June 13, 2025: Ratio Therapeutics Partners with Macrocyclics for Exclusive Manufacturing and Distribution of its Radiopharmaceutical Chelator Platform

On June 13, 2025 Ratio Therapeutics Inc. (Ratio), a pharmaceutical company employing innovative technologies to develop best-in-class radiopharmaceuticals for cancer treatment and monitoring, reported that it entered into an agreement granting Macrocyclics Inc. (Macrocyclics) exclusive manufacturing and distribution rights to Ratio’s proprietary chelator MacropaTM enabling broad access worldwide (Press release, Ratio Therapeutics, JUN 13, 2025, View Source [SID1234653872]).

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Macropa is a proprietary, best-in-class, bifunctional chelator for Actinium-225, known for its strong alpha-particle emissions and its use in targeted alpha therapy (TAT) for the treatment of cancer. Macropa can be tethered to small molecules, peptides, and large polypeptides such as proteins and antibodies to enable the development of targeted radiopharmaceuticals for alpha radiotherapy. By rapidly and quantitatively complexing Ac-225 at room temperature, Macropa’s unique selectivity and stability for Ac-225 enables simple "one-pot" manufacturing and improves in vivo stability of the resulting compound.

"Over the past year, we have been focused on building global scientific awareness and encouraging adoption of our chelator platform across the therapeutic radiopharmaceutical community," said Bill Cupelo, Chief Business Officer of Ratio. "We are proud to see our efforts realized through an expanding global ecosystem of collaborators who can now leverage Macropa to accelerate the development and adoption of radiopharmaceuticals worldwide. By enabling broader access to our platform, we are fostering a global community aligned in the mission to improve patient outcomes through targeted cancer therapies and diagnostics."

Incorporated in 1995, Macrocyclics is a CDMO specialized in chelating agents for radiopharmaceuticals and nuclear medicine. The company maintains a broad catalog of bifunctional chelating agents that are used in R&D and clinical programs across the globe. Under the terms of the agreement, researchers from academia and industry may purchase Macropa directly from Macrocyclics, enabling rapid access in many countries including Japan, Canada, Australia and majority of Europe.

"Ratio’s Macropa is a superior chelator for Ac-225," said Paul Jurek, Ph.D., CEO of Macrocyclics. "The ability to label quickly at room temperature provides a critical advantage, especially when working with proteins or vectors that degrade when heated. We are excited to be the exclusive manufacturer of Macropa and plan to add multiple derivatives to our catalog and provide it under GMP conditions for innovators engaged in clinical research."

Macrocyclics is an exhibitor at the 2025 SNMMI Annual Meeting, located in New Orleans, LA from June 21 to June 24. Ratio will also have representatives in attendance and will host a networking event for current and potential Macropa users.

Enliven Therapeutics Announces Updated Positive Data from Phase 1 Clinical Trial of ELVN-001 in CML at EHA 2025 Congress

On June 13, 2025 Enliven Therapeutics, Inc. (Enliven or the Company) (Nasdaq: ELVN), a clinical-stage biopharmaceutical company focused on the discovery and development of small molecule therapeutics, reported updated, positive data from the Phase 1 ENABLE clinical trial evaluating ELVN-001 in patients with chronic myeloid leukemia (CML) in an oral presentation at the European Hematology Association (EHA) (Free EHA Whitepaper) 2025 Congress taking place June 12-15 in Milan, Italy, and virtually (Press release, Enliven Therapeutics, JUN 13, 2025, View Source [SID1234653888]).

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"Thanks to the success of tyrosine kinase inhibitors (TKIs), patients with CML now have a near-normal life expectancy. As a result, treatment goals have evolved beyond response and survival to also prioritize quality of life and tolerability," said Andreas Hochhaus, Professor of Internal Medicine, Hematology and Oncology and Head of the Department of Hematology and Medical Oncology at the Jena University Hospital, Germany. "However, significant unmet needs remain, particularly related to treatment resistance and intolerance, across all lines of therapy. The data from ELVN-001 are encouraging, showing an efficacy, safety and tolerability profile that compare favorably to approved BCR::ABL1 inhibitors, despite being studied in a more heavily pretreated population. I look forward to future data, which could support ELVN-001 as a promising new option for patients who need better long-term disease management."

