RegulationPriority Review (United States), Breakthrough Therapy (United States), Accelerated Approval (United States), Orphan Drug (United States), Orphan Drug (European Union), Orphan Drug (Japan), Orphan Drug (South Korea), Priority Review (Australia), Fast Track (United States)

Structure/Sequence

Molecular FormulaC20H19Cl2F2N5O3

InChIKeyHGCOOPLEWPBLOY-PFEQFJNWSA-N

CAS Registry2119669-71-3

Clinical Trials associated with Asciminib Hydrochloride

NCT07354074

/ Not yet recruitingPhase 2

A Phase II, Multicenter, Open-label, Single Arm Study to Evaluate the Safety and Efficacy of Asciminib in Pediatric Participants Newly Diagnosed or Previously Treated With Philadelphia Positive Chronic Myelogenous Leukemia in Chronic Phase (Ph+ CML-CP) With or Without Known T315I Mutation

The aim of this study is to support development of asciminib in the pediatric population (1 to < 18 years) with Ph+ CML-CP. The study will evaluate the efficacy and safety of asciminib in pediatric formulation (weigh-based dose, fed state) or adult formulation (fasted) in newly diagnosed and resistant or intolerant Ph+ CML-CP with or without T315I mutation.

Start Date04 May 2026

Sponsor / Collaborator

Novartis Pharmaceuticals Canada, Inc.

NCT07040982

/ Not yet recruitingPhase 1IIT

Pilot Study of Asciminib as a Maintenance Treatment Post Cellular Therapies in Adults With Philadelphia Chromosome Positive Acute Lymphoblastic Leukemia

This phase I trial tests the safety, side effects and best dose of asciminib as maintenance treatment for adults with Philadelphia chromosome positive acute lymphoblastic leukemia (ALL) who have undergone cellular therapies such as hematopoietic stem cell transplantation (HSCT) or chimeric antigen receptor (CAR) T cell therapy. Maintenance treatment is given to help keep cancer from coming back after it has disappeared following initial therapy. Asciminib may stop the growth of cancer cells by blocking some of the enzymes needed for cell growth. Giving asciminib may be safe and tolerable as maintenance treatment for adult patients with Philadelphia chromosome positive ALL who have undergone cellular therapies.

Start Date01 May 2026

Sponsor / Collaborator

City of Hope National Medical Center

[+1]

NCT07039760

/ Not yet recruitingEarly Phase 1IIT

An Early Phase 1 Study of Asciminib With or Without Sildenafil for Brain Tumors

Dissemination of medulloblastoma is an independent risk factor of poor prognosis. Dissemination of medulloblastoma at recurrence is nearly universally fatal. ABL1 and 2 have been recently found to mediate the dissemination of medulloblastoma. Genetically inactivating ABL1 and 2 resulted in decreased leptomeningeal medulloblastoma and improved overall survival (OS) in rodent models. Asciminib is an FDA approved for the treatment of chronic myeloid leukemia and is well tolerated, likely due to its specificity for ABL1 and ABL2. Asciminib is a P-glycoprotein (P-gp) substrate and thus may be susceptible to being pumped out of tumor cells and brain endothelial cells. It is unclear if asciminib can enter the central nervous system (CNS) and brain tumors in adequate concentration to have anti-tumor effects.

Start Date30 Apr 2026

Sponsor / Collaborator

Washington University School of Medicine

100 Clinical Results associated with Asciminib Hydrochloride

100 Translational Medicine associated with Asciminib Hydrochloride

100 Patents (Medical) associated with Asciminib Hydrochloride

329

Literatures (Medical) associated with Asciminib Hydrochloride

01 Apr 2026·Hematology Transfusion and Cell Therapy

Is asciminib an effective tyrosine kinase inhibitor for chronic myeloid leukemia patients with tyrosine kinase inhibitor resistance?

