimab-A is Actinium’s lead clinical radiotherapy delivering Actinium-225, a potent alpha-emitter radioisotope payload that produces lethal double-strand DNA breaks to kill CD33-expressing AML cells. CD33 is expressed ubiquitously in AML and other myeloid malignancies. Actimab-A has been evaluated in more than 150 AML patients across multiple treatment settings, including as monotherapy and in combination with the chemotherapy regimen CLAG-M and with the BCL-2 inhibitor venetoclax, where it has demonstrated compelling clinical activity and a manageable safety profile. Under our Cooperative Research and Development Agreement (CRADA) with the National Cancer Institute (NCI), Actimab-A is being advanced through the NCI’s National Clinical Trials Network, including an ongoing frontline triplet trial combining Actimab-A with venetoclax and the hypomethylating agent ASTX-727 in newly diagnosed AML patients. The data presented at AACR (Free AACR Whitepaper) 2026 further support Actimab-A’s mutation-agnostic mechanism of action and its synergistic activity with targeted therapies approved for patients with the most commonly expressed AML mutations.

Key Data and Highlights of the Actimab-A AACR (Free AACR Whitepaper) Presentation

New data on Actimab-A’s mechanism and combination potential in primary AML patient samples further support its positioning as a foundational backbone therapy across multiple AML treatment settings, significantly expanding its commercial opportunity across the AML treatment continuum. In the relapsed/refractory AML setting Actimab-A in combination with the intensive chemotherapy regimen CLAG-M produced an 83% overall response rate and 75% MRD-negativity in a Phase 1 trial which forms the basis of a Phase 2/3 registrational study for which Actinium has FDA alignment and is seeking a development partner. Actimab-A is also being studied in newly diagnosed patients via the ongoing NCI-sponsored frontline triplet trial of Actimab-A with venetoclax and ASTX-727; and has shown promise in post-remission and MRD-directed settings; as well as myelodysplastic syndrome (MDS) and other CD33-expressing myeloid malignancies.

Transcriptional Reprogramming as a Key Mechanism for Actimab-A Combination Activity

Combination treatment produced consistent pathway-level changes compared with monotherapy. Gene set enrichment analyses (GSEA) showed enhanced myeloid differentiation signatures with the addition of Actimab-A (lintuzumab-Ac225) to revumenib, gilteritinib, and azacitidine.

Across models, combinations were associated with downregulation of proliferative programs, including MYC target genes, E2F targets, and G2/M checkpoint signatures, together with enrichment of p53-associated stress response and apoptosis pathways.

Together, these findings show that Actimab-A combinations don’t just add cytotoxicity — they reprogram AML cells from proliferation toward differentiation and apoptosis, providing the mechanistic basis for deeper, more durable MRD-negative responses and reinforcing Actimab-A’s role as a universal combination backbone across AML.

Broad Activity of Actimab-A as Monotherapy and in Combination in Primary AML Patient Samples

Actimab-A (LinT-Ac225) showed robust cytotoxicity in primary AML patient samples, independent of FLT3, KMT2A, NPM1, IDH1, IDH2, or TP53 mutation status, positioning Actimab-A to treat the full AML population, including TP53-mutant patients who lack effective targeted options, and to serve as a universal combination partner rather than a mutation-restricted therapy.

Combining standard-of-care therapies (SOC) – revumenib (menin-KMT2A inhibitor), gilteritinib (FLT3 inhibitor), and azacitidine (hypomethylating agent) – with Actimab-A enhanced anti-leukemic efficacy across models – demonstrating synergy with one drug from each of the three pillars of modern AML care (targeted kinase inhibitors, menin inhibitors, and hypomethylating agents) and supporting Actimab-A’s positioning as a universal combination partner across frontline, relapsed/refractory, and unfit AML populations.

