On November 3, 2025 Syndax Pharmaceuticals (Nasdaq: SNDX), a commercial-stage biopharmaceutical company advancing innovative cancer therapies, reported that 23 abstracts, including six oral presentations, showcasing compelling Revuforj (revumenib) and Niktimvo (axatilimab-csfr) data were accepted for presentation at the 67th American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting being held in Orlando, Florida, December 6-9, 2025.

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"The breadth of the upcoming data presentations reflects the tremendous promise that Revuforj and Niktimvo hold across the treatment continuum for acute leukemia and chronic GVHD, respectively," said Nick Botwood, MBBS, Head of Research & Development and Chief Medical Officer at Syndax. "In particular, we are excited to present new frontline datasets showcasing the tolerability of Revuforj in combination with standard of care therapies along with high rates of complete remission and MRD negativity, as well as the first real-world evidence for a menin inhibitor, and a retrospective review of usage in the post-transplant setting. We also look forward to the presentation of new data that highlight the potential for Niktimvo to provide long-term benefits in chronic GVHD and the feasibility of combining with ruxolitinib in newly diagnosed chronic GVHD."

The Company will host an in-person investor event, along with a live webcast, at the ASH (Free ASH Whitepaper) Annual Meeting on Monday, December 8, 2025, at 7:00 a.m. ET to discuss key data presented at the meeting. The live webcast will be available on the Investor section of the Company’s website at www.syndax.com, where a replay of the event will also be available for a limited time.

Key abstracts accepted for presentation at ASH (Free ASH Whitepaper) 2025:

Revumenib:

An oral presentation will highlight results from a cohort of newly diagnosed patients in the Phase 2 SAVE trial of revumenib in combination with venetoclax and decitabine/cedazuridine in NPM1 mutated (NPM1m), KMT2A-rearranged (KMT2Ar), or NUP98-rearranged (NUP98r) acute myeloid leukemia (AML).
An oral presentation will report efficacy and safety by leukemia type (AML, ALL, or MPAL) in patients with R/R KMT2Ar acute leukemia in the Phase 2 portion of the pivotal AUGMENT-101 trial.
A poster presentation will highlight the first real-world experience with revumenib outside of a clinical trial setting, including in patients with KMT2Ar, NPM1m, or NUP98r acute leukemia.
Two poster presentations will report preliminary results from Phase 1 trials of revumenib in combination with intensive chemotherapy in newly diagnosed NPM1m, KMT2Ar, or NUP98r AML.
A poster presentation will highlight results from a retrospective review of pediatric patients with KMT2Ar, NUP98r, or NPM1m acute leukemia who received revumenib as a maintenance therapy following hematopoietic stem cell transplantation (HSCT).

Axatilimab:

An oral presentation will describe the safety and feasibility observed among patients with recurrent or refractory chronic graft-versus-host disease (GVHD) who transitioned from 0.3 mg/kg every 2 weeks dosing of axatilimab (FDA-approved dose) to 0.6 mg/kg every 4 weeks in the pivotal Phase 2 AGAVE-201 trial.
A poster presentation will highlight the long-term duration of therapy and safety of axatilimab among patients with recurrent or refractory chronic GVHD in the pivotal Phase 2 AGAVE-201 trial.
A poster presentation will report an interim safety analysis from a Phase 2 trial of axatilimab in combination with ruxolitinib in patients with newly diagnosed chronic GVHD.

The accepted abstracts listed below are now available online at the ASH (Free ASH Whitepaper) conference website. Copies of the oral and poster presentations will be made available in the ‘Publications & Meetings Presentations’ section of the Syndax website after the relevant embargoes lift.

Full list of abstracts accepted for presentation at ASH (Free ASH Whitepaper) 2025 (all times in ET):

Revumenib

Abstract Titles Presentation Details
Phase II study of the all-oral combination of revumenib (SNDX-5613) with decitabine/cedazuridine (ASTX727) and venetoclax (SAVE) in newly diagnosed AML Oral presentation
Abstract #: 47
Saturday, December 6
Session: 9:30-11:00 am
Revumenib for patients with relapsed or refractory (R/R) KMT2Ar acute leukemia: Outcomes by leukemia type in the Phase 2 AUGMENT-101 study Oral presentation
Abstract #: 1001
Monday, December 8
Session: 4:30-6:00 pm
Early real-world experience with revumenib outside of a clinical trial setting: A single center retrospective review of efficacy and tolerability Poster presentation
Abstract #: 3448
Sunday, December 7
Session: 6:00-8:00 pm
Phase 1 study of revumenib in combination with intensive chemotherapy (IC) in patients (pts) with newly diagnosed (ND) acute myeloid leukemia (AML) harboring genetic alterations in KMT2A, NPM1, or NUP98: SNDX-5613-0708 Poster presentation
Abstract #: 3425
Sunday, December 7
Session: 6:00-8:00 pm
Revumenib in combination with intensive induction and consolidation for newly diagnosed patients with NPM1-mutated or KMT2A-rearranged acute myeloid leukemia: Preliminary results from the Phase 1b ETCTN 10596 study Poster presentation
Abstract #: 5206
Monday, December 8
Session: 6:00-8:00 pm
Revumenib for patients with relapsed or refractory (R/R) nucleophosmin 1–mutated (NPM1m) acute myeloid leukemia (AML): Outcomes by prior treatment in the Phase 2 AUGMENT-101 study Poster presentation
Abstract #: 3418
Sunday, December 7
Session: 6:00-8:00 pm
Post-transplant maintenance with revumenib in children with HOX pathway-mutated AML Poster presentation
Abstract #: 3461
Sunday, December 7
Session: 6:00-8:00 pm
Trial in progress: A multicenter Phase I trial evaluating the safety and preliminary efficacy of revumenib as post-transplant maintenance after allogeneic hematopoietic cell transplant in patients with KMT2A-rearranged or NPM1-mutated acute leukemia Poster presentation
Abstract #: 5207
Monday, December 8
Session: 6:00-8:00 pm
Preliminary results of a Phase 1 study of the safety and tolerability of the combination of revumenib (REV) with gilteritinib (GILT) in relapsed/ refractory (R/R) acute myeloid leukemia (AML) Poster presentation
Abstract #: 3427
Sunday, December 7
Session: 6:00-8:00pm
Real-world treatment patterns and outcomes among patients with newly diagnosed NPM1-mutated acute myeloid leukemia in the United States Poster presentation
Abstract #: 3385
Sunday, December 7
Session: 6:00-8:00 pm
Menin inhibition as a new therapeutic option for the myeloproliferative neoplasms Oral presentation
Abstract #: 67
Saturday, December 6
Session: 9:30-11:00 am
Co-targeting menin and RAS in KMT2A-r/NPM1c AML with activated RTK//RAS/MAPK signaling Poster presentation
Abstract #: 5060
Monday, December 8
Session: 6:00-8:00 pm

