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.

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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.

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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.

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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.

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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])

On April 22, 2026 Tempest Therapeutics, Inc. (Nasdaq: TPST) ("Tempest"), a clinical-stage biotechnology company developing a pipeline of advanced CAR-T cell therapy product candidates to treat cancer, reported that it has achieved a key milestone in the development of TPST-2003, Tempest’s dual-targeting CD19/BCMA CAR-T therapy under development for the treatment of relapsed/refractory multiple myeloma ("rrMM"). Earlier this month, Tempest’s manufacturing partner, Cincinnati Children’s Applied Gene and Cell Therapy Center ("AGCTC"), took delivery of the TPST-2003 lentiviral vector, a critical component used in the manufacturing of TPST-2003. This milestone supports Tempest’s plans to initiate the first potentially registrational study to evaluate a dual-targeting CAR-T therapy in patients with rrMM, including patients who are experiencing extramedullary disease ("EMD"), later this year.

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Tempest recently announced that, as of a January 31, 2026 data cutoff, a total of 36 patients with rrMM had received one infusion of TPST-2003, including 24 patients in a prior Phase 1/2 investigator-initiated trial ("IIT") and 12 patients in the ongoing REDEEM-1 trial, representing one of the largest datasets evaluating a CD19/BCMA dual-targeting CAR-T therapy. As of the data cutoff, all six efficacy evaluable patients enrolled in the REDEEM-1 trial had achieved a complete response according to the International Myeloma Working Group uniform response criteria. Among 25 evaluable patients with measurable disease at baseline across both studies, the overall response rate was 100% (25/25). The IIT also demonstrated durable disease control, with median progression-free survival ("PFS") of 23.1 months across all patients and median PFS of 23.1 months in patients with EMD. Tempest plans to present the results of the REDEEM-1 trial and updated results from the IIT at a scientific meeting later this year.

"We are pleased by the rapid progress we have been making in partnership with AGCTC," said Dr. Matt Angel, President and Chief Executive Officer of Tempest. "The delivery of lentiviral vector, which is a critical component in the manufacturing of autologous CAR-T products, has enabled us to proceed with the manufacturing activities required for the pivotal development of TPST-2003. We are grateful for our partnership with AGCTC, and we are looking forward to continued rapid progress toward the initiation of a potentially registrational study for TPST-2003 later this year."

AGCTC is a research, development, and manufacturing hub advancing future cell and gene therapy (CGT) treatments for patients with unmet needs. Established in 2001, the center has evolved into a nationally recognized leader in CTG CDMO services with a proven track record that reflects Cincinnati Children’s commitment to solving unmet medical needs through translational science. AGCTC is part of the Cincinnati Children’s Cancer and Blood Diseases Institute, which is ranked #1 in the nation by U.S. News & World Report for pediatric cancer care.

"We are excited to have achieved this important milestone in the development of TPST-2003," said Dr. Chaozhong Zou, Executive Director and General Manager of AGCTC, Cancer and Blood Diseases Institute, Cincinnati Children’s Hospital Medical Center. "The clinical data generated so far support the idea that the parallel-structure dual-targeting CAR architecture of TPST-2003 could offer patients with rrMM a meaningful new treatment option, and we are grateful to be in position to support the development of TPST-2003 by leveraging our extensive experience making novel CAR-T programs IND-ready. We look forward to generating the information needed to support the pivotal development of TPST-2003."

About TPST-2003

TPST-2003 is an autologous CD19/BCMA dual-targeting CAR-T therapy designed to improve response depth and durability in patients with relapsed/refractory multiple myeloma ("rrMM") through a parallel dual-targeting CAR structure designed to address tumor heterogeneity and antigen escape. TPST-2003 is being developed in China by Tempest’s partner, Novatim Immune Therapeutics ("Novatim"). Under its agreement with Novatim, Tempest has the exclusive right to develop TPST-2003 outside of China, India, Turkey, and Russia.

About REDEEM-1

REDEEM-1 (Study nos. CTR20233309/NCT06223646) is a Phase 1/2a clinical trial evaluating TPST-2003 in patients with relapsed/refractory multiple myeloma, including patients with high-risk cytogenetics and patients with extramedullary disease. The REDEEM-1 trial has a targeted full enrollment of 29 patients. The REDEEM-1 trial is sponsored and being conducted by Tempest’s partner, Novatim Immune Therapeutics, with a total of eight clinical sites registered in China: Peking Union Medical College Hospital (Dr. Jian Li; lead site), The First Affiliated Hospital of Nanchang University (Dr. Fei Li), Peking University First Hospital (Dr. Yujin Dong), Henan Cancer Hospital (Dr. Baijun Fang), Shanxi Provincial Cancer Hospital (Dr. Liping Su), The Second Xiangya Hospital of Central South University (Dr. Hongling Peng), The First Affiliated Hospital of China Medical University (Dr. Xiaojing Yan), and The Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College (Dr. Dehui Zou).

Additional clinical trials evaluating TPST-2003

A Phase 1/2 IIT (Study no. NCT04714827) is evaluating TPST-2003 in patients with relapsed/refractory multiple myeloma, including patients with high-risk cytogenetics and patients with extramedullary disease. The IIT is sponsored and being conducted by Tempest’s partner, Novatim, with a total of two clinical sites registered in China: Shanghai Fourth People’s Hospital (Dr. Weijun Fu; lead site) and Shanxi Provincial Cancer Hospital (Dr. Liping Su).

A Phase 1 trial (Study nos. CTR20242409/NCT06518876) is evaluating TPST-2003 in patients with POEMS, a rare blood disorder caused by abnormal plasma cells. The Phase 1 trial is sponsored and being conducted by Tempest’s partner, Novatim, with a total of three clinical sites registered in China: Peking Union Medical College Hospital (Dr. Jian Li; lead site), Xuanwu Hospital Capital Medical University (Dr. Wanling Sun), and West China Hospital, Sichuan University (Dr. Yu Wu).

(Press release, Tempest Therapeutics, APR 22, 2026, View Source [SID1234664691])