Sandesh Seth, Actinium’s Chairman and CEO, said, "The data presented at AACR (Free AACR Whitepaper) 2026 represent a significant step forward in our mission to establish Actimab-A as the foundational backbone therapy across the AML treatment continuum. For the first time, we have clear molecular evidence – through transcriptional profiling – of how Actimab-A reprograms AML cells to activate p53-driven apoptosis and shut down proliferative signaling, providing the mechanistic basis for deeper, more durable MRD-negative responses and mutation-agnostic activity we have consistently observed clinically. As the only CD33-targeted radiotherapy in development for myeloid malignancies, Actimab-A uniquely leverages the broad, stable expression of CD33 and the potent, mutation-agnostic Ac-225 payload to complement – not compete with – the targeted therapies that define today’s AML standard of care. Building on compelling clinical results across more than 150 patients in multiple treatment settings, and the high visibility of our NCI CRADA – including the ongoing frontline triplet trial with venetoclax and ASTX-727 – these findings will strengthen investigator enthusiasm for Actimab-A and reinforce the significant commercial opportunity ahead as we seek a partner for the registrational Phase 2/3 Actimab-A + CLAG-M study for which we have FDA alignment. We are focused on executing across our ongoing and planned clinical programs to deliver meaningful improvements in outcomes for AML patients, who continue to face high unmet medical need that is not addressed by currently available therapies."

The Actimab-A AACR (Free AACR Whitepaper) presentation is available for viewing on the Presentations & Webinars page of Actinium’s website HERE.

Title: Actimab-A, a CD33-Targeted Actinium-225 Radioconjugate, Drives Mutation-Agnostic Anti-Leukemic Activity and Synergizes with Standard Therapies in AML Through Transcriptional Reprogramming

Abstract Number: 5827

About Actimab-A

Actimab-A (lintuzumab-Ac225) is Actinium’s lead CD33-targeted radiotherapy and the only CD33-targeted radiotherapy in clinical development for myeloid malignancies. Actimab-A pairs a humanized anti-CD33 monoclonal antibody (lintuzumab) with the potent alpha-emitter Actinium-225 (Ac-225), which delivers high-energy, short-range radiation that produces lethal double-strand DNA breaks in CD33-expressing leukemic cells while sparing surrounding healthy tissue. Because CD33 is expressed on the blasts of the large majority of AML patients and the Ac-225 payload kills cells independent of genetic background, Actimab-A is positioned as a mutation-agnostic backbone that can be combined with the targeted and non-targeted therapies that define today’s AML standard of care.

Actimab-A has been studied in more than 150 patients with AML across multiple treatment settings, including as monotherapy and in combination with the intensive chemotherapy regimen CLAG-M and with the BCL-2 inhibitor venetoclax. In a Phase 1 trial in relapsed/refractory AML, Actimab-A plus CLAG-M produced an 83% overall response rate and 75% MRD-negativity at the recommended Phase 2 dose, with meaningful overall survival benefits in a high-risk population including patients with TP53 mutations and prior venetoclax exposure, and a manageable safety profile. Under a Cooperative Research and Development Agreement (CRADA) with the National Cancer Institute (NCI), Actimab-A is being advanced across the NCI’s National Clinical Trials Network – which includes approximately 2,000 clinical trial sites through groups such as ECOG, SWOG, and Alliance – and is the subject of an ongoing frontline triplet combination trial with venetoclax and the hypomethylating agent ASTX-727 (Taiho Oncology) in newly diagnosed AML patients. Actimab-A is advancing toward a Phase 2/3 registrational program, with the goal of establishing Actimab-A as a foundational backbone therapy for patients with AML, myelodysplastic syndrome (MDS), and other CD33-expressing myeloid malignancies – a patient population that continues to face high unmet medical need.

(Press release, Actinium Pharmaceuticals, APR 22, 2026, View Source [SID1234664696])

On April 22, 2026 Actinium Pharmaceuticals, Inc. (NYSE AMERICAN: ATNM) (Actinium or the Company), a pioneer in the development of targeted radiotherapies, reported preclinical results for ATNM-400 across prostate, lung, and breast cancer models presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting in San Diego, CA. ATNM-400 is a novel, first-in-class targeted radiotherapy utilizing the Actinium-225 (Ac-225) radioisotope that targets a non-PSMA membrane antigen overexpressed in advanced and therapy-refractory solid tumors across multiple oncology indications.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

