On December 8, 2025 Protara Therapeutics, Inc. (Nasdaq: TARA) ("Protara"), a clinical-stage company developing transformative therapies for the treatment of cancer and rare diseases, reported the closing of its underwritten public offering of 13,043,479 shares of its common stock at a public offering price of $5.75 per share. In addition, Protara has granted the underwriters a 30-day option to purchase up to an additional 1,956,521 shares of common stock at the public offering price, less underwriting discounts and commissions. The gross proceeds from the offering were approximately $75 million before deducting underwriting discounts and commissions and offering expenses payable by Protara and excluding any exercise of the underwriters’ option to purchase additional shares. Protara intends to use the net proceeds received from the offering to fund the clinical development of TARA-002, as well as the development of other clinical programs. Protara may also use the net proceeds from the offering for working capital and other general corporate purposes.

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J.P. Morgan, TD Cowen and Piper Sandler acted as joint book-running managers of the offering. LifeSci Capital acted as a lead manager of the offering. H.C. Wainwright & Co. acted as a manager of the offering.

The shares of common stock were issued pursuant to an effective shelf registration statement on Form S-3 (File No. 333-275290) that was declared effective on November 14, 2023 by the U.S. Securities and Exchange Commission (the "SEC"). The offering was made only by means of a prospectus supplement and the accompanying prospectus. Copies of the final prospectus supplement and the accompanying prospectus relating to the offering may be obtained from the offices of J.P. Morgan Securities LLC, c/o Broadridge Financial Solutions, 1155 Long Island Avenue, Edgewood, New York 11717 or by email at [email protected] and [email protected]; TD Securities (USA) LLC, c/o Broadridge Financial Solutions, 1155 Long Island Avenue, Edgewood, New York 11717 or by email at [email protected]; or Piper Sandler & Co., 350 North 5th Street, Suite 1000, Minneapolis, Minnesota 55401, Attention: Prospectus Department, by telephone at (800) 747-3924, or by email at [email protected].

This press release shall not constitute an offer to sell or a solicitation of an offer to buy any of these securities, nor shall there be any sale of these securities in any state or jurisdiction in which such an offer, solicitation or sale would be unlawful prior to registration or qualification under the applicable securities laws of such state or jurisdiction.

(Press release, Protara Therapeutics, DEC 8, 2025, View Source [SID1234661270])

On December 8, 2025 Pan Cancer T B.V., a biotech company pioneering next-generation T cell therapies for solid tumours, reported a EUR 10 million financing to advance its lead program, PCT1:CO-STIM, into a first-in-human clinical trial for women with triple-negative breast cancer (TNBC).

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The financing includes EUR 5 million from existing investors Van Herk Ventures, Thuja Capital, Erasmus MC O&O Holdings, and InnovationQuarter, in addition to a EUR 5 million Innovation Credit loan from the Dutch Ministry of Economic Affairs. This funding will enable the company to treat TNBC patients at leading cancer centres in the Netherlands.

"Our mission is to empower a patient’s own immune cells to tackle hard-to-treat cancers like TNBC", said Rachel Abbott, Chief Executive Officer of Pan Cancer T. "This significant investment marks a pivotal moment as we transition from preclinical validation to treating patients with our first novel T-cell receptor (TCR) T cell therapy, PCT1:CO-STIM, following our planned regulatory filing with the EMA in 2026. We are deeply grateful to our investors and the Netherlands Enterprise Agency (RVO) for their confidence in our approach."

"Thuja Capital is dedicated to investing in the most innovative life sciences companies. Pan Cancer T’s TCR-T platform addresses hard-to-treat solid tumours, such as TNBC, that are the greatest challenge in oncology. Following our recent success in the cell and gene therapy field, with AstraZeneca’s acquisition of our portfolio company EsoBiotec, we are delighted to continue backing another pioneer in the C&GT space," said Michel Briejer, Managing Partner at Thuja Capital and member of Pan Cancer T’s Supervisory Board.

The upcoming trial will assess safety, tolerability, and preliminary efficacy of a therapeutic dose of PCT1:CO-STIM in TNBC patients. These patients have an urgent unmet medical need, with a 5-year survival rate following metastatic progression of approximately 12% and median overall survival of less than 6 months.

PCT1:CO-STIM is being developed as an autologous T cell therapy but also has the potential to be delivered in vivo at a later stage. It features a proprietary TCR highly specific for ROPN1, a novel tumour-restricted target expressed in over 90% of TNBC and melanoma cases. The therapy also incorporates a unique co-stimulatory technology designed to overcome immune resistance in solid tumours, aiming to deliver durable responses in patients with few treatment options.