"We are highly encouraged by the ELVN-001 data, specifically as it relates to the consistency of the cumulative and achieved MMR rates as the Phase 1 trial progresses, with more evaluable patients and longer duration of treatment," said Helen Collins, M.D., Chief Medical Officer of Enliven. "While MMR is the efficacy endpoint in CML, safety and tolerability are equally critical given the chronic nature of the disease. ELVN-001 was reported to be well tolerated across all evaluated doses and had low levels of dose reductions and discontinuations, which we believe is the key sign of a favorable safety and tolerability profile. We believe ELVN-001 has the potential to offer best-in-class efficacy and tolerability, which are key attributes for people living with CML. We look forward to sharing additional data in the future."

ELVN-001 is a potent, highly selective, potentially best-in-class small molecule kinase inhibitor designed to specifically target the BCR::ABL gene fusion, the oncogenic driver for patients with CML.

ELVN-001 Data Highlights

Patient Demographics

As of the cutoff date of April 28, 2025, 90 patients have been enrolled in the ongoing Phase 1 trial across dose levels ranging from 10 mg once a day (QD) to 80 mg twice a day (BID).
The vast majority of patients (80%) remain on study with a median treatment duration of ~29 weeks.
Patients enrolled were heavily pretreated:
67% of patients received three or more unique prior TKIs, including 58% of patients who received prior asciminib and 43% of patients who received prior ponatinib.
72% of patients had discontinued their prior TKI due to lack of efficacy.
Encouraging ELVN-001 Efficacy Data by 24 Weeks

Of the enrolled patients, 53 with typical BCR::ABL1 transcripts and without T315I mutations were evaluable for major molecular response (MMR) by 24 weeks.
25 of 53 (47%) evaluable patients were in MMR by 24 weeks, with 13 of 41 (32%) achieving and 12 of 12 (100%) maintaining MMR.
Of those resistant to their last TKI, 14 of 34 (41%) were in MMR by 24 weeks.
Of those previously treated with asciminib or ponatinib, 12 of 34 (35%) were in MMR by 24 weeks.
All patients who achieved or maintained MMR were still in MMR at the time of data cutoff.
These data continued to compare favorably to precedent Phase 1 MMRs for approved BCR::ABL1 TKIs, particularly given the more heavily pretreated patient population in the ELVN-001 clinical trial.
Specifically, the achieved MMR rate by 24 weeks of 32% compares favorably with historical data from less heavily pretreated patients receiving asciminib, which showed achieved MMR rates of 24% in the Phase 1 trial and 25% in the ASCEMBL Phase 3 trial.
ELVN-001’s Safety Profile Consistent with High Selectivity for ABL1

ELVN-001 remains well-tolerated across all evaluated doses.
Only 3.4% (3 of 87) of patients had dose reductions due to treatment-emergent adverse events (TEAEs) and 4.6% (4 of 87) of patients discontinued due to TEAEs.
The majority of TEAEs were low frequency and low grade, and the hematologic TEAE profile was similar to or better than the approved TKIs.
Only 2.3% (2 of 87) of patients experienced ≥ Grade 3 non-hematologic treatment-related AEs.
No evidence to date of enhanced cardiovascular toxicity and no treatment-related arterial occlusive events (AOEs).
The maximum tolerated dose was not reached, and no exposure-toxicity relationship was observed.
ELVN-001 Pharmacokinetic (PK) Profile

The PK profile supports once-daily dosing with flexible administration requirements, including the ability to take with or without food.
There is low potential for drug-drug interactions, an important advantage given that the average CML patient takes approximately five concurrent medications.
"We believe there remains significant opportunity to improve upon existing therapies," said Sam Kintz, Co-founder and Chief Executive Officer of Enliven. "Based on today’s encouraging Phase 1 update, we believe ELVN-001 has the potential to compete across all lines of therapy. We believe that precedent registrational trials in CML provide a roadmap for the regulatory pathway for ELVN-001, and the use of biomarker-based endpoints, like MMR, enables smaller, faster studies. Importantly, historical Phase 1 data in late-line CML trials have predicted success in subsequent pivotal trials. Building off this exciting update, we expect to initiate our first head-to-head Phase 3 pivotal trial in 2026 and remain confident in ELVN-001 and its potential positioning in the future in the CML treatment paradigm."