Axatilimab

Abstract Titles Presentation Details
Safety and feasibility of 0.6 mg/kg every 4 weeks dosing of axatilimab in patients treated in the AGAVE-201 study Oral presentation
Abstract #: 272
Saturday, December 6
Session: 2:00-3:30 pm
Long-term treatment duration and safety of axatilimab among patients with chronic graft-versus-host disease in AGAVE-201 Poster presentation
Abstract #: 6010
Monday, December 8
Session: 6:00-8:00 pm
Axatilimab in combination with ruxolitinib in patients with newly diagnosed chronic graft-versus-host disease: Interim safety analysis of a randomized, Phase 2 study Poster presentation
Abstract #: 6012
Monday, December 8
Session: 6:00-8:00 pm
CSF-1R+ macrophages orchestrate human cutaneous chronic graft-versus-host disease Oral presentation
Abstract #: 588
Sunday, December 7
Session: 12:00-1:30 pm
Safety analysis of axatilimab in patients with chronic graft-versus-host disease in an expanded access program Poster presentation
Abstract #: 6008
Monday, December 8
Session: 6:00-8:00 pm
Trial in progress: A Phase 3, randomized, double-blind, placebo-controlled study of axatilimab and corticosteroids as initial treatment for moderate to severe chronic graft-versus-host disease Poster presentation
Abstract #: 4256
Sunday, December 7
Session: 6:00-8:00 pm
Pharmacodynamic analysis of AGAVE-201 indicates changes in CSF-1R-expressing cells and associated biomarkers potentially contributing to chronic graft-versus-host disease resolution Poster presentation
Abstract#: 2458
Saturday, December 6
Session: 5:30-7:30pm
Clinical and disease characteristics of initial participants at time of enrollment in THRIVE, a prospective, observational cohort study of patients at risk for chronic graft versus host disease Poster presentation
Abstract#: 2446
Saturday, December 6
Session: 5:30-7:30pm
CSF-1R inhibition and lenalidomide synergize to promote myeloma control after autologous stem cell transplantation Oral presentation
Abstract #: 689
Sunday, December 7
Session: 4:30-6:00 pm
CSF1R-CSF1 axis blockade with axatilimab effectively targets leukemia stem cells and monocytes in AML resistant to BH3 mimetics Poster presentation
Abstract #: 3276
Sunday, December 7
Session: 6:00-8:00 pm
Phase 1b/2 study of axatilimab in combination with azacitidine in advanced phase MPN, MDS/MPN overlap and high-risk CMML Poster presentation
Abstract #: 5607
Monday, December 8
Session: 6:00-8:00 pm

About Revuforj (revumenib)

Revuforj (revumenib) is an oral, first-in-class menin inhibitor that is FDA approved for the treatment of relapsed or refractory (R/R) acute leukemia with a lysine methyltransferase 2A gene (KMT2A) translocation as determined by an FDA-authorized test in adult and pediatric patients one year and older. Revuforj is also indicated for the treatment of R/R acute myeloid leukemia (AML) with a susceptible nucleophosmin 1 (NPM1) mutation in adult and pediatric patients one year and older who have no satisfactory alternative treatment options.

Multiple trials of revumenib are ongoing or planned across the treatment landscape, including in combination with standard of care therapies in newly diagnosed patients with NPM1m or KMT2Ar AML.

Revumenib was previously granted Orphan Drug Designation for the treatment of AML, ALL and acute leukemias of ambiguous lineage (ALAL) by the U.S. FDA and for the treatment of AML by the European Commission. The U.S. FDA also granted Fast Track designation to revumenib for the treatment of adult and pediatric patients with R/R acute leukemias harboring a KMT2A rearrangement or NPM1 mutation and Breakthrough Therapy Designation for the treatment of adult and pediatric patients with R/R acute leukemia harboring a KMT2A rearrangement.

About Niktimvo (axatilimab-csfr)

Niktimvo (axatilimab-csfr) is a first-in-class colony stimulating factor-1 receptor (CSF-1R)-blocking antibody approved for use in the U.S. for the treatment of chronic graft-versus-host disease (GVHD) after failure of at least two prior lines of systemic therapy in adult and pediatric patients weighing at least 40 kg (88.2 lbs).

In 2016, Syndax licensed exclusive worldwide rights to develop and commercialize axatilimab from UCB. In September 2021, Syndax and Incyte entered into an exclusive worldwide co-development and co-commercialization license agreement for axatilimab in chronic GVHD and any future indications.

Axatilimab is being studied in frontline combination trials in chronic GVHD – a Phase 2 combination trial with ruxolitinib (NCT06388564) and a Phase 3 combination trial with steroids (NCT06585774) are underway. Axatilimab is also being studied in an ongoing Phase 2 trial in patients with idiopathic pulmonary fibrosis (NCT06132256).

Niktimvo is a trademark of Incyte.
All other trademarks are the property of their respective owners.

Revuforj (revumenib)

IMPORTANT SAFETY INFORMATION

WARNING: DIFFERENTIATION SYNDROME, QTc PROLONGATION, and TORSADES DE POINTES

Differentiation syndrome, which can be fatal, has occurred with Revuforj. Signs and symptoms may include fever, dyspnea, hypoxia, pulmonary infiltrates, pleural or pericardial effusions, rapid weight gain or peripheral edema, hypotension, and renal dysfunction. If differentiation syndrome is suspected, immediately initiate corticosteroid therapy and hemodynamic monitoring until symptom resolution.