(Press release, Pan Cancer T, DEC 8, 2025, https://pancancer-t.com/10-million-investment/ [SID1234661269])

On December 8, 2025 Orum Therapeutics ("Orum" or the "Company") (KRX: 475830), a public biotechnology company pioneering the field of degrader-antibody conjugates (DACs), reported the presentation of preclinical data for ORM-1153 at the 67th American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting, taking place December 6 to 9, 2025, in Orlando, Florida. ORM-1153 is a novel CD123-targeting DAC designed to deliver Orum’s proprietary GSPT1-degrading payload selectively into cancer cells to achieve targeted protein degradation and antitumor activity in acute myeloid leukemia (AML) and other CD123-positive hematological malignancies.

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"These data highlight ORM-1153 as a differentiated therapeutic candidate designed to address the need for more effective and better-tolerated treatments for acute myeloid leukemia," said Sung Joo (SJ) Lee, Ph.D., Founder and CEO of Orum Therapeutics. "AML remains one of the most challenging hematologic cancers to treat, with frequent relapse and limited options, particularly for patients with TP53-mutant disease. These data demonstrate the potential of ORM-1153 to achieve potent antitumor activity with a differentiated safety profile, addressing long-standing limitations of current AML therapies and further validating the versatility of our targeted protein degrader approach."

The preclinical data presented at ASH (Free ASH Whitepaper) show that ORM-1153 drives efficient, CD123-dependent internalization and degradation of GSPT1, resulting in strong and durable antitumor activity in AML models, including TP53-mutant disease. In comparative studies, ORM-1153 demonstrated approximately 1,000-fold higher potency than the unconjugated degrader payload and produced dose-dependent tumor regression in a disseminated AML xenograft model, with complete and durable responses at the highest dose level.

Importantly, ORM-1153 maintained a favorable tolerability profile and showed minimal effects on normal hematopoietic progenitors in colony-forming assays, suggesting potential for a differentiated therapeutic window compared with current standard-of-care. Together, these findings support ORM-1153 as a promising candidate for the treatment of AML and other CD123-positive hematologic malignancies.

About Orum’s TPD² Approach

Orum’s unique Dual-Precision Targeted Protein Degradation (TPD²) approach builds novel targeted protein degraders combined with the precise cell delivery mechanisms of antibodies to generate innovative, first-in-class, cell-selective TPDs for the treatment of cancer and other serious diseases. Orum has developed new targeted protein degrader payloads to specifically degrade an intracellular target protein within cancer cells via the E3 ubiquitin ligase pathway. Conjugated to antibodies, the payloads are designed to be delivered specifically to target cells and precisely degrade the intracellular target protein of interest.

(Press release, Orum Therapeutics, DEC 8, 2025, View Source [SID1234661268])

On December 8, 2025 Nurix Therapeutics, Inc. (Nasdaq: NRIX), a clinical-stage biopharmaceutical company focused on the discovery, development and commercialization of targeted protein degradation medicines in oncology and autoimmune disease, reported new clinical data from patients with relapsed or refractory Waldenström macroglobulinemia (WM) treated in the Phase 1 clinical trial of its Bruton’s tyrosine kinase (BTK) degrader bexobrutideg (NX-5948). These data will be presented by Scott Huntington M.D., MPH, Associate Professor of Internal Medicine (Hematology), Yale School of Medicine, and a clinical investigator on the trial, on December 8, 2025, at 6 p.m. ET at the 67th American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting and Exposition being held in Orlando, FL.

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"The data presented at ASH (Free ASH Whitepaper) in this older and heavily pre-treated WM population that includes patients with MYD88 and CXCR4 mutations continue to demonstrate encouraging activity of bexobrutideg with durable and deepening responses with longer time on treatment," said Paula G. O’Connor, M.D., chief medical officer of Nurix. "Bexobrutideg was well tolerated, consistent with the overall study population and previous disclosures."

"Collectively, these clinical data and recent data highlighting the unique properties of our potent and highly selective BTK degrader contribute to a growing body of evidence that support bexobrutideg’s potential to be the best-in-class and an important new therapeutic option for patients," said Arthur T. Sands, M.D., Ph.D., president and chief executive officer of Nurix. "We believe bexobrutideg is an innovative therapy with the potential to transform care in CLL, WM, and additional NHL indications, while supporting long-term value creation as its development expands into inflammatory and autoimmune settings."

The data presented at the 2025 ASH (Free ASH Whitepaper) Annual Meeting include patients with WM (n=31) treated with bexobrutideg at doses ranging from 200 mg to 600 mg once daily by oral administration from both the Phase 1a dose escalation and Phase 1b cohort expansions. Among the 31 WM patients, the median age was 71.0 years (range 49–88 years), and the median number of prior lines of therapy was 3 (range 1-7). All 31 patients previously had been treated with a BTK inhibitor (100%), 28 had received prior chemotherapy/chemo-immunotherapy (90.3%), four had received prior non-covalent BTK inhibitor (12.9%), and four patients had received prior treatment with a BCL2 inhibitor (12.9%). Twenty-four patients (77.4%) had mutations in MYD88, and six patients (19.4%) had mutations in CXCR4. Three patients (9.7%) had central nervous system (CNS) involvement at baseline.