ATNM-400 is a novel, first-in-class targeted radiotherapy whose differentiation stems from both its target and its isotope. The target is a non-PSMA membrane antigen associated with treatment resistance in advanced solid tumors that is overexpressed across prostate cancer, non-small cell lung cancer (NSCLC), and breast cancer, and is further upregulated following treatment with standard-of-care therapies — providing a strong mechanistic rationale for ATNM-400 in the treatment-resistant disease settings that represent the greatest unmet need, and for combination regimens designed to exploit this treatment-induced target upregulation. The isotope, Actinium-225 (Ac-225), is a potent alpha emitter that, compared to beta emitters such as Lu-177, delivers high-energy radiation capable of inducing irreversible double-stranded DNA breaks, with a shorter path length that may limit off-target effects and enhance therapeutic precision. Together, this target-and-isotope combination positions ATNM-400 to overcome conventional resistance pathways and deliver durable tumor control while potentially avoiding toxicities such as interstitial lung disease that limit the use of antibody-drug conjugates — expanding the population of patients who could benefit from treatment.

Key Data and Highlights From the ATNM-400 AACR (Free AACR Whitepaper) Presentation

New preclinical data support ATNM-400 as a differentiated Ac-225 radioconjugate with potential applicability across multiple high-value solid tumor indications. ATNM-400 demonstrates a favorable tolerability profile, with no significant toxicity observed at therapeutic doses; and additionally:

In Prostate Cancer

Demonstrates in vivo efficacy across prostate cancer models with low, medium, and high PSMA expression, including PSMA-negative models.
Shows superior anti-tumor efficacy versus vehicle control, unconjugated antibody, and 177Lu–PSMA-617 (active ingredient in PLUVICTO) in both high -PSMA, (C4-2) and low (22Rv1) PSMA-expressing models, addressing both patients unlikely to respond to PSMA-targeted radioligand therapy (low-PSMA, 22Rv1) and those who relapse on it (C4-2).
Activity in PSMA-negative (DU145) models supports a differentiated profile, suggesting ATNM-400 could address mCRPC patients who are ineligible for or have progressed on PSMA-targeted radioligand therapy due to low or absent PSMA expression— a population with no currently approved targeted radiotherapy option.

In Lung Cancer

New data in the NCI-H1975 EGFR-mutant NSCLC model – a clinically relevant model of osimertinib-resistant disease – shows ATNM-400 as monotherapy or in combination with osimertinib exceeds the tumor growth inhibition of osimertinib plus chemotherapy, the current standard of care in post-osimertinib progression. These results extend the Company’s prior data demonstrating 100% complete tumor regression with the ATNM-400 plus osimertinib combination.
ATNM-400 monotherapy demonstrates greater anti-tumor activity than Dato-DXd (TROP-2 ADC approved in EGFR-mutant lung cancer) and izalontamab brengitecan (HER3-EGFR bispecific ADC in development for EGFR-mutant lung cancer). ATNM-400 also demonstrates greater anti-tumor activity than the EGFR-cMET bispecific antibody amivantamab (RYBREVANT) as shown in prior studies.

In Breast Cancer

New head-to-head data in the BT474 Clone-5 trastuzumab-resistant HER2+ breast cancer model which is a clinically relevant model of the post-trastuzumab setting, where treatment options are limited, demonstrate that ATNM-400, both as monotherapy and in combination with trastuzumab deruxtecan, achieves anti-tumor activity comparable to the approved HER2-ADC trastuzumab deruxtecan (ENHERTU). These results extend the Company’s SABCS 2025 data and position ATNM-400 as a potential alternative for patients who cannot tolerate HER2 ADCs due to interstitial lung disease, a known class-related toxicity.