Review

Author: Alanazi, Majed A ; Jackson, Denise E ; Omar, Musab Ma

Asciminib represents a significant advancement in the treatment of chronic myeloid leukemia, establishing a novel therapeutic paradigm by specifically targeting the ABL1 myristoyl pocket, a mechanism distinct from that of conventional adenosine triphosphate-competitive inhibitors. Such a selective inhibitor offers an alternative treatment strategy for patients with chronic myeloid leukemia who have developed resistance to previous tyrosine kinase inhibitor therapies. Although asciminib demonstrates a superior safety profile, primarily characterized by a reduction in cardiovascular adverse events associated with prior tyrosine kinase inhibitors, its clinical significance extends further. The effectiveness of asciminib, combined with its capacity to overcome resistance through combination strategies with adenosine triphosphate-binding site tyrosine kinase inhibitors, establishes it as a focal point in emerging chronic myeloid leukemia treatment approaches. It remains essential to continue research and clinical trials to enhance the therapeutic efficacy of asciminib and manage its associated side effects.

04 Mar 2026·Expert Review of Hematology

Addressing unmet needs in chronic myeloid leukemia in chronic phase treated with two or more tyrosine kinase inhibitors: insights from literature and Indian clinical practice

Review

Author: Saini, Kuldeep ; Jain, Rishi ; Gundeti, Sadashivudu ; Sharma, Lalit Mohan ; Bhattacharya, Jina ; Shetty, Disha ; Bagal, Bhausaheb ; Baul, Shuvra Neel ; Kumar, Sujeet ; Sharma, Vishnu ; Nair, Velu ; Malhotra, Hemant ; Nag, Arijit ; Verma, Shailendra Prasad ; Yadav, Sanjeev ; Jena, Rabindra Kumar

INTRODUCTION:

Chronic myeloid leukemia (CML) is a myeloproliferative disorder, usually diagnosed in its chronic phase (CP), often requiring life-long therapy. Despite the effectiveness of targeted therapy with tyrosine kinase inhibitors (TKIs), resistance or intolerance may occur, requiring a switch. The probability of achieving guideline-recommended cytogenetic and molecular responses declines from first (1 L) to second (2 L) and subsequent lines. About half of the patients receiving third line TKI treatment exhibit resistance or intolerance to prior TKIs. Post-2 L, patients experience non-durable responses, persistent adverse events, and a decreased quality of life.

AREAS COVERED:

This narrative review is based on targeted literature search in Medline via PubMed and expert clinical input from Indian hematologists to cover unmet needs of patients with CP-CML post-2 L of TKI therapy. We present an overview of the available clinical data, outline the challenges associated with treatment resistance and intolerance, identify gaps in patient management, and discuss personalized treatment approaches that could bridge these gaps and improve patient outcomes post-2 L.

EXPERT OPINION:

Management of CP-CML beyond 2 L remains a significant clinical challenge due to resistance, intolerance, and suboptimal long-term responses with currently available TKIs. Integrating newer agents like asciminib or ponatinib, can help overcome resistance and improve patient outcomes.

04 Mar 2026·Expert Review of Hematology

Specifically targeting the ABL myristoyl pocket: STAMP inhibitors for chronic myeloid leukemia

Review

Author: Kimura, Shinya ; Ureshino, Hiroshi

INTRODUCTION:

Chronic myeloid leukemia (CML) has been transformed by ATP-competitive BCR:ABL1 tyrosine kinase inhibitors (TKIs); however, resistance, intolerance, and long-term toxicity remain clinically relevant challenges, particularly in patients requiring prolonged therapy or multiple treatment lines. Asciminib, the first-in-class Specifically Targeting the ABL Myristoyl Pocket (STAMP) inhibitor, represents a paradigm shift by restoring physiologic ABL1 autoinhibition through allosteric binding.

