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 Tempest Therapeutics, Inc. (Nasdaq: TPST) ("Tempest"), a clinical-stage biotechnology company developing a pipeline of advanced chimeric antigen receptor T-cell ("CAR-T") product candidates, reported a strategic partnership with Hebei Senlang Biotechnology Co., Ltd. ("Senlang"), a clinical-stage cell therapy company with extensive expertise in CD7-targeted CAR-T development and clinical translation. Under the agreement, Tempest and Senlang will collaborate to develop Tempest’s proprietary TPST-4003 product candidate, beginning with an investigator-initiated trial ("IIT") in China evaluating TPST-4003 in approximately 10 patients with myasthenia gravis ("MG") or multiple sclerosis ("MS"). The company expects first patient enrollment and dosing to occur in the fourth quarter of 2026.

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The initial study is designed to generate clinical evidence of safety, pharmacodynamic ("PD") activity, and therapeutic potential of TPST-4003, building on promising findings from related pipeline preclinical and clinical research. Under the agreement, Senlang will coordinate and support trial execution in China, leveraging its extensive experience in clinical development of advanced CAR-T therapies. Additionally, the agreement grants Senlang an exclusive option to negotiate and enter into a definitive license agreement for TPST-4003 in China.

"This collaboration represents an important step in developing TPST-4003," said Matt Angel, Ph.D., President and Chief Executive Officer of Tempest. "Through this partnership, we plan to rapidly and efficiently advance into first-in-human studies to generate clinical evidence in support of our next generation in vivo CAR-T pipeline and platform technologies. We expect to begin dosing patients in the fourth quarter of this year with initial safety and PD data from the first patients expected as early as the first half of 2027."

"Based on our extensive clinical-stage experience in CD7-targeted CAR-T therapies, we believe CD7 represents a highly attractive target for next-generation cell therapies," said Shengmin Guo, Founder and Chief Executive Officer of Senlang Biotechnology. "We are excited to partner with Tempest to combine our CD7 expertise with Tempest’s innovative CD7-targeted mRNA/LNP delivery platform and clinically validated CD19/BCMA CAR architecture to advance TPST-4003 into first-in-human studies."

The initial trial is expected to assess the safety, cellular kinetics and pharmacodynamic activity of TPST-4003 in patients with MG or MS. Key assessments are expected to include treatment-emergent adverse events; the generation and expansion of peripheral blood CD4+ and CD8+ CAR-T cells and CD56+ CAR-NK cells; CAR transgene copy number; and the depth and kinetics of CD19+ B-cell depletion and B-cell subset reconstitution. Where clinically appropriate, exploratory assessments may also include the detection of CAR-positive immune cells in cerebrospinal fluid and the evaluation of B-cell depletion in lymphoid tissue. Disease-specific clinical activity will be evaluated using established measures.

About TPST-4003

TPST-4003 is an in vivo dual-targeting CD19/BCMA CAR-T product candidate that combines proprietary CD7-targeted mRNA/LNP delivery with a clinically validated dual-target CAR architecture utilized in the company’s TPST-2003 CAR-T program. Targeting broad B-cell lineage depletion and reset, TPST-4003 is being designed to address a range of autoimmune and oncology indications, initially including myasthenia gravis and multiple sclerosis. TPST-4003 differentiates from other in vivo CAR-T approaches through its CD7-targeted mRNA/LNP delivery strategy, which is designed to enable direct engagement of endogenous CD4+ and CD8+ T-cell populations for CAR generation in vivo.

(Press release, Tempest Therapeutics, JUL 21, 2026, https://ir.tempesttx.com/news-releases/news-release-details/tempest-announces-development-collaboration-senlang [SID1234669342])

On July 21, 2026 Propanc Biopharma, Inc. (Nasdaq: PPCB) ("Propanc" or the "Company"), a biopharmaceutical company focused on developing novel treatments for chronic diseases, including recurrent and metastatic cancer, reported that the Company and its joint research partners at the Universities of Jaén and Granada published key findings in a peer reviewed journal, Microbial Cell Factories, regarding the evaluation of recombinant trypsinogen and chymotrypsinogen for improving production for applications in biotechnology research. Specifically, human therapeutic use intended for the treatment of a range of chronic diseases including cancer and fibrosis. The Microbial Cell Factories journal is a leading peer-reviewed journal that focuses on applied microbiology. The publication, entitled, "Evaluation of recombinant trypsinogen and chymotrypsinogen production in Komagataella phaffii through co-expression of HAC1 and PDI1," is available online.

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Funded and coordinated by Propanc in collaboration with the Company’s joint research partners, the program is designed to produce a backup, clinical compound to the Company’s lead product candidate, PRP, from bovine sources, initially targeting metastatic cancer from solid tumors. According to Emergen Research, the global metastatic cancer market is projected to be worth over $111 Billion by 2027. Key findings from the research conducted by Dr. Aitor González determined that it is possible to scale up production of both proenzymes trypsinogen and chymotrypsinogen using recombinant technology resulting in stable purified proteins.

The recombinant proenzyme product candidate, designated rec-PRP, will be produced at small scale quantities under non-GMP (Good Manufacturing Practice) conditions to establish compatibility with the naturally derived, bovine sourced product before determining the regulatory pathway for entering the clinic. Rec-PRP is a follow-on product to the Company’s lead asset, PRP, which is targeting a Phase 1b First-In-Human clinical study in advanced cancer patients suffering from solid tumors early 2027.