In the same post-trastuzumab failure setting, ATNM-400 produces durable tumor growth inhibition after treatment discontinuation which exceeds both vehicle control and trastuzumab deruxtecan, supporting the potential for less frequent dosing and more durable disease control than ADCs.Sandesh Seth, Actinium’s Chairman and CEO, said, "The data we presented at AACR (Free AACR Whitepaper) are an important new piece of a much larger picture for ATNM-400. As a single agent, ATNM-400 continues to demonstrate activity across prostate, lung, and breast cancer in the treatment-resistant settings that represent the greatest unmet need, and also in combinations which can expand the available opportunity to additional patient populations. These data build on our previously disclosed results showing significant tumor regression when ATNM-400 is combined with osimertinib in EGFR-mutant lung cancer, and when combined with enzalutamide in prostate cancer, with similar combination potential emerging in breast cancer. What is becoming increasingly clear is that ATNM-400’s target antigen is upregulated by standard-of-care therapies, which creates a strong mechanistic rationale for ATNM-400 to rescue patients who progress approved agents and also to extend the benefit of these approved agents through combinations. We look forward to continuing to advance ATNM-400 toward the clinic with additional data to come in 2026."

The ATNM-400 AACR (Free AACR Whitepaper) presentation is available for viewing on the Presentations & Webinars page of Actinium’s website HERE.

Title: Preclinical Development of ATNM-400, a First-in-Class Actinium-225 Radioconjugate with Pan-Tumor Efficacy in Solid Tumors

Abstract Number: 5824

(Press release, Actinium Pharmaceuticals, APR 22, 2026, View Source [SID1234664695])

On April 22, 2026 Nurix Therapeutics, Inc. (Nasdaq: NRIX), a clinical-stage biopharmaceutical company developing targeted protein degradation therapies, reported new preclinical data from multiple oncology programs at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

The presentations highlight continued progress across Nurix’s oncology pipeline, including programs targeting pan-mutant BRAF, CBL-B and Aurora Kinase A (AURKA), as well as a featured AACR (Free AACR Whitepaper) Advances session presentation highlighting the broader scientific progress and clinical translation of targeted protein degradation. Collectively, these data provide additional mechanistic validation of Nurix’s approach to CBL-B, Aurora kinase A (AURKA) and mutant BRAF to address key limitations of traditional approaches, including resistance, incomplete pathway suppression, and inability to target non-enzymatic protein functions.

"These data, together with our participation in the AACR (Free AACR Whitepaper) Advances session, highlight the growing clinical and scientific validation of targeted protein degradation as a new therapeutic modality," said Arthur T. Sands, M.D., Ph.D., president and chief executive officer. "Across multiple programs, we are seeing consistent evidence that these therapies can drive deeper and more durable biological responses, supporting their potential to deliver meaningful benefit for patients."

AACR Advances Session
Later today, April 22, 2026, Gwenn Hansen, Ph.D., chief scientific officer of Nurix, will present "Designing Effective Degrader Therapeutics: What Early Clinical Experience Has Taught Us" as part of the AACR (Free AACR Whitepaper) Advances session "Induced Proximity Pharmacology: Degraders and Beyond." Dr. Hansen’s remarks will provide a broad perspective on recent advances in targeted protein degradation, including insights from early clinical experience and the evolving potential of induced proximity approaches to expand the druggable target space and improve therapeutic outcomes.

Pan-Mutant BRAF Degrader Program
In a poster presentation titled "NRX-0305, an orally bioavailable, CNS penetrant pan-mutant BRAF degrader demonstrates robust efficacy in intracranial models of melanoma brain metastasis and primary glioma," Nurix reported that NRX-0305 achieves dose-proportional pharmacokinetics across plasma, tumor, and brain, enabling robust degradation of mutant BRAF and downstream pathway inhibition. These properties translate into potent antitumor activity in intracranial glioma and melanoma models while selectively sparing wildtype BRAF and avoiding paradoxical MAPK pathway activation. In a clinically relevant BRAF inhibitor–resistant melanoma brain metastasis patient-derived xenograft (PDX) model, NRX-0305 significantly extended survival versus both vehicle and dabrafenib, delivering a 142% increase in lifespan, compared with approximately 12% for the approved BRAF inhibitor.