QTc prolongation and Torsades de Pointes have occurred in patients receiving Revuforj. Correct hypokalemia and hypomagnesemia prior to and during treatment. Do not initiate Revuforj in patients with QTcF > 450 msec. If QTc interval prolongation occurs, interrupt, reduce, or permanently discontinue Revuforj.

WARNINGS AND PRECAUTIONS

Differentiation Syndrome: Revuforj can cause fatal or life-threatening differentiation syndrome (DS). Symptoms of DS, including those seen in patients treated with Revuforj, include fever, dyspnea, hypoxia, peripheral edema, pleuropericardial effusion, acute renal failure, rash, and/or hypotension.

In clinical trials, DS occurred in 60 (25%) of 241 patients treated with Revuforj at the recommended dosage for relapsed or refractory acute leukemia. Among those with a KMT2A translocation, DS occurred in 33% of patients with acute myeloid leukemia (AML), 33% of patients with mixed-phenotype acute leukemia (MPAL), and 9% of patients with acute lymphoblastic leukemia (ALL); DS occurred in 18% of patients with NPM1m AML. DS was Grade 3 or 4 in 12% of patients and fatal in 2 patients. The median time to initial onset was 9 days (range 3-41 days). Some patients experienced more than 1 DS event. Treatment interruption was required for 7% of patients, and treatment was withdrawn for 1%.

Reduce the white blood cell count to less than 25 Gi/L prior to starting Revuforj. If DS is suspected, immediately initiate treatment with systemic corticosteroids (e.g., dexamethasone 10 mg IV every 12 hours in adults or dexamethasone 0.25 mg/kg/dose IV every 12 hours in pediatric patients weighing less than 40 kg) for a minimum of 3 days and until resolution of signs and symptoms. Institute supportive measures and hemodynamic monitoring until improvement. Interrupt Revuforj if severe signs and/or symptoms persist for more than 48 hours after initiation of systemic corticosteroids, or earlier if life-threatening symptoms occur such as pulmonary symptoms requiring ventilator support. Restart steroids promptly if DS recurs after tapering corticosteroids.

QTc Interval Prolongation and Torsades de Pointes: Revuforj can cause QT (QTc) interval prolongation and Torsades de Pointes.

Of the 241 patients treated with Revuforj at the recommended dosage for relapsed or refractory acute leukemia in clinical trials, QTc interval prolongation was reported as an adverse reaction in 86 (36%) patients. QTc interval prolongation was Grade 3 in 15% and Grade 4 in 2%. The heart-rate corrected QT interval (using Fridericia’s method) (QTcF) was greater than 500 msec in 10%, and the increase from baseline QTcF was greater than 60 msec in 24%. Revuforj dose reduction was required for 7% due to QTc interval prolongation. QTc prolongation occurred in 21% of the 34 patients less than 17 years old, 35% of the 146 patients 17 years to less than 65 years old, and 46% of the 61 patients 65 years or older. One patient had a fatal outcome of cardiac arrest, and one patient had non-sustained Torsades de Pointes.

Correct electrolyte abnormalities, including hypokalemia and hypomagnesemia, prior to and throughout treatment with Revuforj. Perform an electrocardiogram (ECG) prior to initiation of Revuforj, and do not initiate Revuforj in patients with QTcF >450 msec. Perform an ECG at least once weekly for the first 4 weeks and at least monthly thereafter. In patients with congenital long QTc syndrome, congestive heart failure, electrolyte abnormalities, or those who are taking medications known to prolong the QTc interval, more frequent ECG monitoring may be necessary. Concomitant use with drugs known to prolong the QTc interval may increase the risk of QTc interval prolongation.

Interrupt Revuforj if QTcF increases >480 msec and <500 msec, and restart Revuforj at the same dose twice daily after the QTcF interval returns to ≤480 msec
Interrupt Revuforj if QTcF increases >500 msec or by >60 msec from baseline, and restart Revuforj twice daily at the lower-dose level after the QTcF interval returns to ≤480 msec
Permanently discontinue Revuforj in patients with ventricular arrhythmias and in those who develop QTc interval prolongation with signs or symptoms of life-threatening arrhythmia

Embryo-Fetal Toxicity: Revuforj can cause fetal harm when administered to a pregnant woman. Advise pregnant women of the potential risk to a fetus. Advise females of reproductive potential and males with female partners of reproductive potential to use effective contraception during treatment with Revuforj and for 4 months after the last dose of Revuforj.

ADVERSE REACTIONS

Fatal adverse reactions occurred in 9 (4%) patients who received Revuforj, including 4 with sudden death, 2 with differentiation syndrome, 2 with hemorrhage, and 1 with cardiac arrest.

Serious adverse reactions were reported in 184 (76%) patients. The most frequent serious adverse reactions (≥10%) were infection (29%), febrile neutropenia (20%), bacterial infection (15%), differentiation syndrome (13%), and hemorrhage (11%).

The most common adverse reactions (≥20%) including laboratory abnormalities, were phosphate increased (51%), hemorrhage (48%), nausea (48%), infection without identified pathogen (46%), aspartate aminotransferase increased (44%), alanine aminotransferase increased (40%), creatinine increased (38%), musculoskeletal pain (37%), febrile neutropenia (37%), electrocardiogram QT prolonged (36%), potassium decreased (34%), parathyroid hormone intact increased (34%), alkaline phosphatase increased (33%), diarrhea (29%), bacterial infection (27%), triglycerides increased (27%), phosphate decreased (25%), differentiation syndrome (25%), fatigue (24%), edema (24%), viral infection (23%), decreased appetite (20%), and constipation (20%).

DRUG INTERACTIONS

Drug interactions can occur when Revuforj is concomitantly used with:

Strong CYP3A4 inhibitors: reduce Revuforj dose
Strong or moderate CYP3A4 inducers: avoid concomitant use with Revuforj
QTc-prolonging drugs: avoid concomitant use with Revuforj. If concomitant use is unavoidable, obtain ECGs when initiating, during concomitant use, and as clinically indicated. Withhold Revuforj if the QTc interval is >480 msec. Restart Revuforj after the QTc interval returns to ≤480 msec

SPECIFIC POPULATIONS

Lactation: advise lactating women not to breastfeed during treatment with Revuforj and for 1 week after the last dose.

