On July 21, 2026 Calidi Biotherapeutics, Inc. (NYSE American: CLDI) ("Calidi" or the "Company"), a clinical-stage biotechnology company pioneering the development of systemically delivered, targeted genetic medicines, reported 2026 successes to date and provided an update on the Company’s upcoming milestones.

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"Calidi continues to execute on its goal of bringing its RedTail platform to the clinic and expanding the utility of this groundbreaking technology," said Calidi Chief Executive Officer Eric Poma, PhD. "We have had productive discussions with the FDA that support our strategy and timeline for CLD-401 IND filing and we continue to expand the reach of RedTail with the development of in situ TCEs."

1H26 Accomplishments

Successful pre-IND meeting with FDA with agreement on pharmacology, toxicology, CMC, and phase I protocol strategy for CLD-401 phase I trial
In Situ TCEs have the potential to overcome current limitations around T-cell engagers in solid tumors by their ability to deliver high levels of a TCE in situ while simultaneously activating T-cells in the tumor microenvironment. Proof-of-concept data presented in 2026 underscore this potential
Strengthened the Board of Directors with the addition of Corsee Sanders, Ph.D. Dr. Sanders has served as strategic advisor to Celgene’s Chief Medical Officer (CMO) following Celgene’s acquisition of Juno where she was an Executive Vice President of Development Operations. She also served as Transition Advisor to Bristol Myers Squibb (BMS), which acquired Celgene. Prior to that, Dr. Sanders held numerous leadership positions over the course of 23 years at Genentech/Roche, including serving as Senior Vice President, Global Head of Clinical Operations and Industry Collaboration, for six years
Reduced debt and G&A expenses by approximately $1M in 1Q26 over 1Q25. Company will maintain a continued focus on cost cutting to ensure sufficient capital to advance pipeline
Upcoming Key Value Drivers

New data to be presented quantifying positive results from cytotoxicity and IL-15 SA expression in murine tumor cells at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Drug Discovery and Development (AACR D3) conference being held in Boston, MA from July 21-24, 2026
New data to be presented expanding in situ TCEs from the RedTail platform to include EpCAM-targeted TCEs, in addition to TROP-2, at the European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) conference being held in Madrid, Spain from October 23-27, 2026
New data to be presented including results from GLP toxicity and IND-enabling studies, as agreed to with the FDA at June 2026 pre-IND meeting, at the Society for Immunology of Cancer (SITC) (Free SITC Whitepaper) conference being held in Phoenix, AZ from November 4-8, 2026
Company targeting first patient dosed in CLD-401 phase I trial in Q1 2027. On track for regulatory submissions with positive feedback from FDA in pre-IND meeting
First patients’ data in CLD-401 trial anticipated in Q2 2027. The Company believes that early signs of activity and expression in tumor microenvironment (TME) would prove the platform is working as designed and viral and protein payloads are being effectively deployed in the TME

(Press release, Calidi Biotherapeutics, JUL 21, 2026, View Source [SID1234669358])

On July 21, 2026 Atossa Therapeutics, Inc. (NASDAQ: ATOS) ("Atossa" or the "Company"), a clinical-stage biopharmaceutical company developing novel therapies in oncology and other areas of significant unmet clinical need, reported that a poster presentation titled "Dual estrogen receptor and PKC-β signaling modulation by (Z)-Endoxifen: A mechanism-driven therapeutic strategy for estrogen-driven pathology in McCune-Albright Syndrome" was presented at the AACR (Free AACR Whitepaper) Special Conference in Cancer Research: Breaking Barriers in the Fight Against Rare Cancers, which took place July 18-20, 2026, in Vancouver, BC, Canada.

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Presentation Details

Session Type: Poster Session A

Date: Saturday, July 18, 2026, 7:30-9:30 pm PT

Abstract Number: A010

Location: AACR (Free AACR Whitepaper) Special Conference in Cancer Research: Breaking Barriers in the Fight Against Rare Cancers, Vancouver, BC, Canada

Poster Title: Dual estrogen receptor and PKC-β signaling modulation by (Z)-Endoxifen: A mechanism-driven therapeutic strategy for estrogen-driven pathology in McCune-Albright Syndrome

Presenter: Sandra Hammer, PhD, Atossa Therapeutics Inc.

Summary: The poster supports a dual mechanism of action for (Z)-endoxifen in estrogen-driven pathology relevant to McCune Albright Syndrome-associated Peripheral Precocious Puberty (MAS-PPP): the blockade of ER-mediated transcription downstream of autonomous estrogen production and suppression of PKC-β/AKT-associated proliferative and cell-cycle signaling. This multi-pathway profile may address a key therapeutic gap in MAS-PPP, where estrogen suppression alone may not fully mitigate downstream proliferative signaling.