The oral presentation titled: "ENABLE: A Phase 1a/1b Study of ELVN-001, a selective active site inhibitor of BCR::ABL1, in patients with previously treated CML" will be presented by Andreas Hochhaus, Professor of Internal Medicine, Hematology and Oncology and Head of the Department of Hematology and Medical Oncology at the Jena University Hospital, Germany later today. A copy of the presentation will be available on the "Program Presentations & Publications" section of the Company’s website at www.enliventherapeutics.com.

Webcast and Conference Call Information
Enliven will host a live webcast and conference call today at 1:30 p.m. ET / 7:30 p.m. CEST. To participate in the live event, please register using this link. Following registration, participants will have access to dial in numbers and a unique passcode should they prefer to participate by phone. The event and accompanying slides can also be accessed by visiting the investor relations section of the Company’s website at View Source An archived webcast will be available on the Company’s website following the event.

About the ENABLE Trial
The ENABLE study (NCT05304377) is a Phase 1 study of ELVN-001 in patients with previously treated CML. The trial is currently in Phase 1a/1b development and is a dose escalation and expansion trial designed to evaluate safety and tolerability and to determine the recommended dose for further clinical evaluation of ELVN-001 in patients with CML with and without T315I mutations that is relapsed, refractory or intolerant to TKIs. Secondary endpoints include pharmacokinetics, MMR by central quantitative reverse transcriptase polymerase chain reaction, duration of MMR, BCR::ABL1 transcript levels and complete hematologic response. Enliven is preparing for the potential start of a pivotal trial for ELVN-001 in 2026.

About ELVN-001
ELVN-001 is a potent, highly selective, potentially best-in-class small molecule kinase inhibitor designed to specifically target the BCR::ABL gene fusion, the oncogenic driver for patients with chronic myeloid leukemia. As a highly selective active site inhibitor, ELVN-001 has a mechanism of action that is complementary to allosteric BCR::ABL1 inhibitors, which may play an increasingly important role in the standard of care. ELVN-001 was also designed to have activity against the T315I mutation, the most common BCR::ABL1 mutation, which confers resistance to nearly all approved TKIs, as well as activity against mutations known to confer resistance to allosteric BCR::ABL1 inhibitors.

Arvinas Presents Preclinical Data for PROTAC BCL6 Degrader, ARV-393, at the European Hematology Association 2025 Congress

On June 13, 2025 Arvinas, Inc. (Nasdaq: ARVN), a clinical-stage biotechnology company working to develop a new class of drugs based on targeted protein degradation, reported data from preclinical studies of ARV-393, the company’s investigational PROteolysis TArgeting Chimera (PROTAC) B-cell lymphoma 6 protein (BCL6) degrader (Press release, Arvinas, JUN 13, 2025, View Source [SID1234653873]). BCL6 is a transcriptional repressor protein and a known driver of B-cell lymphomas. ARV-393 demonstrated significant single-agent activity in a patient derived xenograft (PDX) model of nodal T-follicular helper cell lymphoma, angioimmunoblastic-type (nTFHL-AI also known as AITL) and PDX models of transformed follicular lymphoma (tFL). In combination with oral small molecule inhibitors (SMIs), ARV-393 demonstrated enhanced antitumor activity, including tumor regressions, in cell line-derived xenograft (CDX) models of high-grade B-cell lymphoma (HGBCL) and aggressive diffuse large B-cell lymphoma (DLBCL). The results from these preclinical studies were shared at the European Hematology Association (EHA) (Free EHA Whitepaper) 2025 Congress in Milan, Italy.

