This phase II trial tests how well ziftomenib works in treating patients with NPM1 mutated or KMT2A rearranged acute myeloid leukemia (AML) and are not eligible to receive standard therapy. AML is often due to genetic changes in the cancer cells, including mutations in the NPM1 gene and rearrangements involving the KMT2A gene. These mutations result in activation of the menin pathway. Menin is a type of protein in the body that helps to regulate some of the naturally occurring processes in the body, but can also be involved in some types of cancers. Ziftomenib blocks this menin pathway and may prevent the cancer cells from continuing to grow. Giving ziftomenib may kill more cancer cells in patients with NPM1 mutated or KMT2A rearranged AML that are not eligible to receive standard therapy.

Start Date10 Apr 2026

Sponsor / Collaborator

Ohio State University Comprehensive Cancer Center

[+1]

NCT07507760

/ Not yet recruitingPhase 2IIT

A Phase II, Multicentre, Open Label Clinical Trial Evaluating the Efficacy and Safety of Oral Decitabine Plus Ivosidenib in Adult Patients With Newly Diagnosed Acute Myeloid Leukemia Older Than 60 Years Old and/or Who Are Ineligible for Standard Induction Chemotherapy

The goal of this clinical trial is to learn if the combination of oral decitabine plus ivosidenib works to treat naïve adult patients with acute myeloid leukemia (AML) with IDH1 R132 mutation older than 60 years old or those who are older than 18 years old with defined comorbidities that make them not suitable for standard induction therapy. The main objectives of this clinical trial are:
* Asses the Complete Remission (CR) and Complete Remission with incomplete marrow recovery (CRi) rates of this treatment.
* Determine the incidence and severity of all adverse events (AEs).
All participants will receive oral ivosidenib and oral decitabine in treatment cycles of 28 days until disease progression, lack of clinical benefit or the end of the study. Patients who achieve CR/CRi will be elegible to receive allogeneic stem cell transplantation.

Start Date01 Apr 2026

Sponsor / Collaborator-

NCT06871410

/ RecruitingPhase 1IIT

CD83 CAR T in Relapsed or Refractory Acute Myeloid Leukemia (AML): A Phase I Trial

This phase I trial tests the safety, side effects, and best dose of genetically engineered cells (CD83 chimeric antigen receptor [CAR] T cells) in treating patients with acute myeloid leukemia (AML) that has come back after a period of improvement (relapsed) or has not responded to previous treatment (refractory). CD83 is a protein that is found on AML blasts. Blasts are abnormal immature white blood cells that can multiply uncontrollably: filling up the bone marrow and preventing the production of other cells important for survival. CD83 CAR T cells represent a new cell therapy to eliminate AML blasts, while avoiding the risk for graft versus host disease (GVHD) after stem cell transplant to replace bone marrow or, tumor toxicity like myeloid aplasia where the body's own immune system causes damage to the bone marrow stem cells. Therefore, human CD83 CAR T cells are a promising cell-based approach to preventing two critical complications of stem-cell transplant - GVHD and relapse. Giving CD83 CAR T cells may be safe, tolerable, and/or effective in treating patients with relapsed or refractory AML.

Start Date02 Mar 2026

Sponsor / Collaborator

Roswell Park Comprehensive Cancer Center

100 Clinical Results associated with Hydroxycarbamide

100 Translational Medicine associated with Hydroxycarbamide

100 Patents (Medical) associated with Hydroxycarbamide

13,138

Literatures (Medical) associated with Hydroxycarbamide

01 Dec 2026·Molecular & general genetics : MGG

Impairment of ribosomes and DNA biosynthesis confers resistance to Inhibition of sphingolipid biosynthesis

Article

Author: Matsuzaki, Momoko ; Tani, Motohiro ; Kawaguchi, Takahiro ; Tabuchi, Mitsuaki ; Yamagata, Satomi ; Sugihara, Saki