AREAS COVERED:

This Special Report reviews the mechanistic basis, preclinical development, and clinical evidence supporting asciminib in CML. We summarize key data from pivotal trials, including ASCEMBL and ASC4FIRST, as well as emerging real-world studies, focusing on molecular response depth, safety, resistance mechanisms, and patient selection. Particular attention is paid to how STAMP inhibition differs from ATP-competitive TKIs in terms of selectivity, toxicity profile, and resistance patterns, and how asciminib can be positioned relative to ponatinib in later-line settings.

EXPERT OPINION:

Asciminib has established itself as an effective and generally well-tolerated option for patients with TKI-resistant or -intolerant CML and is poised to expand into earlier lines of therapy. Its ability to induce rapid and deep molecular responses with reduced off-target toxicity may have important implications for long-term disease control and future treatment-free remission (TFR) strategies. Ongoing studies will clarify its optimal sequencing, combination potential, and role in facilitating durable TFR.

154

News (Medical) associated with Asciminib Hydrochloride

25 Mar 2026

·www.fiercebiotech.com

Merck, girding for Keytruda cliff, flies toward promising CML asset with $6.7B Terns acquisition

The crown jewel of the acquisition is an oral treatment candidate for patients with chronic myeloid leukemia.\n Merck and Terns Pharmaceuticals have agreed to a $6.7 billion all-cash buyout that delivers a prized leukemia asset to the New Jersey Big Pharma.The crown jewel of the deal is TERN-701, an oral treatment that demonstrated encouraging efficacy and safety signals in a recent trial while also offering greater convenience for patients with chronic myeloid leukemia (CML), a rare cancer of the blood and bone marrow caused by a genetic mutation.Merck will acquire Terns for $53 a share, a 6% premium over Tuesday’s closing price, according to a March 25 release. The deal values the biotech at $5.7 billion when factoring in its $1 billion in cash holdings.A note from William Blair analysts said the deal undervalues TERN-701, which the team believes is poised to disrupt the CML treatment paradigm and challenge Novartis’ Scemblix franchise. Meantime, analysts at Mizuho say the deal value may leave room for another bidder for the CML asset. The agreement, expected to close in the second quarter of this year, will help Merck replenish its oncology pipeline as Keytruda approaches its loss of exclusivity in 2028.TERN-701 is a novel oral allosteric BCR::ABL tyrosine kinase inhibitor (TKI) currently being evaluated in a phase 1/2 trial in patients with Philadelphia chromosome-positive (Ph+) chronic-phase CML who were previously treated with one TKI and experienced treatment failure. In March 2024, TERN-701 received orphan drug designation from the FDA.In a presentation at the American Society of Hematology late last year, TERN-701 reduced the number of diseased white blood cells in patients’ bloodstreams. Although the study was primarily designed to assess safety, Terns described the results as “unprecedented” among CML treatments.TERN-701 has shown promising rates of major molecular response and deep molecular response by week 24, including in patients with high disease burden who had received multiple prior lines of therapy, according to the biotech. Most treatment-emergent adverse events recorded in the study were low grade, with a low incidence of severe adverse events and discontinuations. No meaningful changes in blood pressure were observed, and rates of lipase elevation were low.Terns is preparing to launch late-stage trials toward the end of the year or in early 2027. According to the American Cancer Society, CML accounts for 15% of all new leukemia cases, with about 9,650 people expected to be diagnosed this year.The data prompted bullish reactions from analysts, who noted that Novartis recently raised its peak global sales guidance for Scemblix from $3 billion to $4 billion. First approved for third-line treatment, Scemblix has since been cleared by the FDA for patients with newly diagnosed Ph+ CML. A note from BMO Capital Markets predicts that TERN-701 could achieve unadjusted peak sales of more than $4 billion.The deal is a boost for Terns, which abandoned its oral GLP-1 obesity candidate last year after a phase 2 trial fell short of expectations and showed signs of liver injury. While the company initially planned to seek a partner to advance the asset, the data ultimately ended its development.Still, investor sentiment in the wake of the announcement “appears mixed,” Leerink analysts wrote to clients Wednesday. Some Terns investors were happy to enjoy the stock’s quick appreciation and buyout, while others thought the company left value on the table by selling for the price it did. Merck\'s Keytruda LOE positioning Merck, which remained pharma\'s top R&D spender in 2025, has been on an acquisition streak. Last July, it acquired Verona for $10 billion to bolster its respiratory portfolio with potential chronic obstructive pulmonary disease blockbuster Ohtuvayre. In November, Merck spent $9.2 billion on Cidara Therapeutics, targeting its lead influenza antiviral, which had previously been abandoned by Johnson & Johnson in 2024.As part of last month’s full-year earnings presentation, Merck CEO Robert Davis said the Cidara and Verona acquisitions will help drive the company toward more than $70 billion in annual revenue opportunities by the “mid-2030s.” Merck reported $65 billion in revenue in 2025, up 1% from 2024, with Keytruda accounting for $31.7 billion in sales.Wednesday, Davis said in a statement that the Terns acquisition allows Merck to add a potential best-in-class candidate for patients with CML as the company continues “to look for opportunities to broaden our portfolio into other therapeutic areas.”