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Key findings from the preclinical studies included:

Single-agent ARV-393 significantly reduced tumor burden in peripheral blood, bone marrow and spleen in a systemic PDX model of nTFHL-AI derived from a patient who relapsed post chemotherapy. This is potentially the first preclinical evidence of anti-tumor activity with an efficacious BCL6-targeted small-molecule degrader in a human nTFHL-AI model.
ARV-393 monotherapy treatment resulted in robust (≥95%) tumor growth inhibition (TGI) in two PDX models of tFL.
ARV-393 in combination with 5 classes of SMIs targeting potentially cooperative oncogenic drivers (tazemetostat, palbociclib, everolimus, acalabrutinib, or venetoclax) demonstrated increased TGI in CDX models of HGBCL and aggressive DLBCL compared with the respective monotherapy treatments. Tumor regressions were observed when ARV-393 was combined with tazemetostat, palbociclib, acalabrutinib, or venetoclax.
RNA sequencing studies carried out to further characterize downstream mechanism of action suggested that ARV-393 inhibits tumor cell cycle progression and promotes differentiation, driving antitumor activity and broad combinability in preclinical models.
"We are encouraged by the marked single-agent activity of ARV-393 in PDX models of AITL and transformed follicular lymphoma and by the enhanced antitumor activity of ARV-393 in combination with five classes of small molecule inhibitors in models of aggressive DLBCL," said Noah Berkowitz, M.D., Ph.D., Chief Medical Officer at Arvinas. "We believe these preclinical data potentially suggest the broad utility of ARV-393 across non-Hodgkin lymphoma subtypes with unmet need beyond DLBCL and provide a compelling rationale for considering combination strategies including chemotherapy-free approaches as we work to bring forward new therapeutic options for adult patients with lymphoma."

A Phase 1 study of ARV-393 is enrolling adult patients with relapsed/refractory non-Hodgkin lymphoma, including DLBCL and nTFHL-Al (AITL) (NCT06393738).

Additional detail on the ARV-393 data presentation at the EHA (Free EHA Whitepaper) 2025 Congress:

Poster Title: ARV-393, a PROteolysis TArgeting Chimera (PROTAC) BCL6 Degrader, is Efficacious in Preclinical Models of Diffuse Large B-Cell Lymphoma, Nodal T-Follicular Helper Cell Lymphoma, and Transformed Follicular Lymphoma

Abstract: PF1000
Session Title: Lymphoma biology & translational research 
Date: Thursday, June 13, 2025
Time: 6:30-7:30 pm CEST

About ARV-393
ARV-393 is an investigational orally bioavailable PROteolysis TArgeting Chimera (PROTAC) designed to degrade B-cell lymphoma 6 protein (BCL6), a transcriptional repressor and major driver of B-cell lymphomas. The BCL6 protein facilitates B cell tolerance of rapid proliferation and somatic gene recombination via repressing cell cycle checkpoints, terminal differentiation, apoptosis, and the DNA damage response. PROTAC-mediated degradation has the potential to address the traditional undruggable nature of BCL6. ARV-393 is currently being evaluated in a Phase 1 clinical trial in patients with relapsed/refractory non-Hodgkin lymphoma.

Biomea Fusion Presents Updated Preliminary Clinical Data for Covalent FLT3 Inhibitor BMF-500 in Relapsed or Refractory Acute Leukemia at EHA 2025

On June 13, 2025 Biomea Fusion, Inc. ("Biomea" or the "Company") (Nasdaq: BMEA), a clinical-stage diabetes and obesity medicines company, reported updated preliminary clinical data from the ongoing Phase I COVALENT-103 trial of BMF-500 in adults with relapsed or refractory ("R/R") acute leukemia ("AL") (Press release, Biomea Fusion, JUN 13, 2025, View Source [SID1234653874]). The results will be presented in a poster presentation at the European Hematology Association (EHA) (Free EHA Whitepaper) ("EHA") 2025 Congress in Milan, Italy.

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The presentation by Dr. Farhad Ravandi of The University of Texas MD Anderson Cancer Center will highlight emerging safety, pharmacokinetics/pharmacodynamics, and early clinical activity data for BMF-500, a highly selective covalent FMS-like tyrosine kinase 3 ("FLT3") inhibitor, in heavily pretreated patients with R/R AL.