Additional data were presented in a poster titled "NRX-0305 is an orally bioavailable, pan-mutant BRAF degrader that exhibits single-agent and combination efficacy with MEKi or anti-EGFR across Class 1/2/3 BRAF-mutant cancers." In preclinical tumor models, NRX-0305 demonstrates broad activity across mutant BRAF classes, including activity across 14 PDX models spanning Class 1 treatment-resistant, Class 2, and Class 3 BRAF mutations. Combination of NRX-0305 with MEK inhibitors or anti-EGFR therapy enhanced tumor regressions in Class 2 and drove complete responses in Class 1 and 3 models. Notably, the complete regressions are achieved at lower MEK inhibitor dose levels, supporting the potential for an improved therapeutic window relative to current treatment approaches.

CBL-B Program
In an oral presentation titled "Discovery and characterization of CBL-B intramolecular glue inhibitors that increase T cell activation and suppress tumor growth," Nurix reported the discovery and characterization of novel intramolecular glue inhibitors targeting CBL-B, an E3 ubiquitin ligase that negatively regulates T, B, and NK cell activation. Using mechanism-agnostic screening assays guided by CBL-B biology, Nurix identified a novel series of intramolecular glue inhibitors that stabilize the closed, inactive conformation of CBL-B, representing a first-in-class mechanism of action. Through structure-guided optimization, this series was advanced to NX-1607, a potent and selective CBL-B inhibitor with sub-nanomolar binding affinity. In preclinical studies, NX-1607 enhanced T cell activation, as evidenced by increased IL-2 and IFN-γ secretion in response to TCR stimulation, and demonstrated single-agent anti-tumor activity across multiple syngeneic tumor models, including colorectal, triple-negative breast cancer, and B cell lymphoma. NX-1607 also synergized with anti-PD-1 therapy to significantly enhance survival across multiple models. Early clinical data demonstrated dose-dependent pharmacokinetics and modulation of the proximal pharmacodynamic biomarker pHS1 in CD8 T cells, providing initial evidence of target engagement in patients.

Aurora Kinase A (AURKA) Degrader Program
In a poster presentation titled "NRX-4972, a selective, oral, Aurora kinase A degrader, demonstrates increased efficacy in an SCLC tumor model, and greater in vitro synergy than an AURKA inhibitor," Nurix reported new data demonstrating that targeted degradation of AURKA enables more complete biological modulation compared to inhibition alone. NRX-4972 exhibits central nervous system penetration and a favorable pharmacokinetic and pharmacodynamic profile, translating into superior antitumor activity in aggressive small cell lung cancer models, particularly with an optimized twice-daily dosing regimen. In the H82 SCLC model, twice-daily administration of NRX-4972 resulted in 60% of mice surviving to the end of the study, whereas none of the mice treated with AURKA inhibitors alisertib or LY3295668 survived. Mechanistically, degradation of AURKA results in downregulation of MYC and enhanced induction of DNA damage, apoptosis, and G2/M arrest. NRX-4972 also demonstrated broader and more potent synergy than an AURKA inhibitor in an in vitro screen of combination agents across triple-negative breast cancer, SCLC, and NSCLC cell lines, further supporting its therapeutic potential.

About NRX-0305
NRX-0305 is a potent, selective, and orally bioavailable central nervous system (CNS)-penetrant pan-mutant BRAF degrader that Nurix is exploring for use in oncology. Nurix has reported preclinical data demonstrating potent anti-tumor activity in multiple cell line-derived and patient-derived xenograft disease models representing Class 1, Class 2, and Class 3 B-RAF mutations. Anti-tumor activity was also observed in the setting of CNS disease and treatment-resistance, suggesting the potential for utility across a broad range of solid tumor types.

About NX-1607
NX-1607 is an investigational first-in-class oral inhibitor of the E3 ligase Casitas B-lineage lymphoma proto-oncogene B (CBL-B) being developed for immuno-oncology indications, including a range of solid tumor types. CBL-B is a cytoplasmic E3 ubiquitin ligase that negatively regulates T cell activation, making it an attractive target for immuno-oncology and offering a novel therapeutic approach to treat solid tumors. Inhibition of CBL-B in preclinical studies reverses T cell exhaustion, alleviates tumor induced immunosuppression, and may also exert direct antitumor effects. Nurix is evaluating NX-1607 in an ongoing Phase 1 trial in adults in a range of oncology indications. This study includes a thorough investigation of both dose and schedule in the Phase 1a portion. Additional information on the NX-1607 clinical trial can be accessed at www.clinicaltrials.gov (NCT05107674).