Clinical ResultAcquisitionDrug ApprovalOrphan DrugASH

25 Mar 2026

·endpoints.news

Merck to buy Terns for $6.7B, taking a leukemia drug that could challenge Scemblix

Merck is looking to further solidify its oncology pipeline via a $6.7 billion cash acquisition of Terns Pharmaceuticals and its investigational treatment for chronic myeloid leukemia. The Wednesday morning M&A move gives the New Jersey drug giant access to TERN-701, a small molecule that Terns anticipates will enter the market before 2031 and could set it up for competition with Novartis’ blockbuster treatment Scemblix. Merck will pay $53 per share $TERN , a 31% premium to Terns’ 60-day average stock price. “This transaction further diversifies and strengthens our position in oncology as we continue to look for opportunities to broaden our portfolio into other therapeutic areas,” Merck CEO Rob Davis said in a press release. Merck has been acquiring assets and partnering with biotechs left and right over the past few years to build out a broad pipeline of cancer drugs to weather the patent cliff for Keytruda. The pharma has budgeted at least $15 billion on acquisitions of cancer biotechs and assets since the beginning of 2019, according to an Endpoints News analysis. Additional money has gone toward earlier-stage pacts, licensing deals and research collaborations. TERN-701 is a potential treatment for certain patients with a blood and bone marrow cancer known as CML. The small molecule is an allosteric BCR-ABL tyrosine kinase inhibitor that has FDA orphan drug designation. Early TERN-701 clinical data jolted the company’s stock in December, with the candidate hitting a 64% major molecular response rate by 24 weeks in a Phase 1 study. That data presentation at the American Society of Hematology annual conference led to a $747 million public offering. At the time, Terns CEO Amy Burroughs told Endpoints that Terns could try going up against Novartis’ Scemblix as an independent biotech. Burroughs said it was “ unlikely ” Terns would seek a partner to compete with the Swiss drugmaker’s treatment, which was first approved in 2021 and reached $1.3 billion in 2025 net sales. Terns’ experimental medicine is projected to enter a pivotal trial later this year or in early 2027, the California biotech said in a corporate presentation earlier this month. The company added it had about $1 billion in cash, or enough money to last it into 2031 and take TERN-701 into the market. In 2020, Hansoh Pharma took the Greater China rights to the medicine from Terns. Those licensing terms were amended in January so Terns no longer needed sign-off from its Shanghai partner if Terns wanted to do additional deals on the drug. At the time, Mizuho analyst Graig Suvannavejh wrote that the updated arrangement “should make for a cleaner situation if and when the company evaluates potential commercial partnerships.” As a flurry of biotechs emerge with obesity drugs, or pivot to the cardiometabolic field, Terns recently ditched those efforts. The biotech debuted in 2018 with three MASH drugs that it licensed from Eli Lilly, with operations across both the US and China. Terns worked in the burgeoning obesity and MASH spaces for years before shelving a GLP-1 agonist in October . That pill, TERN-601, “was not a best-in-class type of asset,” Burroughs told Endpoints in December. “We’d already planned, from an operational standpoint, to move people into oncology, and so it wasn’t very disruptive to the company. It really was just a loss of potential.” Terns’ decision to hone in on cancer appears to have paid off. Merck anticipates the deal will close in the second quarter. And Merck likely has additional dealmaking capacity. The company was reportedly in talks to spend about $30 billion on Revolution Medicines earlier this year, but had balked. The pharma spent almost $20 billion on two deals last year, on influenza drug developer Cidara Therapeutics and respiratory treatment maker Verona Pharma . Its powerhouse cancer medicine Keytruda reeled in $31.7 billion in sales last year, accounting for 48% of the pharma’s sales. Earlier this year, Merck split its human health business into two separate units, with one focused on oncology and the other devoted to specialty, pharma and infectious disease. Editor’s note: This story was updated to correct which metabolic drug Amy Burroughs was referring to in the December interview.