Key Results from the EHA (Free EHA Whitepaper) 2025 Poster Presentation
27 patients were enrolled across two study arms, Arm A (no CYP3A4 inhibitor; n=10) and Arm B (CYP3A4 inhibitor; n=17). All patients had R/R AL, with a median of 4 prior lines of therapy. 18 of the 27 patients were FLT3 mutations ("FLT3m") while the other 9 patients had FLT3 wild-type AL. Frequent co-mutations included WT1, TP53, IDH1/2, and NRAS. All 18 FLT3m patients had failed gilteritinib in the R/R setting and 9 of the 18 had received at least two FLT3 inhibitors prior to study entry. 26 of 27 (96%) enrolled patients had also received and failed the BCL2 inhibitor venetoclax. Key findings include:

Clinical Activity Observed:

9 of 11 efficacy-evaluable FLT3m patients, defined as all patients enrolled who received at least one dose and had at least one disease assessment, showed bone marrow (BM) blast reduction; 5 of 11 achieved >50% BM blast reduction.
1 FLT3m patient achieved complete remission with incomplete hematologic recovery (CRi), sustained for 6 cycles.
1 FLT3m patient achieved morphologic leukemia-free state (MLFS); response is ongoing.
1 FLT3m patient met all criteria for partial response (PR) except platelet recovery; categorized as near PR.
2 of 4 efficacy-evaluable FLT3 wild-type patients achieved durable disease control ≥120 days, with treatment ongoing for one patient.
Additional clinical improvements include reductions in peripheral blasts, transfusion dependency, and frequency of hydroxyurea use.
Pharmacokinetics/Pharmacodynamics:

FLT3 inhibition correlated with BMF-500 systemic exposures.
Bone marrow and plasma concentrations of BMF-500 and its metabolites were comparable, suggesting good compartmental penetration.
Survival:

Median overall survival (mOS) among all treated FLT3m patients (n=18) was 3.8 months (Arm A) and 3.5 months (Arm B) during dose escalation.
For the efficacy-evaluable FLT3m patients (n=12), the mOS for Arms A and B was 3.8 and 3.6 months, respectively during dose escalation.
These survival durations compare favorably to historical mOS of 2.1 months in patients with R/R FLT3m acute myeloid leukemia ("AML") post-failure with both gilteritinib and venetoclax. 1
Ongoing Dose Escalation:

Dose escalation continues at 200 mg BID (Arm A) and 75 mg BID (Arm B).
Based on observed activity and tolerability, further evaluation is underway to determine optimal biologic dose ("OBD") and recommended Phase II dose ("RP2D").
Safety and Tolerability

BMF-500 was generally well-tolerated across dose levels.
No dose-limiting toxicities (DLTs), QT prolongation, or discontinuations due to treatment-related adverse events were reported.
Escalation is ongoing without safety restrictions.
"The updated COVALENT-103 results continue to support the potential of BMF-500 as a selective, covalent FLT3 inhibitor," said Mick Hitchcock, Ph.D., Interim Chief Executive Officer of Biomea Fusion. "We are encouraged by the depth of bone marrow responses, the achievement of MLFS and CRi, and the early survival benefit in heavily pretreated patients with FLT3 mutations who had progressed following prior FLT3 inhibitor therapy. These data speak to BMF-500’s potential to meaningfully improve outcomes in a high-risk AML population with no currently available treatment options."

Following completion of the COVALENT-103 dose escalation phase in R/R AL patients with FLT3m, Biomea plans to conclude its internal development of BMF-500 in oncology and is actively exploring strategic partnerships to advance the program.

Poster Presentation Details

Date/Time: Saturday, June 14 (18:30-19:30 CEST)
Title: Covalent FLT3 Inhibitor BMF-500 in Relapsed or Refractory (R/R) Acute Leukemia (AL): Preliminary Phase 1 Data from the COVALENT-103 Study (NCT05918692)
Poster Number: PS1520
Presenter: Farhad Ravandi, M.D., University of Texas MD Anderson Cancer Center
About COVALENT-103
COVALENT-103 is a multicenter, open-label, non-randomized trial seeking to evaluate the safety and efficacy of BMF-500, a twice daily oral treatment, in adult patients with R/R AL with FLT3 wild-type or FLT3m. The Phase I COVALENT-103 study aims to evaluate the safety and tolerability of BMF-500, determine the optimal biologic dose and recommended Phase II dose, and identify initial efficacy signals. Additional information about the Phase I clinical trial of BMF-500 can be found at ClinicalTrials.gov using the identifier, NCT05918692.