About NRX-4972
NRX-4972 is a CNS-penetrant, orally bioavailable and highly selective degrader of Aurora A kinase (AURKA). AURKA is an oncogene frequently overexpressed in adult solid tumors, hematologic malignancies, and pediatric cancers. Several AURKA inhibitors are effective in preclinical tumor models, but this activity has failed to translate into clinical efficacy. To address the limitations of inhibitors, Nurix has designed bifunctional targeted protein degraders of AURKA that enable removal of both enzymatic and scaffolding functions.

(Press release, Nurix Therapeutics, APR 22, 2026, View Source [SID1234664694])

On April 22, 2026 Xenetic Biosciences, Inc. (NASDAQ:XBIO) ("Xenetic" or the "Company"), a biopharmaceutical company focused on advancing innovative immuno-oncology technologies addressing difficult to treat cancers, reported that its abstract has been accepted for presentation at the 2026 American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Annual Meeting, taking place May 29 – June 2, 2026, in Chicago, IL.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

The accepted abstract, titled "Targeting cfDNA and NETs with DNase I to augment CAR T cell function and antitumor efficacy," highlights preclinical research supporting Xenetic’s DNase-based therapeutic approach designed to enhance CAR T-cell activity and improve antitumor responses.

Presentation Details:

Session Title: Hematologic Malignancies – Plasma Cell Dyscrasia (Poster Session)

Abstract Title: Targeting cfDNA and NETs with DNase I to augment CAR T cell function and antitumor efficacy

Poster Board: 410

Presentation Date & Time: June 1, 2026, 9:00 AM – 12:00 PM CDT

Presenter: Alexey V. Stepanov, PhD

The poster will be available to conference attendees during the scheduled session. For more information, please visit asco.org.

(Press release, Xenetic Biosciences, APR 22, 2026, View Source [SID1234664693])

On April 22, 2026 TuHURA Biosciences, Inc. (NASDAQ:HURA) ("TuHURA" or the "Company"), a Phase 3 immuno-oncology company developing novel therapeutics to overcome resistance to cancer immunotherapy, reported that it has entered into a loan agreement providing a credit facility of up to $50 million in funding to support the Company’s pipeline, ongoing clinical trials, and general corporate expenses. The lender is an affiliate of the Company’s largest stockholder, K&V Investment One LLC.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

Under the terms of the loan agreement, TuHURA will have the ability to draw down monthly on the facility on an as-needed basis to fund monthly expenses for ongoing clinical development and operations. The facility bears a 12% annual interest rate on outstanding funds drawn, with interest paid monthly and principal repayment due at a 5-year maturity date of April 21, 2031. The loan facility is secured by the assets of the Company and its subsidiaries. In connection with the credit facility, the Company granted the lender a low to mid-single digit percentage royalty on annual commercial sales by the Company or its sublicensees of products based on IFx-2.0.

"We are gratified to have established this non-equity based source of operating capital on what we believe are attractive terms for a company such as TuHURA. This agreement allows us to fund operations through anticipated key milestones this year and beyond through anticipated top-line Phase 3 results of our lead IFx-2.0 program. Importantly, we control the timing and amount of funds drawn under this facility while preserving the ability to be opportunistic in securing other potential sources of capital, including corporate partnerships or equity financings," said Dr. James Bianco, President and Chief Executive Officer of TuHURA Biosciences. "We believe that it is unusual to access such an attractive source of capital in advance of a BLA submission or pending FDA approval. This funding is a testament to the conviction our largest shareholder has in our strategy and in the potential for the clinical and commercial success of IFx-2.0."

Additional information regarding the credit facility and royalty agreement, including the terms and provisions of the loan agreement, can be found in the Company’s Current Report on Form 8-K filed today with the Securities and Exchange Commission.

(Press release, TuHURA Biosciences, APR 22, 2026, View Source [SID1234664692])