Sphingolipids are essential components of eukaryotic membranes and play central roles in cellular growth and stress responses. In the budding yeast Saccharomyces cerevisiae, Lcb1 and Lcb2 constitute the serine palmitoyltransferase complex, which catalyzes the initial step of sphingolipid biosynthesis. Repression of LCB1 expression leads to inhibition of sphingolipid biosynthesis, resulting in severe growth defects. Here, we aimed to identify novel genes functionally associated with sphingolipid metabolism by screening for suppressor mutations that confer resistance to sphingolipid biosynthesis inhibition. To conditionally suppress sphingolipid biosynthesis, we employed a tetracycline-repressible promoter to control LCB1 expression. This screen revealed that deletion of SAC7, YTA7, RNR1, RPL23B, or RPL35A confers resistance to LCB1 repression. The suppressive effect of YTA7, RNR1, RPL23B, and RPL35A deletions was also observed under conditions in which growth inhibition was induced by repression of AUR1, a gene involved in the conversion of ceramides to complex sphingolipids. These genes encode proteins related to ribosomal subunits or DNA biosynthesis. Furthermore, sublethal concentrations of cycloheximide (a translation inhibitor), diazaborine (a ribosome maturation inhibitor), hydroxyurea (a DNA biosynthesis inhibitor), and zeocin (a DNA double-strand break inducer) alleviated growth defects caused by LCB1 repression. Diazaborine or hydroxyurea partly suppressed the decrease in complex sphingolipids induced by Lcb1 repression. Additionally, these treatments suppressed the reduction in Lcb1 and Aur1 protein expression levels. These findings reveal a previously unappreciated link between ribosome function, DNA biosynthesis, and sphingolipid metabolism and provide insight into how cells adapt to metabolic stress.

01 Sep 2026·Value in Health Regional Issues

Cost-Effectiveness of Hydroxyurea for Treatment of Children With Sickle Cell Anemia in Ghana

Article

Author: Chola, Lumbwe ; Asare, Brian ; Dias, Sinaï Francisco

OBJECTIVES:

Most African children born with sickle cell disease (SCD) will die before their fifth birthday. Hydroxyurea has proven therapeutic benefits for SCD yet remains inaccessible to many children in low- and middle-income countries. To inform policy on coverage and reimbursement, this study evaluates the cost-effectiveness of hydroxyurea for pediatric SCD in Ghana, compared with the standard of care.

METHODS:

We developed a Markov model of SCD progression, incorporating costs and effects from a Ghanaian payer perspective, over a 17-year time horizon. Outcomes were life-years gained and disability-adjusted life-years averted. Cost-effectiveness was determined using the World Health Organization willingness-to-pay threshold of 1 times the per-capita gross domestic product and an alternative country-specific threshold based on health opportunity cost ($580.52). One-way and probabilistic sensitivity analyses were undertaken. Costs and effects were discounted at 3% per annum.

RESULTS:

In the base case, the incremental cost-effectiveness ratio was $1440.34 per disability-adjusted life-year averted and $1823.89 per life-year gained. The intervention was potentially cost-effective using the World Health Organization threshold but not cost-effective using the alternative threshold. The 1-way sensitivity analysis highlighted the incremental cost-effectiveness ratio's sensitivity to price changes, emphasizing the importance of price negotiations.

CONCLUSIONS:

Hydroxyurea can provide substantial health benefits for Ghanaian children with SCD. The results provide a strong argument for the incorporation of hydroxyurea into the Ghana national health insurance benefits package. Future research should address the disparity in threshold outcomes and the need for country-specific data on the long-term effects and broader economic impact of hydroxyurea in Ghana.

01 May 2026·BLOOD CELLS MOLECULES AND DISEASES

Inflammatory markers in sickle cell disease during vaso-occlusive crisis

Article

Author: Meher, Kamal Kumar ; Mohanty, Pradeep Kumar ; Meher, Satyabrata

Sickle cell disease (SCD) is a monogenic blood disorder in which vaso-occlusive crises (VOC) are the main cause of hospitalization. Along with vascular adhesion, inflammation plays a central role in VOC. This study compared inflammatory and hematological markers in SCD patients during VOC and steady state, examined their association with outcomes such as hospital stay, acute chest syndrome (ACS), and mortality, and evaluated the impact of hydroxyurea. A total of 109 VOC patients admitted to the Department of General Medicine, VIMSAR, and 40 steady-state patients attending the outpatient clinic were included. Hematological (HbF, HbS, hemoglobin, WBC, neutrophils, platelets), biochemical (bilirubin, AST, ALT, urea, creatinine), and inflammatory markers (IL-6,CRP, ferritin, LDH, ESR) were measured. Data were analyzed using GraphPad Prism; comparisons were made by unpaired t-test and correlations by Pearson analysis. VOC patients showed significantly lower hemoglobin and higher WBC and neutrophil counts compared to controls. Inflammatory markers were markedly elevated during VOC: IL-6 (41.95 vs2.1 pg/mL), CRP (61.34 vs3.2 mg/L), ferritin (847.6 vs116.7 ng/mL), and LDH (1151.7 vs719.5 U/L). Platelet count and ESR did not differ significantly. Hydroxyurea use was associated with lower inflammatory marker levels. Inflammation strongly influences VOC severity and outcomes, and hydroxyurea mitigates this effect. Routine monitoring of inflammatory markers may support predicting course and management in SCD.