License out/inPhase 1ASHOrphan DrugDrug Approval

25 Mar 2026

·allsci.com

Merck acquires Terns for USD 6.7b to boost hematology pipeline with CML drug

Merck (NYSE: MRK) has entered into a definitive agreement to acquire Terns Pharmaceuticals (Nasdaq: TERN), a clinical-stage oncology company, for USD 53.00 per share in an all-cash transaction valued at approximately USD 6.7 billion. The Merck Terns Pharmaceuticals acquisition positions the pharma company to consolidate its presence in hematology through TERN-701, an oral allosteric BCR::ABL1 tyrosine kinase inhibitor currently in Phase I/II development for chronic myeloid leukemia. The transaction represents approximately USD 5.7 billion net of acquired cash and carries a premium of 31% to the 60-day and 42% to the 90-day volume-weighted average stock price as of March 24, 2026. The deal contains no disclosed milestone payments, contingent value rights, or earn-out provisions. Merck will execute the acquisition through a tender offer requiring a majority of Terns stockholders to tender their shares, with closing expected in Q2 2026 following expiration of the Hart-Scott-Rodino waiting period. The transaction will be accounted for as an asset acquisition, resulting in an approximately USD 5.8 billion charge (approximately USD 2.35 per share) recognized in both Q2 and full-year 2026 GAAP and non-GAAP results. The asset acquisition classification means the acquired in-process R&D will be expensed immediately rather than capitalized. TERN-701: Mechanism and clinical status TERN-701 is a BCR-ABL1 tyrosine kinase inhibitor designed to bind to the ABL myristoyl pocket, an allosteric site distinct from the ATP-binding domain targeted by earlier-generation TKIs. CML is driven by the Philadelphia chromosome, a translocation between chromosomes 9 and 22 that produces constitutive activation of the BCR::ABL1 fusion protein, which fuels malignant white blood cell proliferation. The compound is being evaluated in the CARDINAL trial (NCT06163430), a global multi-center dose escalation and expansion study enrolling patients with Ph+ chronic phase CML who experienced treatment failure, suboptimal response, or intolerance to at least one prior TKI. The dose escalation portion completed in January 2025 with no dose-limiting toxicities observed up to 500 mg QD. Dose expansion initiated in April 2025 across two cohorts (320 mg and 500 mg QD), and in January 2026 an additional cohort was added to evaluate activity against BCR::ABL1 resistance mutations including T315I, M244V, and F359I/C/V. The FDA granted Orphan Drug Designation for TERN-701 in CML in March 2024. Clinical data reported to date indicate rates of major molecular response and deep molecular response by week 24, including in patients with high disease burden who had received multiple prior therapy lines, with low rates of severe adverse events and discontinuations. Specifically, Terns reported a 75% cumulative MMR rate by 24 weeks in 32 efficacy-evaluable patients. The strategic context The TERN-701 CML program joins a Merck hematology pipeline that already includes three Phase III candidates: bomedemstat (LSD1 inhibitor), nemtabrutinib (non-covalent BTK inhibitor), and zilovertamab vedotin (ROR1-targeting ADC), along with MK-1045 (CD19×CD3 T-cell engager) in Phase Ib/II. The Terns buyout extends a pattern of aggressive deal-making driven by the approaching Keytruda patent cliff (~2028). Merck’s recent transactions include the USD 9 billion purchase of influenza-focused Cidara Therapeutics, Inc. (Nasdaq: CDTX), the USD 10 billion purchase of Verona Pharma for a COPD therapy, and the USD 10.8 billion acquisition of immunology-focused Prometheus Biosciences. In the chronic myeloid leukemia treatment landscape, TERN-701 enters a competitive field. Novartis markets asciminib (Scemblix), the first approved allosteric BCR::ABL1 inhibitor, which received FDA approval in 2022 for Ph+ CML after two or more prior TKIs and gained a first-line CML indication based on the ASC4FIRST trial. Sun Pharma Advanced Research is developing denimsertib, another allosteric BCR::ABL1 inhibitor in clinical development. Earlier-generation ATP-competitive TKIs from Novartis (imatinib, nilotinib), Bristol Myers Squibb (dasatinib), and Pfizer (bosutinib) remain standards of care, though resistance mutations and tolerability limitations persist across these agents. Your email address will not be published. Required fields are marked * Comment * Name * Email * Website