Pregnancy and testing: Revuforj can cause fetal harm when administered to a pregnant woman. Verify pregnancy status in females of reproductive potential within 7 days prior to initiating Revuforj.

Infertility: based on findings in animals, Revuforj may impair fertility. The effects on fertility were reversible.

Pediatric: monitor bone growth and development in pediatric patients.

Geriatric: no overall differences were observed in the effectiveness of Revuforj between patients who were 65 years and older, and younger patients. Compared to younger patients, the incidences of QTc prolongation and edema were higher in patients 65 years and older.

To report SUSPECTED ADVERSE REACTIONS, contact Syndax Pharmaceuticals at 1-888-539-3REV or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.

Please see Full Prescribing Information, including BOXED WARNINGS.

Niktimvo (axatilimab-csfr)

IMPORTANT SAFETY INFORMATION

WARNINGS AND PRECAUTIONS
Infusion-Related Reactions
Niktimvo (axatilimab-csfr) can cause infusion-related reactions. Infusion-related reactions, including hypersensitivity reactions, occurred in 18% of patients who received Niktimvo in the clinical trial (AGAVE-201), with Grade 3 or 4 reactions in 1.3%.

Premedicate with an antihistamine and an antipyretic for patients who have previously experienced an infusion-related reaction to Niktimvo. Monitor patients for signs and symptoms of infusion-related reactions, including fever, chills, rash, flushing, dyspnea, and hypertension. Interrupt or slow the rate of infusion or permanently discontinue Niktimvo based on severity of the reaction.

Embryo-Fetal Toxicity
Based on its mechanism of action, Niktimvo may cause fetal harm when administered to a pregnant woman. Advise pregnant women of the potential risk to the fetus. Advise females of reproductive potential to use effective contraception during treatment with Niktimvo and for 30 days after the last dose.

ADVERSE REACTIONS
Serious adverse reactions occurred in 44% of patients who received Niktimvo (N=79). Serious adverse reactions in >2 patients included infection (pathogen unspecified) (14%), viral infection (14%) and respiratory failure (5.1%). Permanent discontinuation of Niktimvo due to an adverse reaction occurred in 10% of patients and dose reduction due to adverse reaction occurred in 8% of patients. Dose interruptions due to an adverse reaction occurred in 44% of patients. The adverse reactions leading to dose interruption in >2 patients were viral infection, infection (pathogen unspecified), bacterial infection, musculoskeletal pain, and pyrexia.

The most common (≥15%) adverse reactions, including laboratory abnormalities, were increased aspartate aminotransferase (AST), infection (pathogen unspecified), increased alanine aminotransferase (ALT), decreased phosphate, decreased hemoglobin, viral infection, increased gamma glutamyl transferase (GGT), musculoskeletal pain, increased lipase, fatigue, increased amylase, increased calcium, increased creatine phosphokinase (CPK), increased alkaline phosphatase (ALP), nausea, headache, diarrhea, cough, bacterial infection, pyrexia, and dyspnea.

Clinically relevant adverse reactions in <10% of patients who received Niktimvo included:

Eye disorders: periorbital edema
Skin and subcutaneous skin disorders: pruritus
Vascular disorders: hypertension

Immunogenicity: Anti-Drug Antibody–Associated Adverse Reactions
Across treatment arms in patients with cGVHD who received Niktimvo in clinical trials, among the patients who developed anti-drug antibodies (ADAs), hypersensitivity reactions occurred in 26% (13/50) of patients with neutralizing antibodies (NAb) and in 4% (2/45) of those without NAb.

USE IN SPECIFIC POPULATIONS
Lactation
Because of the potential for serious adverse reactions in a breastfed child, advise women not to breastfeed during treatment and for 30 days after the last dose of Niktimvo.

Females and Males of Reproductive Potential
Pregnancy Testing
Verify pregnancy status in females of reproductive potential prior to initiating Niktimvo.

Contraception
Females
Advise females of reproductive potential to use effective contraception during treatment with Niktimvo and for 30 days after the last dose of Niktimvo.

DOSAGE AND ADMINISTRATION
Dosage Modifications for Adverse Reactions
Monitor aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), creatine phosphokinase (CPK), amylase, and lipase prior to the start of Niktimvo therapy, every 2 weeks for the first month, and every 1 to 2 months thereafter until abnormalities are resolved. See Table 1 in the Prescribing Information for more recommendations.

(Press release, Syndax, NOV 3, 2025, View Source [SID1234659281])

On November 3, 2025 Star Therapeutics, a clinical stage biotechnology company discovering and developing best-in-class antibodies for bleeding disorders and other diseases, reported that the company will present an oral presentation on interim data from its Phase 1/2 multidose study of VGA039 for von Willebrand disease (VWD), along with additional posters on the program, at the 67th American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting and Exposition, being held December 6-9, 2025, in Orlando, Fla. VGA039 is a first-in-class monoclonal antibody therapy with a novel mechanism of action that targets Protein S, thereby restoring balance to the blood clotting process.

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Presentation details include:

Oral Presentation

Title: Subcutaneous, Every-Four-Week Maintenance Dosing of a Novel Protein S Antibody is Well-Tolerated and Substantially Reduces Bleeding Rates: Results from a Phase 1/2 Multidose Study of VGA039 in Patients with Von Willebrand Disease
Publication Number: 308
Oral Session: 323. Disorders of Coagulation, Bleeding, or Fibrinolysis, Excluding Congenital Hemophilias: Clinical and Epidemiological: Novel Insights into Diagnostics and Therapeutics of Bleeding in Inherited, Acquired Coagulopathies and BDUC
Presentation Date and Time: Saturday, December 6, 2025, 4:15 – 4:30 p.m. ET
Presenter: Allison Wheeler, M.D., MSCI
Poster Presentations