About BMF-500
BMF-500 is an investigational, orally bioavailable, covalent small molecule inhibitor of FLT3, discovered in-house using Biomea’s proprietary FUSION System. Designed to be highly potent and selective, BMF-500 has demonstrated encouraging potential in extensive preclinical studies. Its kinase inhibitory profile indicates strong target selectivity, which may translate to a reduced risk of off-target effects.

City of Hope Developed a Foundational Map of Tumor Cells for Personalized Brain Cancer Treatments

On June 13, 2025 City of Hope, one of the largest and most advanced cancer research and treatment organizations in the U.S. with its National Medical Center named top 5 in the nation for cancer by U.S. News & World Report, reported the first study to demonstrate that characterizing genetic material near chromosomes forecasts how mutated, cancer-causing genes reengineer DNA and alter the tumor microenvironment (Press release, City of Hope, JUN 13, 2025, View Source [SID1234653890]). The leading-edge brain cancer research provides foundational knowledge that one day will improve the practice of precision medicine and allow oncologists to deliver more personalized therapies to cancer patients.

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Tiny DNA molecules outside of chromosomes were once disregarded, but in the past decade research has revealed that these circles called extrachromosomal DNA, or ecDNA, fuel cancer by breaking the laws of biology.

"Our study offers new insights into the interplay between different ecDNA. Importantly, when there is a prevalence of ecDNA and cancer-causing ingredients like the EGFR protein or tumor protein p53, the tumor microenvironment becomes hypoxic. It falls into a state of reduced oxygen, which has been linked to cancer progression, resistance to therapy and poor clinical outcomes," said David Craig, Ph.D., professor and chair of the Department of Integrative Translational Sciences at City of Hope and co-corresponding author of a study published today in Nature Communications.

Spatial transcriptomics (measuring and mapping of DNA activity) combined with genomic data can help identify groups of cells within a tumor that share a common ancestor but have acquired additional mutations. How they are distributed spatially informs the understanding of tumor evolution. The new translational science data underpins City of Hope’s precision medicine research, which applies innovation to create better outcomes with fewer side effects for more patients. City of Hope aspires to cure more cancer patients.

City of Hope researchers led a team that performed bulk RNA sequencing, tumor/normal DNA sequencing and spatial transcriptomics in a small sample of gliomas — tumors that develop in the brain or spinal cord. Through varied experiments and validation cohorts, they were able to identify common and distinct characteristics of the tumor microenvironment, developing an integrated analysis framework that can be leveraged by others.

"While our paper solely evaluated different types of brain cancers, the spatial transcriptomic principles and genome sequencing techniques we outlined will one day enable physicians to provide more personalized therapies for cancer patients," said Gabriel Zada, M.D., a neurosurgeon with Keck Medicine of USC, professor of neurological surgery and physiology and neuroscience at the Keck School of Medicine of USC, co-director of the USC Brain Tumor Center and co-corresponding study author. "Cancer and its treatment is not one-size-fits-all. Understanding the molecular activity of ecDNA near inheritable and non-inheritable cells provides deep insights into potential therapeutic targets and risk of cancer recurrence."

The researchers demonstrated that ecDNA drives rapid cancer cell (oncogene) proliferation outside of chromosomes, the thread-like structures inside the cell nucleus that houses DNA and RNA. EcDNA contributes to the development of gliomas, genetic instability and distinct tumor cell populations within a single tumor, making cancer more difficult to eliminate.

The dynamic nature of ecDNA may be what enables cancer cells to adapt and reprogram their genomes, driving tumor progression in response to changes in their microenvironment, including changes resulting from therapies.

"We have now demonstrated how cancer cells dynamically reprogram their own genome to control and respond to the tumor microenvironment. By uncovering these mechanisms, we are paving the way for more precise and effective treatments tailored to the unique biology of each patient," Dr. Craig said.

The Nature Communications study entitled "Resolving Subclonal Genomic Heterogeneity in Gliomas by Integrating Spatial Transcriptomics with Loss of Heterozygosity and Extrachromosomal DNA Analysis" was supported by the National Center for Advancing Translational Science of the U.S. National Institutes of Health (KL2TR001854).