These findings support further evaluation of (Z)-endoxifen as a targeted therapeutic strategy for MAS-PPP and illustrate how transcriptomic and kinase-network integration can enable therapeutic repositioning for rare endocrine-driven diseases with limited dedicated drug development. They also highlight the potential relevance of (Z)-endoxifen to estrogen-driven neoplasms.

Key Highlights

McCune-Albright Syndrome (MAS) is a rare mosaic disorder driven by activating GNAS mutations that can result in autonomous estrogen production and chronic estrogen receptor activation.
Activating GNAS alterations are recognized oncogenic drivers in multiple neoplasms, positioning MAS a genetically defined model of chronic proliferative signaling that is highly relevant to rare tumor biology.
The poster evaluates (Z)-endoxifen, the active metabolite of tamoxifen, as a mechanism-driven strategy to modulate both estrogen receptor signaling and non-ER proliferative kinase pathways relevant to estrogen-driven MAS symptomatology, peripheral precocious puberty.
The analysis used weighted gene expression signatures in ER-positive MCF7 cells and integrated published phosphoproteomic and RNA-seq datasets to assess modulation of PKC-β and AKT signaling pathways.
The analysis identified a shared estrogen-responsive gene network and showed that (Z)-endoxifen markedly downregulated cell-cycle progression programs, including G2M Checkpoint and E2F Targets, while concurrently modulating estrogen-response pathways.
Integration of published mechanistic data further demonstrated that (Z)-endoxifen targets PKC-β1, promotes its dephosphorylation and degradation, and inhibits PMA-induced PKC-β1 and AKT phosphorylation.
"MAS related PPP remains a rare and underserved condition where current approaches focus primarily on reducing estrogen production but may not fully address downstream ER-dependent and proliferative signaling," said Dr. Steven C. Quay, M.D., Ph.D., President and Chief Executive Officer of Atossa Therapeutics. "These data support the potential of (Z)-endoxifen as a differentiated, mechanism-driven candidate that may simultaneously modulate estrogen receptor biology and PKC-β/AKT-associated cell-cycle signaling. This finding has direct relevance to several tumor types."

About McCune-Albright Syndrome

MAS is an extremely rare genetic disorder caused by activating mutations in the GNAS gene, leading to mosaic endocrine dysregulation. Because it is so rare and has a broad spectrum of symptoms, diagnosis can be challenging. The disease is characterized by a triad of symptoms: Polyostotic Fibrous Dysplasia: replacement of normal bone with weak, fibrous tissue, leading to fractures, deformities, and pain; Café-au-lait Spots: hyperpigmented skin patches with irregular, "jagged" borders that typically respect the body’s midline; and Hyperfunctioning Endocrinopathies: commonly known as precocious puberty, where children (especially girls) may begin puberty as early as age two. In pediatric patients, MAS commonly presents with gonadotropin-independent precocious puberty, particularly in females, which can result in accelerated growth, premature epiphyseal closure, and reduced adult height. Additional complications may include thyroid dysfunction, growth hormone excess, and other endocrine abnormalities. There are currently limited effective treatment options, highlighting the need for new therapeutic approaches.

(Press release, Atossa Therapeutics, JUL 21, 2026, View Source [SID1234669343])

On July 21, 2026 Acrivon Therapeutics, Inc. ("Acrivon" or "Acrivon Therapeutics") (Nasdaq: ACRV), a clinical stage biotechnology company discovering and developing precision medicines utilizing its proprietary Generative Phosphoproteomics AP3 (Acrivon Predictive Precision Proteomics) platform deployed for rational drug design and predictive clinical development, reported that the company will deliver an oral presentation and present a poster at the upcoming American Association for Cancer Research (AACR) (Free AACR Whitepaper) Drug Discovery and Development, or AACR (Free AACR Whitepaper) D3, Conference, taking place July 21–24, 2026 in Boston.

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The presentations will highlight the broad and actionable capabilities of the AP3 platform to rapidly identify and advance promising compounds into clinical development, focusing on the discovery of ACR-2316, the company’s novel clinical-stage, selective WEE1/PKMYT1 inhibitor.