240

News (Medical) associated with Hydroxycarbamide

18 Mar 2026

·www.edisononcology.com

Edison Oncology to Present Two Posters at the 2026 AACR Annual Meeting

Preclinical data for EO1001 an orally bioavailable, irreversible pan-ErbB inhibitor targeting EGFR extracellular domain (ECD) mutant solid tumors. Preclinical data for EO4426 (tezacitabine), an orally bioavailable brain-penetrant, dual inhibitor of DNA polymerase alpha (Pol α) and ribonucleotide reductase (RNR), targeting CDA-mediated resistance in solid tumors and mesenchymal GBM. Presentations’ highlight – Edison Oncology’s expanding precision oncology pipeline focused on biomarker-directed therapies for molecularly-defined patient populations with significant unmet need. MENLO PARK, CA / ACCESS Newswire / March 18, 2026 / Edison Oncology Holding Corp. (“Edison Oncology” or the “Company”) today announced the presentation of two posters at the upcoming American Association for Cancer Research (AACR) Annual Meeting 2026, taking place April 17-22, in San Diego, California. The presentations showcased Edison Oncology’s advancements in precision oncology, including EO1001, an irreversible pan-ErbB TKI with CNS penetration, and EO4426, a brain-penetrant dual inhibitor of DNA polymerase alpha (Pol α) and ribonucleotide reductase (RNR). “We are pleased to present these two programs at the AACR Annual Meeting, which together reflect Edison Oncology’s focus on developing biomarker-directed oncology targeted therapies for molecularly-defined patient populations with significant unmet need,” said Jeffrey A. Bacha, Chief Executive Officer, Edison Oncology Holding Corp. “EO1001 addresses the critical gap in treatment for EGFR extracellular domain mutant cancers and is currently being evaluated in clinical studies, while EO4426 targets the CDA-mediated resistance mechanisms that limit the efficacy of current cytidine-based therapies.” EO1001 EGFR extracellular domain (ECD) mutations, including EGFRvIII, A289 substitutions, R108 variants, and related structural alterations, drive ligand-independent EGFR activation and highly aggressive tumor biology. These mutations occur in head and neck, lung, and gastrointestinal cancers and glioblastoma (GBM), where they are associated with therapeutic resistance and poor patient outcomes. EGFR-ECD mutations are generally resistant to approved EGFR TKIs, including osimertinib, erlotinib, gefitinib, and afatinib, because the structural alterations lie outside the ATP-binding pocket and may preserve receptor signaling despite drug engagement. EO1001 is an orally bioavailable, irreversible pan-ErbB inhibitor designed to inhibit signaling from both wild-type and structurally altered ErbB receptors. Early signals of clinical activity in EGFR-ECD mutant GBM patients have been observed in an ongoing Phase 1-2a study (ANZCTR: ACTRN12620000583943), underscoring the need for mechanistic validation. To further investigate this, Edison Oncology initiated a focused, preclinical program assessing EO1001 activity in patient derived xenograft (PDX) tumor models harboring clinically relevant EGFR-ECD variants. Preliminary preclinical data from the program will be presented at the AACR Annual Meeting. This preclinical program will further explore mechanisms of EO1001’s activity in EGFR-ECD mutant cancers, providing