AcquisitionOrphan DrugClinical ResultDrug ApprovalPhase 3

100 Deals associated with Asciminib Hydrochloride

External Link

KEGG	Wiki	ATC	Drug Bank
D11403 D11404	-	-	DB12597

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Philadelphia chromosome-positive chronic myeloid leukemia in chronic phase with the T315I mutation	United States	Novartis Pharmaceuticals Corp.	29 Oct 2024
Philadelphia chromosome-positive chronic myeloid leukemia in chronic phase	Australia	Novartis Pharmaceuticals Australia Pty Ltd.	15 Jul 2022
Chronic Myelogenous Leukemia	Japan	Novartis Pharmaceuticals KK	28 Mar 2022
Philadelphia chromosome positive chronic myelogenous leukemia	United States	Novartis Pharmaceuticals Corp.	29 Oct 2021

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Philadelphia Chromosome Positive Leukemia	Phase 3	Italy	Novartis Pharma AG	23 Aug 2021
Philadelphia positive acute lymphocytic leukaemia	Phase 3	Germany	Novartis Pharma AG	23 Aug 2021
Bone Marrow Neoplasms	Phase 3	France	Novartis Pharma AG	05 Aug 2021
Chronic phase chronic myeloid leukemia	Phase 3	Italy	Novartis Pharma AG	18 Jul 2017
Blast Phase Chronic Granulocytic Leukemia	Phase 2	Hong Kong	Novartis AG	30 Mar 2026
Recurrent Ph-Like Acute Lymphoblastic Leukemia	Phase 2	-	Novartis Pharmaceuticals Canada, Inc.	26 Mar 2026
Metastatic human epidermal growth factor 2 positive carcinoma of breast	Phase 2	-	Novartis AG	01 Feb 2026
Aggressive-Phase Chronic Myelocytic Leukemia	Phase 2	France	Novartis Pharmaceuticals Canada, Inc.	18 Feb 2025
Aggressive-Phase Chronic Myelocytic Leukemia	Phase 2	France	Novartis Pharma SAS	18 Feb 2025
Solid tumor	Phase 2	United States	Novartis AG	14 Feb 2025