Data being presented illustrate how AP3 can uncover drug-induced resistance mechanisms, in this case WEE1 inhibition-induced activation of PKMYT1, resulting in phosphorylation of CDK1 on Thr14, a direct PKMYT1 phosphorylation site. Moreover, AP3 enabled the development of ACR-2316 based on optimal intracellular pathway effects, including sustained activation of CDK1, CDK2, but importantly and also of PLK1, to drive potent pro-apoptotic tumor cell death.

"We are excited to present at AACR (Free AACR Whitepaper) D3 and to highlight the actionable power of our AP3 platform to rapidly translate intracellular pathway biology into differentiated drug candidates," said Kristina Masson, Ph.D., co-founder and EVP at Acrivon, and president and CEO of the company’s research subsidiary, Acrivon AB, in Lund, Sweden. "Our presentations underscore how AP3 moves beyond traditional target-centric drug discovery by directly measuring drug-regulated pathway activity in intact cells, enabling optimal biology-based design of compounds for superior clinical activity and patient benefit. ACR-2316 is a compelling example of this strategy, and we look forward to sharing our findings at the conference."

ACR-2316 is currently in a Phase 1/2 clinical study advancing toward the dose expansion phase. Initial observations have shown tumor shrinkage, including PRs, and durable clinical benefit in subjects with small cell lung cancer (SCLC), squamous non-small cell lung cancer (sqNSCLC), and adenosarcoma NSCLC (adNSCLC), AP3-predicted tumor types not previously shown to be sensitive to other clinical WEE1 or PKMYT1 inhibitors. The compound has also demonstrated a favorable, differentiated tolerability profile observed in studies conducted to date, with adverse events primarily limited to only transient, mechanism-based neutropenia and a notable absence of non-hematological adverse events.

Presentations and Details

Oral Podium Presentation

Title: Acrivon Predictive Precision Proteomics (AP3): Next Generation Precision Medicine for Phosphoproteomics-Guided Drug Discovery
Presenter: Lei Shi, Ph.D., Director and Head, AP3 Pathway Discovery, Acrivon Therapeutics
Session: Biotech Spotlight Session 1: Novel Therapeutics
Date and Time: Thursday, July 23, 2026, 3:50–4:00 p.m. ET
Location: Grand Ballroom

Poster Presentation

Title: AP3-guided biological SAR enables discovery of ACR-2316, a novel clinical-stage WEE1/PKMYT1 inhibitor designed for CDK1/2 and PLK1 pathway activation
Poster Number: A082
Session: Poster Session A
Date and Time: Wednesday, July 22, 2026, 6:15–8:45 p.m. ET
Location: Back Bay Ballroom

(Press release, Acrivon Therapeutics, JUL 21, 2026, View Source [SID1234669359])

On July 21, 2026 Verismo Therapeutics, a clinical-stage multi-chain CAR T cell therapy company pioneering a novel KIR-CAR platform technology, reported a new preclinical KIR-CAR program targeting the clinically validated Claudin 6 (CLDN6) antigen to treat CLDN6-expressing solid tumors via a novel binder developed at the University of Pennsylvania Perelman School of Medicine (Penn) through a Verismo-sponsored research agreement. The program is designed to complement Verismo’s lead solid tumor asset SynKIR-110, which targets mesothelin antigen and is currently being evaluated at multiple sites in the U.S. in the STAR-101 Phase 1 clinical trial (NCT05568680). The new CLDN6 novel binder is the second binder discovered in collaboration with Penn. The first binder, DS191, is used in SynKIR-310, which is being evaluated in the CELESTIAL-301 Phase 1 trial for treating patients with relapsed or refractory B cell non-Hodgkin lymphomas (NCT06544265).

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"Penn has been a foundational scientific partner for Verismo, particularly in the development of novel binders to advance our multi-chain KIR-CAR platform," said Laura Johnson, Ph.D., Chief Scientific Officer and Chief Operating Officer of Verismo Therapeutics. "We are excited to expand our preclinical assets with CLDN6 for targeting solid tumors in cancers with high unmet needs, especially as a complement to our lead candidate SynKIR-110, which recently reported positive early clinical data at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) meeting, for advanced mesothelin-expressing solid tumors, including ovarian cancer, mesothelioma, and cholangiocarcinoma. Our goal is simple: to make life better for patients with cancer who have run out of options."

Recent clinical advancements have established CLDN6 as a validated solid tumor target for CAR T cells, antibody-drug conjugates (ADCs), and bispecific immune therapies demonstrating anti-tumor activity across multiple CLDN6-positive cancers.¹ CLDN6 has emerged as a promising target for next-generation immunotherapies due to its expression in a variety of cancers and its limited or absent expression in healthy adult tissues. Improving the persistence and durability of response — a leading cause of CAR T failure in solid tumors — has been identified as the next major hurdle in the field, a challenge that the design of Verismo’s multi-chain KIR-CAR platform is built to address.