"A fully synthetic recombinant version of PRP is the next phase of our strategic plan in building a new therapeutic drug class aimed at treating a range of chronic diseases that remain a high unmet medical need and life threatening for many patients, but not at the expense of severe toxicity often associated with standard treatment options," said Mr. James Nathanielsz, Propanc’s Chief Executive Officer. "Our novel technology uses proteolytic action (breakdown of proteins) to enforce malignant cells to return to a natural state that restores cellular function and so they die off naturally, which induces anti-cancer and anti-tumor effects by altering the micro-immune environment. Our vision is to produce both products as cost-effective and practical solutions that can be administered globally. We are pleased with our progress as the Company enters a transformative stage with its R&D programs."

Rec-PRP could have additional benefits to the global healthcare system that could further capitalize on a new therapeutic approach to chronic diseases such as cancer and fibrosis. For example, both proenzymes are synthesized by an in vivo (living organism) system to produce crystallized proteins that could be maintained for long periods without suffering degradation in the absence of refrigeration. This will be useful for a longer shelf life as well as global distribution of the product, particularly in warmer climates and developing regions where refrigeration may not be available.

(Press release, Propanc, JUL 21, 2026, View Source [SID1234669341])

On July 21, 2026 Pasithea Therapeutics Corp. (NASDAQ: KTTA) ("Pasithea" or the "Company"), a clinical-stage biotechnology company developing PAS-004, a next-generation macrocyclic oral MEK inhibitor, for the long-term treatment of chronic diseases including the neurocutaneous manifestations of neurofibromatosis type 1 (NF1), reported that an abstract detailing the Phase 1 dose-escalation study of PAS-004 in patients with MAPK pathway-driven advanced solid tumors has been accepted for poster presentation in the Developmental Therapeutics track at the European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) Congress 2026, taking place October 23-27, 2026, at the IFEMA Madrid Convention Center in Madrid, Spain.

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Details of the Poster Presentation:

Title: Phase I Dose-Escalation Study of the Safety and Pharmacokinetics of PAS-004, a Macrocyclic MEK Inhibitor, for the Treatment of Patients with MAPK Pathway Driven Advanced Solid Tumors

Presenter: Kartik Krishnan, Miami, Florida, United States

Authors: Ildefonso I. Rodriguez Rivera (San Antonio, TX); Kartik Krishnan, Tiago Reis Marques, Joy Cannon, Yohana Sebhat (Miami, FL)

Abstract/Poster Number: 1050P

Session: Developmental Therapeutics

Date/Time: Friday, October 23, 2026, 15:15–16:00 CEST

The full abstract will be published on the ESMO (Free ESMO Whitepaper) Congress website in accordance with the meeting’s embargo policy. The Company plans to issue a follow-up release with detailed results at the time of presentation.

(Press release, Pasithea Therapeutics, JUL 21, 2026, View Source [SID1234669340])

On July 21, 2026 Innate Pharma SA (Euronext Paris: IPH; Nasdaq: IPHA) ("Innate" or the "Company"), reported the completion of enrollment in the dose escalation of the Phase 1 study of IPH4502 (NCT06781983), its proprietary Nectin-4 exatecan ADC. Preliminary data are expected by year-end and will include data from 76 patients, guiding Phase 1 dose optimization in selected tumor types.

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The IPH4502-101 Phase 1 study is an open-label, multi-center study evaluating the safety, tolerability, and preliminary anti-tumor activity of IPH4502 as a single agent in patients with advanced solid tumors known to express Nectin-4, including but not limited to urothelial carcinoma (UC), non-small cell lung cancer (NSCLC), head and neck squamous cell carcinoma (HNSCC), breast, ovarian, gastric, esophageal, and colorectal cancers. The Phase 1 dose-escalation part has recruited 76 patients in France and the United States.

To date, IPH4502 continues to show a favorable safety profile, with limited hematological toxicity, supporting the hypothesis that the Company’s proprietary linker leads to a slow release of free exatecan, minimizing toxicity. Preliminary anti-tumor activity continues to be observed in heavily pre-treated patients with advanced solid tumors, with objective responses reported in UC post enfortumab vedotin, as well as in NSCLC and HNSCC.

"Completing enrollment in the dose escalation marks an important milestone for IPH4502. The data generated to date continue to support the differentiated design of IPH4502, notably through the limited hematological toxicity observed to date, which we believe might reflect the benefits of our proprietary linker. We look forward to the dose escalation dataset by year-end, which will guide our path into dose optimization and further define the clinical potential of IPH4502," said Sonia Quaratino, EVP Chief Medical Officer of Innate Pharma.

About IPH4502

IPH4502 is Innate Pharma’s proprietary Nectin-4 antibody-drug conjugate (ADC), built on three differentiated components. The payload is exatecan, a potent topoisomerase I inhibitor, with the potential to overcome key limitations associated with monomethyl auristatin E (MMAE)-based ADCs, including multidrug resistance protein 1 (MDR1)-mediated resistance, and without the need for CYP2D6 genotyping. IPH4502 incorporates a proprietary stable linker designed to slow the release of free exatecan into the circulation. The binder is a proprietary humanized anti-Nectin-4 antibody with high affinity and a distinct, non-overlapping epitope compared with enfortumab vedotin (EV). In preclinical studies, IPH4502 demonstrated anti-tumor activity in EV-resistant tumor models and in tumors with low and heterogeneous Nectin-4 expression, supporting its potential applicability across solid tumor types beyond urothelial carcinoma (UC). IPH4502 is currently being evaluated in the Phase 1 IPH4502-101 study (NCT06781983) in patients with advanced solid tumors known to express Nectin-4.

(Press release, Innate Pharma, JUL 21, 2026, View Source [SID1234669339])