Title: The First Characterization of Disease Burden and Healthcare Resource Utilization for the Recent Definition of Severe Von Willebrand Disease Using a Large United States Real-World Dataset
Publication Number: 2611
Poster Session: 901. Health Services and Quality Improvement: Non-Malignant Conditions Excluding Hemoglobinopathies: Poster I
Session Date and Time: Saturday, December 6, 2025, 5:30 – 7:30 p.m. ET
Presenter: Angela Weyand, M.D.
Title: VGA039 as a Protein S-Targeted Hemostatic Promoting Monoclonal Antibody, Promotes in-vitro Thrombin Generation in Plasma Samples from Subjects Across a Broad Range of Bleeding Disorders, Including Von Willebrand Disease, Hemophilia A, Hemophilia B and Hemophilia C
Publication Number: 1277
Poster Session: 321. Coagulation and Fibrinolysis: Basic and Translational: Poster I
Session Date and Time: Saturday, December 6, 2025, 5:30 – 7:30 p.m. ET
Presenter: Alina He, B.S.
Title: A Protein S-Targeting Monoclonal Antibody, VGA039, Improves Both Primary and Secondary Hemostatic Activity of Von Willebrand Disease Patient Blood in an ex vivo Vascularized Hemostasis-on-a-Chip
Publication Number: 3051
Poster Session: 321. Coagulation and Fibrinolysis: Basic and Translational: Poster II
Session Date and Time: Sunday, December 7, 2025, 6:00 – 8:00 p.m. ET
Presenter: Yumiko Sakurai, M.S.
About VGA039
VGA039 is a monoclonal antibody therapy with a novel mechanism of action that targets Protein S, thereby restoring balance to the blood clotting process. VGA039 has potential to be a universal hemostatic therapy that can treat numerous bleeding disorders, starting with VWD. As a subcutaneously self-administered antibody therapy with a convenient once monthly dosing regimen, VGA039 has the potential to dramatically reduce treatment burden for patients. VGA039 has received Fast Track and orphan drug designations from the United States Food and Drug Administration (FDA).

Interim positive data from a Phase 1 single ascending dose study of VGA039 in patients with VWD were previously reported at the Annual Meeting of the American Society of Hematology (ASH) (Free ASH Whitepaper) in December 2024. A Phase 1/2 multidose study is ongoing (NCT05776069), with an interim readout planned for presentation at the 2025 ASH (Free ASH Whitepaper) Annual Meeting. VGA039 has advanced into a Phase 3 study (NCT07115004), a global single arm cross-over study designed to investigate the safety and efficacy of subcutaneous administration of VGA039 as prophylaxis for bleeding in patients with every type of VWD. For additional information on our VIVID trials of VGA039, including how to enroll, please visit the website here.

About von Willebrand disease
Von Willebrand disease (VWD) is the most common inherited bleeding disorder in which the blood does not clot properly, caused by absent or defective von Willebrand factor (VWF). VWD patients may experience excessive bleeding with variability in severity and frequency, negatively impacting their daily lives. Current therapies for VWD prophylaxis include factor replacement therapies requiring multiple intravenous (IV) infusions every week. More than 130,000 people in the U.S. are diagnosed with VWD.

(Press release, Star Therapeutics, NOV 3, 2025, View Source [SID1234659280])

On November 3, 2025 Rigel Pharmaceuticals, Inc. (Nasdaq: RIGL), a commercial stage biotechnology company focused on hematologic disorders and cancer, reported that data from the ongoing Phase 1b study of R2891, a potent and selective inhibitor of dual interleukin receptor-associated kinases 1 and 4 (IRAK1/4), in patients with lower-risk myelodysplastic syndrome (MDS) who are relapsed or refractory (R/R) to prior therapies will be presented in an oral session at the 67th American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting and Exposition on Sunday, December 7, 2025. In addition, the ASH (Free ASH Whitepaper) Annual Meeting will feature four poster presentations with data for REZLIDHIA (olutasidenib) for the treatment of R/R mutated isocitrate dehydrogenase-1 (mIDH1) acute myeloid leukemia (AML). The ASH (Free ASH Whitepaper) Annual Meeting is being held December 6-9, 2025, in Orlando, Florida and virtually.

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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

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"We are very pleased to have the opportunity to highlight our hematology and oncology portfolio at ASH (Free ASH Whitepaper) this year," said Lisa Rojkjaer, M.D, Rigel’s chief medical officer. "In particular, we are delighted that updated results from our Phase 1b study in patients with relapsed or refractory lower-risk MDS have been accepted for oral presentation. Despite the availability of approved agents, there remains an unmet need for additional therapies to treat patients with transfusion dependent lower-risk MDS, and we look forward to advancing the dose expansion phase of the study to completion."

ASH Annual Meeting abstracts may be accessed online at www.hematology.org. Details of the oral and poster presentations, which will be available in the poster hall and via the virtual event platform, are as follows:

Oral Presentation

Sunday, December 7, 2025, 9:45am to 10:00am ET
Publication #: 489
Session Name: 637. Myelodysplastic Syndromes: Clinical and Epidemiological: Moving the Needle Through Novel Approaches in MDS and CMML
Presentation Title: An Update of Safety and Efficacy Results from a Phase 1b Study of R289, a Dual IRAK 1/4 Inhibitor, in Patients with Relapsed/Refractory (R/R) Lower Risk Myelodysplastic Syndrome (LR-MDS)
Presenter: Guillermo Garcia-Manero, M.D.

As of the data cutoff date (July 15, 2025), 33 patients were enrolled in the dose escalation part of the study. Patients had a median age of 75 with a median of 3 prior therapies and 61% were high transfusion burden at baseline.
Patients received R289 at doses ranging from 250 mg QD (once daily) to 500 mg BID (twice daily). For the 500 mg BID dose group, five patients were not yet evaluable (<16 weeks follow up) for determination of hematologic responses and one patient withdrew consent.
R289 was generally well tolerated across all dose groups, with the most frequent treatment emergent adverse events (≥20%) being diarrhea (28.1%), constipation/fatigue (25% each), and creatinine/alanine aminotransferase (ALT) increased (21.9% each), the majority being Grade 1/2. One (1) dose limiting toxicity (DLT) (Grade 4 aspartate aminotransferase (AST) increase/Grade 3 ALT increase) was reported in the 750 mg dose group.
For evaluable transfusion dependent patients (≥16 weeks follow up) at dose levels of at least 500 mg QD and higher, 4/13 patients (31%) achieved durable red blood cell transfusion independence (RBC-TI) for >8 weeks (500 mg QD [1/3], 750 mg QD [2/5], 500/250 mg QD [1/5]). Duration of RBC-TI was >16 weeks in 3 patients, >24 weeks in 2 patients, and >12 months in 1 patient. The median time to onset of RBC-TI was 2.2 months and the median duration of RBC-TI was 24.3 weeks.
All responding patients had R835 plasma concentrations similar to those at which ≥50% LPS-induced inhibition of cytokine release was observed in healthy volunteers, indicating a potential threshold for dose response (≥500 mg QD).
Updated data as of an October 28, 2025, data cutoff will be presented during the oral presentation.
Poster Presentations

Saturday, December 6, 2025, 5:30pm to 7:30pm ET
Publication #: 1659
Title: Clinical Characteristics and Response in Olutasidenib-Treated Relapsed/Refractory mIDH1 Acute Myeloid Leukemia (AML) Patients With Stable Disease Following Two Treatment Cycles
Presenter: Justin M. Watts, M.D.