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


AACR2026	Not Applicable	Chronic Myelogenous Leukemia	291	Ponatinib	xrblevupiy(faywurpbma) = xyelptvhpo ddfdlhnffi (qhildvymvl )	Positive	21 Apr 2026
				Bosutinib	kxwsirbyiu(pzzaurtpxd) = dvcathrjcu baxnelibiv (lzqekygdsi ) View more
NCT04216563 (CTgov)	Phase 2	Chronic phase chronic myeloid leukemia \| Residual Neoplasm \| Philadelphia chromosome positive chronic myelogenous leukemia	7	Asciminib	ozixybolrp = dcmkfgigib oswbpoobci (nqvlqoawjc, rkazipuutj - tnlalservp) View more	-	09 Jan 2026
ASH2025	Not Applicable	Chronic phase chronic myeloid leukemia	530	imatinib	zhbnrniuzs(mvlcomsumd) = ofceuuvksx xgoqrslpnd (vzczcivbcv ) View more	Positive	06 Dec 2025
				nilotinib	zhbnrniuzs(mvlcomsumd) = ekdeimehmk xgoqrslpnd (vzczcivbcv ) View more
NCT05384587 (ASC2ESCALATE, ASH2025)	Phase 2	Philadelphia chromosome-positive chronic myeloid leukemia in chronic phase First line	95	Asciminib (ASC)	ayjrzqecck(nlrgekszlr) = dtckchjawe uqsumtrapr (kupdmoyggf ) View more	Positive	06 Dec 2025
ASH2025	Not Applicable	Chronic Myelogenous Leukemia	68	Asciminib	ldvlsygidn(aoypwoaljy) = gmvvhqehvv towhsfckou (cvbtzqfxfv ) View more	Negative	06 Dec 2025
				Asciminib (Somatic mutations (SM) presence)	qzbbrjuwvh(lddyvbrqfr) = poaaduntdl ldirgxtlbh (mdtlbjpmbr ) View more
NCT05384587 (ASC2ESCALATE, ASH2025)	Phase 2	Philadelphia chromosome-positive chronic myeloid leukemia in chronic phase	101	Asciminib (ASC) 80 mg QD	ijbqmlsrkc(xojpdxuvkr) = vtiovitllu lkjdjravps (zjswuusvyl ) View more	Positive	06 Dec 2025
NCT04971226 (ASC4FIRST, ASH2025)	Phase 4	Chronic phase chronic myeloid leukemia ASXL1 mutation	341	Asciminib	lzpprensgl(koowuymwmu) = tcxhvjbnqg misdhkltzh (dwskwvumot ) View more	Positive	06 Dec 2025
				Investigator-selected tyrosine kinase inhibitors (IS-TKI)	lzpprensgl(koowuymwmu) = kkopwmerrx misdhkltzh (dwskwvumot ) View more
NCT04971226 (ASC4FIRST, ASH2025)	Phase 3	Chronic phase chronic myeloid leukemia	501	Asciminib	pcpthpvhyw(sflrqkutqi): OR = 2.58 (95.0% CI, 1.67 - 3.98) View more	Positive	06 Dec 2025
				Dasatinib
ASH2025	Not Applicable	Chronic phase chronic myeloid leukemia Second line	392	Asciminib	wjogwixebe(embjjtmltz) = gdjsxxdjda tlqslmiaud (gpflsobcvk ) View more	Positive	06 Dec 2025
				ATP-competitive TKIs (dasatinib, nilotinib, bosutinib, imatinib)	wjogwixebe(embjjtmltz) = pftkmlztzq tlqslmiaud (gpflsobcvk ) View more
NCT04971226 (ASC4FIRST, ASH2025)	Phase 3	Chronic Myelogenous Leukemia	415	Asciminib	myietskqbb(yrdhdoieei) = dxzukzcjol xtwsuekont (bsjuvmwuwt ) View more	Positive	06 Dec 2025
				2G TKIs (dasatinib, nilotinib, bosutinib)	myietskqbb(yrdhdoieei) = konnzqmyqs xtwsuekont (bsjuvmwuwt ) View more

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