support for biomarker-guided clinical development. EO4426 EO4426 (tezacitabine) is a novel brain-penetrant, deamination-resistant, cytidine analog that exhibits dual inhibition of both DNA polymerase-α (Polα) and ribonucleotide reductase (RNR), resulting in depletion of deoxynucleotide pools, replication-fork collapse, and accumulation of DNA damage in rapidly proliferating tumor cells. Unlike gemcitabine and hydroxyurea, EO4426 resists cytidine deaminase (CDA)-mediated inactivation. Tumors with high CDA expression such as mesenchymal GBM, TNBC, NSCLC, and ovarian cancer are predicted to exhibit heightened dependence on Polα/RNR function and may therefore be particularly susceptible to dual-targeting strategies. Prior nonclinical studies demonstrate that EO4426 retains activity in CDA-high tumor environments and is less susceptible to rapid deamination than gemcitabine. Historically, EO4426 has been evaluated in multiple third-party Phase I and Phase II trials, demonstrating a generally manageable safety profile with reversible myelosuppression reported as the principal dose-limiting toxicity and evidence of clinical activity in heavily pretreated solid-tumor populations. New data are being developed to support further investigation of EO4426 in biomarker guided clinical development strategies for CDA-high solid tumors. Preliminary results of these ongoing non-clinical studies will be presented at the meeting. Additional details on key presentations at AACR are available below and further information on the AACR Annual Meeting 2026 is available here. Title: Preclinical evaluation of EO1001 in EGFR-ECD mutant solid tumor models: Toward biomarker-directed therapy Date/Time: Tuesday April 21, 2026, 2:00-5:00PM PT Session: Poster, Experimental and Molecular Therapeutics, Tyrosine Kinase, Phosphatase, and Other Inhibitors Abstract Number: 5889 Title: Overcoming cytidine deaminase (CDA) mediated resistance via EO4426 dual DNA-replication targeting: Implications for CDA-high solid tumors and mesenchymal GBM Date/Time: Wednesday April 22, 2026, 9:00AM – noon PT Session: Poster, Experimental and Molecular Therapeutics, Novel Antitumor Agents Abstract Number: 7102 About Edison Oncology Holding Corp. Edison Oncology Holding Corp. is a clinical-stage biopharmaceutical company developing a pipeline of first-in-class, small-molecule, biomarker-driven therapies designed to overcome key resistance mechanisms and address critical unmet needs in aggressive and underserved cancers. Leveraging existing clinical data and a modern understanding of cancer biology, the Edison Oncology focuses on genetically defined cancers, advancing its programs through a capital-efficient combination of internal development and strategic partnerships while retaining meaningful development and commercial rights. To learn more, please visit https://www.edisononcology.com/ and follow us for updates on LinkedIn. Contact Hayden IR Brett Maas (646) 536-7331 brett@haydenir.com or James Carbonara (646)-755-7412 james@haydenir.com SOURCE: Edison Oncology Holding Corp. View Original Press Release Here Edison Oncology to Present Two Posters at the 2026 AACR Annual Meeting Society for NeuroOncology: EO-4426: A Brain-Penetrant Dual DNA Polymerase α and Ribonucleotide Reductase Inhibitor for High-Grade Gliomas and Other Aggressive Cancers