In the pivotal cohort of the Phase 2 registrational study, of 147 patients with R/R mIDH1 AML who received olutasidenib, 36 (24%) patients maintained stable disease (SD) after 2 cycles of treatment. Treatment duration ranged from 2.6 to 51.1 months. In these 36 patients, the subsequent response rate was 33% (n=12), including 6 (17%) complete remission (CR), 2 (6%) CR with partial hematologic recovery (CRh), 1 (3%) CR with incomplete recovery, 1 (3%) morphologic leukemia-free state, and 2 (6%) partial remission.
Median time to best response from the start of treatment was 3.7 months (range: 2.8-5.7). 8 patients (22%) remained in SD and 16 (44%) had subsequent disease progression on study.
In the 12 late responders, median duration of response (DOR), duration of CR/CRh, and duration of CR were 9.9 months, 17.3 months, and not reached, respectively. Additionally, of the late responders who were transfusion dependent for platelets (n=6) or red blood cells (n=9) at baseline, 5 (83%) and 8 (89%), respectively, became transfusion independent.
Patients who achieved any late response had a longer median treatment duration (10.1 months) than non-responders. Median overall survival (OS) for late responders was 23.9 months and 32.7 months for those with CR/CRh.
Patients with SD after 2 cycles of olutasidenib may experience meaningful clinical benefit with continued treatment, as one-third of these patients subsequently achieved a late response, resulting in a lower risk of death compared to patients with no later response. These findings suggest that early SD may not predict treatment failure and support continuing olutasidenib for at least 6 cycles or until disease progression.
Sunday, December 7, 2025, 6:00pm to 8:00pm ET
Publication #: 4616
Title: Assessment of Real-World Treatment Patterns and Outcomes of Olutasidenib in Patients with Mutated Isocitrate Dehydrogenase 1 Acute Myeloid Leukemia Previously Treated with Venetoclax Using Electronic Health Record Data
Presenter: Catherine Lai, M.D., MPH

This retrospective cohort study analyzed data from Loopback Analytics’ electronic health records data in the U.S. until September 2024, incorporating structured clinical data and abstracted data from physician notes. Fourteen olutasidenib-treated patients in the Loopback database met inclusion criteria for the study.
The overall response rate (ORR) was 50% (7/14) and the composite complete remission (CRc) rate was 36% (5/14). Among patients who achieved any response, 86% (6/7) received venetoclax immediately prior to olutasidenib.
Median OS from olutasidenib initiation in the full cohort was 12.2 months, with the proportion of patients surviving 6, 9, and 12 months estimated to be 88%, 70%, and 53%, respectively.
In this real-world cohort, despite the small sample size, 50% of patients responded to post-venetoclax olutasidenib, consistent with the clinical efficacy observed in the pivotal Phase 2 trial. These findings support the use of olutasidenib as a viable therapeutic option in post-venetoclax treatment settings.
Publication #: 3439
Title: Analysis of Hematologic Improvement (HI) by Time to Response in Relapsed/Refractory Acute Myeloid Leukemia (AML) Patients Treated with Olutasidenib
Presenter: Shira N. Dinner, M.D

In the pivotal cohort of the Phase 2 registrational study (n=147), increases in hemoglobin were seen early in the course of treatment and levels continued to increase over 12 cycles. Similarly, platelet counts increased and blast percentages decreased over the course of treatment.
A total of 71 patients (48%) achieved an overall response; 47 patients (32%) achieved CR and 51 (35%) achieved CR/CRh. Among CR/CRh responders, 28 (55%) achieved a response in <2 months, 17 (33%) from 2 to 4 months, and 6 (12%) at >4 months.
Patients with a longer time to response tended to have lower baseline platelet counts and higher bone marrow blast percentages compared with earlier responders, suggesting lower hematopoietic reserve and greater disease burden.
In 37 patients (25%) who had a best response of SD, several showed improvement in platelets and hemoglobin levels by end of treatment. 7 of 21 (33%) patients with prior platelet transfusion dependence became independent and 7 of 23 (30%) with prior red blood cell transfusion dependence became independent.
This report highlights the hematological responses to olutasidenib in these patients with R/R mIDH1 AML and suggests that continuing olutasidenib treatment beyond 2 cycles may offer hematologic benefits, even in the absence of an early clinical response.
Monday, December 8, 2025, 6:00pm ET to 8:00pm ET
Publication #: 5213
Title: Olutasidenib Monotherapy in Patients With mIDH1 Acute Myeloid Leukemia Who Received Prior Intensive Chemotherapy
Presenter: Jay Yang, M.D.