Bexobrutideg was well tolerated in patients with WM, consistent with the overall study population and previous disclosures. Adverse events (AEs) were predominantly low grade with the most common being neutropenia (29.0%), petechiae (29.0%), diarrhea (25.8%), anemia (22.6%), purpura/contusion (22.6%), and thrombocytopenia (19.4%). There were no dose limiting toxicities observed and no grade 5 AEs. Two treatment emergent AEs led to drug discontinuation. No new onset atrial fibrillation was observed.​

As of the September 19, 2025 data cut, 28 patients were evaluable for response. Bexobrutideg demonstrated an objective response rate (ORR) of 75.0%, including very good partial responses (VGPR) in three patients (10.7%), partial responses (PR) in 14 patients (50.0%), and minor responses (MR) in four patients (14.3%). Six patients (21.4%) had a best response of stable disease (SD). In a subgroup analysis of patients with 2 or more disease assessments (n=23), ORR was 82.6% and disease control rate (DCR) was 100.0%.

Responses were observed in patients regardless of their baseline mutations in MYD88 and CXCR4. Out of three patients with CNS involvement (2 with systemic disease), two have responded and none progressed. Overall, responses were durable. With a median follow up of 8.1 months, median duration of response and median progression-free survival were not reached. As of the September 19, 2025 data cut, fourteen patients had continued on treatment for more than six months, and six patients had remained on treatment for more than one year.

Nurix Webcast Details
Date and time: Monday, December 8, 2025, 8:15 p.m. ET
Access Details: The live webcast and subsequent archived replay will be available in the Events section of the Investor page of the Nurix website at ir.nurixtx.com.

About Bexobrutideg (NX-5948)
Bexobrutideg is an investigational, orally bioavailable, brain penetrant, highly selective small molecule degrader of BTK currently being evaluated in the DAYBreak CLL-201 clinical trial (NCT07221500), a pivotal single-arm Phase 2 study of bexobrutideg in patients with relapsed or refractory chronic lymphocytic leukemia. Nurix also continues enrollment in the NX-5948-301 Phase 1a/1b clinical trial (NCT05131022) of bexobrutideg in patients with relapsed or refractory B cell malignancies.

(Press release, Nurix Therapeutics, DEC 8, 2025, View Source [SID1234661267])

On December 8, 2025 Moleculin Biotech, Inc., (Nasdaq: MBRX) ("Moleculin" or the "Company"), a late-stage pharmaceutical company with a broad portfolio of drug candidates targeting hard-to-treat cancers and viral infections, reported it has entered into a research and material transfer agreement with CIC biomaGUNE, a non-profit research organization created to promote scientific research and technological innovation at the highest levels in the Basque Country, Spain, for investigator-initiated preclinical research evaluating Annamycin for the treatment of glioblastoma multiforme (GBM), a form of brain cancer.

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Under the terms of the agreement Moleculin will supply Annamycin and Jesús Ruiz-Cabello, Principal Investigator at CIC biomaGUNE will conduct the planned preclinical research. The studies covered under this agreement will evaluate tumor progression following intra-arterial delivery of liposomal Annamycin (L-Annamycin) and Free-Annamycin as compared to Doxil and Free-doxorubicin in mouse models.

Walter Klemp, Chairman and CEO of Moleculin, commented, "We are excited to further expand our efforts to advance and develop Annamycin across a number of investigator-initiated studies. Annamycin has demonstrated clinical activity in acute myeloid leukemia and soft tissue sarcomas while also showing potential in preclinical models in pancreatic, GBM, and certain liver cancers amongst others."

Mr. Klemp continued, "GBM remains an area of profound unmet medical need, with current therapies offering only limited survival benefit and no meaningful long-term solutions. Collaborating with the premier research team at CIC biomaGUNE provides an important opportunity to explore Annamycin’s potential to overcome the challenges of drug delivery and resistance in central nervous system tumors. This work highlights the potential breadth of Annamycin and underscores our commitment to advancing innovative therapies for patients facing cancers with few or no effective options."

Glioblastoma is a common type of tumor originating in the brain. The average annual age-adjusted incidence rate of glioblastoma is 3.19 per 100,000 persons in the United States.1 Glioblastoma is the most aggressive malignant primary brain tumor with a median survival of only 15 months2. It is the most common malignant primary brain tumor making up 54% of all gliomas and 16% of all primary brain tumors.3 Despite advancements for other cancers, the survival rate for glioblastoma has not changed significantly in the last three decades.4

Annamycin, also known by its non-proprietary name of naxtarubicin, currently has Fast Track Status and Orphan Drug Designation from the FDA for the treatment of relapsed or refractory AML, in addition to Orphan Drug Designation for the treatment of STS lung metastases. Furthermore, Annamycin has Orphan Drug Designation for the treatment of relapsed or refractory AML from the EMA.

(Press release, Moleculin, DEC 8, 2025, View Source [SID1234661266])