Phase 1AACR

04 Mar 2026

·www.fiercepharma.com

Sanofi strikes $1.5B global licensing deal for Sino Biopharm's first-in-class JAK/ROCK asset

Sanofi’s interest in rovadicitinib, or the drug’s “core value” on the global market, is driven by its potential in chronic graft-versus-host disease, according to Sino Biopharmaceutical. Sanofi is betting $1.53 billion on a novel drug from Sino Biopharmaceutical, securing global rights to a first-in-class JAK/ROCK inhibitor that could play a double role in the French pharma’s hematology and immunology pipeline.Sanofi will pay $135 million upfront to Sino Biopharm’s subsidiary Chia Tai Tianqing Pharmaceutical to bag exclusive rights to the Chinese company’s rovadicitinib, according to a securities filing (PDF).Beyond the initial payment, Sanofi has pledged up to $1.395 billion in potential development, regulatory and sales milestones as well as up to double-digit tiered royalties based on net sales of rovadicitinib. The oral drug is the first inhibitor that targets both JAK and ROCK to achieve anti-inflammation and anti-fibrosis effects. In February, rovadicitinib received its first approval from Chinese authorities for the treatment of patients with certain forms of myelofibrosis, a rare blood cancer. While the initial approval focuses on myelofibrosis, Sanofi’s interest, or the drug’s “core value” on the global market, is driven by its potential in chronic graft-versus-host disease (cGVHD), according to Sino Biopharm. In cGVHD, a phase 3 study is already underway in China, and the FDA has cleared the drug to enter phase 2 trials in the U.S. “Through this partnership, Sanofi—a global leader in vaccines, immunology, and rare diseases—will leverage its global clinical and commercial infrastructure to unlock rovaciditinib’s international potential and maximize its long-term value,” Sino Biopharm said in a March 4 release (local time) provided to Fierce Pharma.The deal marks another addition to Sanofi’s specialty care business, drawing parallels to the company’s recent acquisition of Blueprint Medicines. That 2025 deal, worth up to $9.5 billion, gave Sanofi Ayvakit, a commercial product for the rare blood disorder systemic mastocytosis (SM), plus a next-generation SM candidate and an early-stage KIT inhibitor that has potential in immunology indications. Rovadicitinib, by inhibiting the JAK1/2-STAT3/5 signaling pathway, reduces inflammatory cytokines produced by myeloid cells to alleviate abnormal enlargement of the spleen and systemic inflammatory symptoms. Simultaneously, by inhibiting ROCK1/2, the drug lowers overactivated helper T cells and enhances the function of regulatory T cells, further enhancing its anti-inflammatory effect, according to Sino Biopharm.In a trial undertaken in China, rovadicitinib showed better spleen responses than hydroxyurea did in patients with intermediate-2 or high-risk myelofibrosis. At Week 24, 58% of patients who took rovadicitinib achieved at least a 35% reduction in spleen volume compared with baseline, versus 23% for the hydroxyurea group. In terms of the proportion of patients who achieved at least a 50% reduction in total symptom score in myelofibrosis at Week 24, the rate was 61% in the rovadicitinib group, versus 46% in the comparator arm. As to the drug’s potential in cGVHD. Phase 1b/2a data released a year ago showed a best overall response rate of 86.4% among 44 patients who took two different dosages of rovadicitinib. The 12-month failure-free survival rate was 85.2%, which Sino Biopharm noted is “significantly superior to approved therapies.”In terms of safety, investigators reported that the drug was “well tolerated” with no dose-limiting toxicity and that no drug-related adverse events led to discontinuation. For Sino Biopharm, the Sanofi deal marks the first significant innovative drug out-licensing project the company has signed with a Big Pharma company in recent years. More than 10 years ago, Chia Tai Tianqing Pharmaceutical had partnered with Johnson & Johnson on a treatment for hepatitis B, a disease area the U.S. pharma is no longer interested in. More recently, the Chinese pharma giant has out-licensed drugs to smaller Western biotechs. In January, another Sino Biopharm subsidiary, Chia Tai Feng Hai Pharmaceutical, penned a deal transferring ex-China rights to an autoimmune candidate targeting miR-124 to artificial-intelligence-fueled Formation Bio. Licensing drug projects from Chinese companies have become commonplace among Western biopharmas these days. The number of cross-border licensing deals of drugs developed by Chinese biotechs increased from 42 in 2022 to 93 in 2025, according to data by Evaluate. As is the case for the Formation Bio deal, most Chinese firms would carve out their own country in their licensing agreements. But, as Sino Biopharm noted, the Sanofi deal represents a rare case, in which an established Chinese pharma company sells the full rights for a late-stage or commercial asset.As a large pharma company with 2025 half-year revenue of 17.6 billion Chinese yuan (about $2.6 billion), Sino Biopharm itself has been quite acquisitive as its chairwoman Theresa Tse puts an increased emphasis on innovative drugs. Last year, Sino Biopharm bought Merck & Co.’s PD-1xVEGF partner LaNova Medicines in a deal worth up to $951 million. Then, in January, the company unveiled a deal to acquire Hangzhou Hygieia Pharmaceuticals for 1.2 billion yuan (about $175 million) to gain a small interfering RNA platform.