About the CLDN6 Binder Discovery and Verismo-Penn Collaboration

Our new preclinical program is built around a novel CLDN6-directed binder discovered at Penn through a Verismo-sponsored research agreement. The binder was identified by Prof. Donald Siegel, M.D., Ph.D., Co-Founder and Co-Chair of Verismo’s Scientific Advisory Board and Professor of Pathology and Laboratory Medicine and Founding Director of the Division of Transfusion Medicine & Therapeutic Pathology at Penn. Dr. Siegel previously led the discovery of Verismo’s DS191 binder.

"CLDN6 is one of the most compelling tumor-specific antigens to emerge in solid tumor immunotherapy, with highly restricted expression in healthy adult tissues and clinically validated activity across multiple solid tumor cancers," said Dr. Siegel. "We identified this CLDN6 binder through the same rigorous in-house discovery approach that produced the DS191 binder now being used to treat patients in the CELESTIAL-301 Phase 1 SynKIR-310 trial. We look forward to continuing our work with Verismo to expand the potential impacts of the multi-chain KIR-CAR platform across different cancers with unmet need."

Bryan Kim, CEO and Co-Founder of Verismo Therapeutics, said, "Pairing the CLDN6 antigen with Verismo’s multi-chain KIR-CAR architecture is a deliberate strategy designed to address challenges that have limited prior CLDN6-directed (and other solid-tumor) approaches. We are fortunate to be working with Dr. Siegel and the outstanding research team at Penn to assess the potential for our multi-chain KIR-CAR platform to overcome the limitations of current CAR T therapies in the treatment of solid tumors."

(Press release, Verismo Therapeutics, JUL 21, 2026, View Source [SID1234669344])

On July 21, 2026 Telix Pharmaceuticals Limited (ASX: TLX, NASDAQ: TLX, "Telix") reported publication of results from the ProstACT SELECT study in Cancers, a peer-reviewed journal. The Phase 1 study evaluated TLX591-Tx (lutetium-177 (177Lu) rosopatamab tetraxetan), Telix’s first-in-class prostate-specific membrane antigen (PSMA) targeting radio antibody-drug conjugate (rADC) therapy candidate. The study’s scientific purpose was to evaluate lesion concordance between 68Ga-PSMA-PET5 and multi-time point SPECT6 imaging for patient selection using a "theranostic" approach.

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The publication highlights TLX591-Tx’s differentiated clinical profile, including an intensified dosing schedule, prolonged tumor retention and low exocrine (salivary) gland irradiation. The authors also concluded that in a heterogeneous population representative of a real-world setting, TLX591-Tx therapy in combination with standard of care (SOC) demonstrated a manageable and predictable safety profile, and indicative efficacy with a median radiographic progression-free survival (rPFS) of 8.8 months reported in evaluable patients.

Nat Lenzo, MD, Nuclear Medicine Oncologist and Principal Investigator on the ProstACT SELECT study commented, "A key objective of ProstACT SELECT was to determine whether PSMA-PET imaging could reliably identify patients suitable for TLX591-Tx therapy, and the results clearly support this approach. The results provide compelling evidence that the PSMA-PET imaging agent and TLX591-Tx are targeting the same disease sites, supporting the ongoing ProstACT Global trial for mCRPC7, where there remains significant unmet need for additional treatment options."

David N. Cade, MD, Group Chief Medical Officer, Telix, said, "The publication of ProstACT SELECT data further strengthens the scientific foundation for Telix’s lead therapeutic candidate, TLX591-Tx. The peer-reviewed results support our patient-selection strategy and demonstrate a differentiated pharmacologic profile characterized by durable tumor targeting, hepatobiliary clearance, and a manageable safety profile. Telix is further evaluating TLX591-Tx in the international multi-center Phase 3 ProstACT Global study, where we aim to meaningfully improve outcomes for patients living with advanced prostate cancer."

The full paper is available at: View Source

About ProstACT SELECT

The purpose of the ProstACT SELECT trial was to evaluate the utility of 68Ga-PSMA-PET imaging (Illuccix) to select patients for TLX591-Tx rADC therapy. The primary objectives were to determine whole body biodistribution and organ radiation dosimetry and assess the safety and tolerability of TLX591-Tx in patients with advanced mCRPC. rPFS was a secondary study objective.

(Press release, Telix Pharmaceuticals, JUL 21, 2026, View Source [SID1234669360])