In the pivotal cohort of the Phase 2 registrational study (n=147), in patients with prior intensive chemotherapy (IC), the ORR was 50% with 35/105 (33%) achieving CR and 38/105 (36%) achieving CR/CRh. Median DOR was 15.5 months, with median duration of CR not reached and CR/CRh of 17.6 months.
After a median follow up of 37.3 months, the median OS was 12.5 months. In comparison, in the 38 patients who received prior non-intensive therapy the ORR was 42%; 9/38 achieved CR and 10/38 achieved CR/CRh. The median DOR in this group was 16.2 months, with a median duration of CR and CR/CRh of 28.1 months and 29.0 months, respectively.
Among this cohort of patients with R/R mIDH1 AML who had received prior IC, treatment with olutasidenib monotherapy produced clinically meaningful response rates that closely align with those observed in the overall population, with durable responses and acceptable tolerability.
About R289
R289 is a prodrug of R835, an IRAK1/4 dual inhibitor, which has been shown in preclinical studies to block inflammatory cytokine production in response to toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) family signaling. TLRs and IL-1Rs play a critical role in the innate immune response and dysregulation of these pathways can lead to various inflammatory conditions. Chronic stimulation of both these receptor systems is thought to cause the pro-inflammatory environment in the bone marrow responsible for persistent cytopenias in lower-risk MDS patients.2

About AML
Acute myeloid leukemia (AML) is a rapidly progressing cancer of the blood and bone marrow that affects myeloid cells, which normally develop into various types of mature blood cells. AML occurs primarily in adults and accounts for about 1 percent of all adult cancers. The American Cancer Society estimates that there will be about 22,010 new cases in the United States, most in adults, in 2025.3

Relapsed AML affects about half of all patients who, following treatment and remission, experience a return of leukemia cells in the bone marrow.4,5 Refractory AML, which affects between 10 and 40 percent of newly diagnosed patients, occurs when a patient fails to achieve remission even after intensive treatment.6 Quality of life declines for patients with each successive line of treatment for AML, and well-tolerated treatments in relapsed or refractory disease remain an unmet need.

About REZLIDHIA

INDICATION
REZLIDHIA is indicated for the treatment of adult patients with relapsed or refractory acute myeloid leukemia (AML) with a susceptible isocitrate dehydrogenase-1 (IDH1) mutation as detected by an FDA-approved test.

IMPORTANT SAFETY INFORMATION

WARNING: DIFFERENTIATION SYNDROME

Differentiation syndrome, which can be fatal, can occur with REZLIDHIA treatment. Symptoms may include dyspnea, pulmonary infiltrates/pleuropericardial effusion, kidney injury, hypotension, fever, and weight gain. If differentiation syndrome is suspected, withhold REZLIDHIA and initiate treatment with corticosteroids and hemodynamic monitoring until symptom resolution.

WARNINGS AND PRECAUTIONS

Differentiation Syndrome
REZLIDHIA can cause differentiation syndrome. In the clinical trial of REZLIDHIA in patients with relapsed or refractory AML, differentiation syndrome occurred in 16% of patients, with grade 3 or 4 differentiation syndrome occurring in 8% of patients treated, and fatalities in 1% of patients. Differentiation syndrome is associated with rapid proliferation and differentiation of myeloid cells and may be life-threatening or fatal. Symptoms of differentiation syndrome in patients treated with REZLIDHIA included leukocytosis, dyspnea, pulmonary infiltrates/pleuropericardial effusion, kidney injury, fever, edema, pyrexia, and weight gain. Of the 25 patients who experienced differentiation syndrome, 19 (76%) recovered after treatment or after dose interruption of REZLIDHIA. Differentiation syndrome occurred as early as 1 day and up to 18 months after REZLIDHIA initiation and has been observed with or without concomitant leukocytosis.

If differentiation syndrome is suspected, temporarily withhold REZLIDHIA and initiate systemic corticosteroids (e.g., dexamethasone 10 mg IV every 12 hours) for a minimum of 3 days and until resolution of signs and symptoms. If concomitant leukocytosis is observed, initiate treatment with hydroxyurea, as clinically indicated. Taper corticosteroids and hydroxyurea after resolution of symptoms. Differentiation syndrome may recur with premature discontinuation of corticosteroids and/or hydroxyurea treatment. Institute supportive measures and hemodynamic monitoring until improvement; withhold dose of REZLIDHIA and consider dose reduction based on recurrence.

Hepatotoxicity
REZLIDHIA can cause hepatotoxicity, presenting as increased alanine aminotransferase (ALT), increased aspartate aminotransferase (AST), increased blood alkaline phosphatase, and/or elevated bilirubin. Of 153 patients with relapsed or refractory AML who received REZLIDHIA, hepatotoxicity occurred in 23% of patients; 13% experienced grade 3 or 4 hepatotoxicity. One patient treated with REZLIDHIA in combination with azacitidine in the clinical trial, a combination for which REZLIDHIA is not indicated, died from complications of drug-induced liver injury. The median time to onset of hepatotoxicity in patients with relapsed or refractory AML treated with REZLIDHIA was 1.2 months (range: 1 day to 17.5 months) after REZLIDHIA initiation, and the median time to resolution was 12 days (range: 1 day to 17 months). The most common hepatotoxicities were elevations of ALT, AST, blood alkaline phosphatase, and blood bilirubin.

Monitor patients frequently for clinical symptoms of hepatic dysfunction such as fatigue, anorexia, right upper abdominal discomfort, dark urine, or jaundice. Obtain baseline liver function tests prior to initiation of REZLIDHIA, at least once weekly for the first two months, once every other week for the third month, once in the fourth month, and once every other month for the duration of therapy. If hepatic dysfunction occurs, withhold, reduce, or permanently discontinue REZLIDHIA based on recurrence/severity.

ADVERSE REACTIONS
The most common (≥20%) adverse reactions, including laboratory abnormalities, were aspartate aminotransferase increased, alanine aminotransferase increased, potassium decreased, sodium decreased, alkaline phosphatase increased, nausea, creatinine increased, fatigue/malaise, arthralgia, constipation, lymphocytes increased, bilirubin increased, leukocytosis, uric acid increased, dyspnea, pyrexia, rash, lipase increased, mucositis, diarrhea and transaminitis.

DRUG INTERACTIONS

Avoid concomitant use of REZLIDHIA with strong or moderate CYP3A inducers.
Avoid concomitant use of REZLIDHIA with sensitive CYP3A substrates unless otherwise instructed in the substrates prescribing information. If concomitant use is unavoidable, monitor patients for loss of therapeutic effect of these drugs.
LACTATION
Advise women not to breastfeed during treatment with REZLIDHIA and for 2 weeks after the last dose.

GERIATRIC USE
No overall differences in effectiveness were observed between patients 65 years and older and younger patients. Compared to patients younger than 65 years of age, an increase in incidence of hepatotoxicity and hypertension was observed in patients ≥65 years of age.

HEPATIC IMPAIRMENT
In patients with mild or moderate hepatic impairment, closely monitor for increased probability of differentiation syndrome.

Click here for Important Safety Information and Full Prescribing Information, including Boxed WARNING.

To report side effects of prescription drugs to the FDA, visit www.fda.gov/medwatch or call 1-800-FDA-1088 (800-332-1088).

REZLIDHIA is a registered trademark of Rigel Pharmaceuticals, Inc.

(Press release, Rigel, NOV 3, 2025, View Source [SID1234659279])

On November 3, 2025 Regeneron Pharmaceuticals, Inc. (NASDAQ: REGN) reported it will webcast management participation as follows:

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!

Jefferies London Healthcare Conference at 3:30 p.m. GMT (10:30 a.m. ET) on Monday, November 17, 2025
7th Annual Wolfe Research Healthcare Conference at 9:20 a.m. ET on Monday, November 17, 2025
8th Annual Evercore Healthcare Conference at 1:20 p.m. ET on Tuesday, December 2, 2025
Citi 2025 Global Healthcare Conference at 10:30 a.m. ET on Wednesday, December 3, 2025

The sessions may be accessed from the "Investors & Media" page of Regeneron’s website at View Source Replays and transcripts of the webcasts will be archived on the Company’s website for at least 30 days.

(Press release, Regeneron, NOV 3, 2025, View Source [SID1234659278])

On November 3, 2025 Pyxis Oncology, Inc. (Nasdaq: PYXS), a clinical-stage company developing next-generation therapeutics for difficult-to-treat cancers, reported a business update, and announced financial results for the quarter ended September 30, 2025.

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

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"In the dynamic landscape of emerging clinical-stage therapies for patients with recurrent and metastatic head and neck squamous cell carcinoma, a significant unmet medical need remains despite the potential improvements in treatment options," said Lara S. Sullivan, M.D., President, Chief Executive Officer and Chief Medical Officer of Pyxis Oncology. "We look forward to presenting our preliminary data from the ongoing clinical studies evaluating MICVO as a novel potential treatment option for recurrent and metastatic head and neck squamous cell carcinoma. We believe that the breadth of the MICVO clinical program, encompassing monotherapy and combination approaches, holds significant promise and this inflection point will further underscore our first-in-concept ADC’s potential to improve outcomes across multiple lines of therapy."

Pipeline & Corporate Updates
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Pyxis Oncology expects to report preliminary data from the ongoing Phase 1 clinical studies of micvotabart pelidotin (MICVO) in patients with recurrent and metastatic head and neck squamous cell carcinoma (R/M HNSCC) in 4Q25.

o
Clinical update to focus on preliminary data from the Phase 1 monotherapy dose expansion study of MICVO for 2L/3L R/M HNSCC patients, including both the post platinum and anti-PD(L)-1 experienced arm and the post EGFRi and anti-PD(L)-1 experienced arm.
o
Additional preliminary clinical data from the Phase 1/2 combination dose escalation study of MICVO and KEYTRUDA (pembrolizumab) for 1L/2L+ R/M HNSCC patients will also be provided. The combination study is part of a Clinical Trial Collaboration Agreement with Merck (known as MSD outside of the US and Canada).
o
Pyxis Oncology expects to announce next steps in the clinical development plan for MICVO for R/M HNSCC along with the preliminary data update.

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Pyxis Oncology presented new translational data in October 2025 in two posters at the European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) Congress 2025 and in six posters at the AACR (Free AACR Whitepaper)-NCI-EORTC International Conference, as well as three clinical trial in progress posters at ESMO (Free ESMO Whitepaper). The presentation posters at ESMO (Free ESMO Whitepaper) and AACR (Free AACR Whitepaper)-NCI-EORTC provided deeper insights into the pharmacodynamic responses of tumors to MICVO as well as MICVO’s unique mechanism of action and its potential to exert anti-tumor activity through three mechanisms: direct tumor cell killing, bystander killing and immunogenic cell death.
o
Translational findings highlighted MICVO’s effects on tumor microenvironment remodeling and immune activation, further reinforcing the potential benefit of MICVO as both a monotherapy and in combination with anti-PD1 therapy.
o
Observations included changes in circulating tumor DNA (ctDNA) tumor fraction (TF) to the vast majority of 37 clinical samples tested. Notably, reduction in ctDNA TF after treatment with MICVO, particularly in HNSCC and at the 5.4 mg/kg dose, support a positive molecular response to MICVO and strengthen rationale for continued development for this tumor type and dose in the monotherapy dose expansion study.
o
Additionally, features observed in nonclinical samples of the stromal architecture detected using AI-enabled hyper-resolution digital pathology may correlate with sensitivity to MICVO – a finding that may be unique compared to tumor cell surface targeting ADCs, due to MICVO’s targeting of a non-cellular structural component of the extracellular matrix.

Third Quarter 2025 Financial Results

•
As of September 30, 2025, Pyxis Oncology had cash and cash equivalents, including restricted cash, and short-term investments, of $77.7 million. The Company believes that its current cash, cash equivalents, and short-term investments will be sufficient to fund its operations into the second half of 2026.

•
Research and development expenses were $17.8 million for the quarter ended September 30, 2025, compared to $17.7 million for the quarter ended September 30, 2024. MICVO program-specific research and development costs increased by $2.0 million, primarily due to a $1.0 million increase in contract manufacturing costs and a $1.3 million increase in clinical trial related expenses related to monotherapy and combination therapy of MICVO. The increase in expenses was partially offset by a $1.8 million reduction in expenses related to PYX-106, as the clinical development of PYX-106 was paused in December 2024.

•
General and administrative expenses were $5.6 million for the quarter ended September 30, 2025, compared to $6.0 million for the quarter ended September 30, 2024. The decrease was primarily due to lower corporate insurance costs and a decrease in legal, professional and consulting fees.

•
Net loss was $22.0 million, or ($0.35) per common share, for the quarter ended September 30, 2025, compared to $21.2 million, or ($0.35) per common share, for the quarter ended September 30, 2024. Excluding non-cash stock-based compensation expense, the net loss for the quarter ended September 30, 2025 was $18.9 million, compared to a net loss of $18.2 million for the quarter ended September 30, 2024.

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As of October 31, 2025, the outstanding number of shares of Common Stock of Pyxis Oncology was 62,264,215.

(Press release, Pyxis Oncology, NOV 3, 2025, View Source [SID1234659277])