License out/inDrug ApprovalClinical ResultPhase 3Acquisition

04 Mar 2026

·firstwordpharma.com

Sanofi taps Sino Biopharm unit for oral JAK/ROCK inhibitor

Sanofi is paying $135 million upfront for exclusive rights to develop and commercialise Chia Tai Tianqing Pharmaceutical's experimental oral JAK/ROCK inhibitor rovadicitinib. The deal — disclosed in a regulatory filing by the Chinese company's parent Sino Biopharmaceutical — includes further milestones of up to $1.395 billion, as well as up to double-digit tiered sales royalties.Last month, rovadicitinib gained approval in China under the name Anxu for the first-line treatment of adults with intermediate-2 or high-risk primary myelofibrosis (MF), post-polycythemia vera MF or post-essential thrombocythemia MF. The clearance was supported by findings from a Phase II study, in which rovadicitinib demonstrated superior efficacy compared to hydroxyurea in patients with intermediate-2 or high-risk MF.Results showed that 58.33% of patients given rovadicitinib achieved a ≥35% reduction in spleen volume (SVR35) at week 24 compared with baseline and 63.89% achieved SVR35 at any time point, with an average SVR35 duration of 8.31 months. Sino Biopharm noted that the best ≥50% reduction in total symptom score (TSS50) rate was 77.78% in the rovadicitinib group. The small molecule drug is also being investigated in a Phase III trial in China for the treatment of chronic graft-versus-host disease, having demonstrated superior 12-month failure-free survival and enhanced responses in fibrosis-dominated organs compared to other approved therapies in earlier studies. In the US, rovadicitinib has been cleared to start Phase II development. According to Sino Biopharm, rovadicitnib exerts synergistic anti-inflammatory and anti-fibrotic effects through a dual mechanism of action. The drug targets the JAK/STAT pathway to directly suppress inflammatory signalling, while inhibiting the ROCK pathway modulates STAT3/STAT5 phosphorylation to downregulate overactivated T-helper cells and enhance the function of regulatory T-cells, restoring immune homeostasis.

Clinical ResultDrug ApprovalPhase 3License out/inPhase 2

100 Deals associated with Hydroxycarbamide

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KEGG	Wiki	ATC	Drug Bank
D00341	Hydroxycarbamide	L01XX05	DB01005

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Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Polycythemia Vera	Japan	Clinigen KK	25 Mar 2013
Polycythemia Vera	Japan	Bristol-Myers Squibb KK	25 Mar 2013
Vaso-occlusive crisis	European Union	Theravia SAS	29 Jun 2007
Vaso-occlusive crisis	Iceland	Theravia SAS	29 Jun 2007
Vaso-occlusive crisis	Liechtenstein	Theravia SAS	29 Jun 2007
Vaso-occlusive crisis	Norway	Theravia SAS	29 Jun 2007
Chronic Myelogenous Leukemia	Japan	CHEPLAPHARM Arzneimittel GmbH	03 Jul 1992
refractory chronic myelocytic leukemia	Japan	Clinigen KK	03 Jul 1992
Thrombocythemia, Essential	Japan	Clinigen KK	03 Jul 1992
Head and Neck Neoplasms	China	Sinopharm Group Co., Ltd.	01 Jan 1981
Kidney Neoplasms	China	Sinopharm Group Co., Ltd.	01 Jan 1981
Melanoma	China	Sinopharm Group Co., Ltd.	01 Jan 1981
Philadelphia chromosome positive chronic myelogenous leukemia	China	Sinopharm Group Co., Ltd.	01 Jan 1981
Squamous Cell Carcinoma of Head and Neck	China	Sinopharm Group Co., Ltd.	01 Jan 1981
Anemia, Sickle Cell	United States	Waylis Therapeutics LLC	07 Dec 1967
Pain	United States	Waylis Therapeutics LLC	07 Dec 1967

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Albuminuria	Phase 2	Côte d'Ivoire	Theravia SAS	28 May 2019
Albuminuria	Phase 2	France	Theravia SAS	28 May 2019
Albuminuria	Phase 2	Guadeloupe	Theravia SAS	28 May 2019
Albuminuria	Phase 2	Mali	Theravia SAS	28 May 2019
Albuminuria	Phase 2	Martinique	Theravia SAS	28 May 2019
Albuminuria	Phase 2	Senegal	Theravia SAS	28 May 2019
Beta-Thalassemia	Phase 2	Jamaica	Nova Laboratories Ltd.	03 Jan 2019
Beta-Thalassemia	Phase 2	United Kingdom	Nova Laboratories Ltd.	03 Jan 2019
Hemoglobin SC Disease	Phase 2	Jamaica	Nova Laboratories Ltd.	03 Jan 2019
Hemoglobin SC Disease	Phase 2	United Kingdom	Nova Laboratories Ltd.	03 Jan 2019

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT00305175 \| NCT01966731 \| NCT01976416 \| NCT02556099 \| NCT02286154 (EXTEND, Pubmed \| Blood Adv)	Not Applicable	Anemia, Sickle Cell	451	Hydroxyurea (United States)	bsmhbquyzs(zvdjqoyhln) = crmwgwmoqa afobemqybv (uxjeunrihe, 5.9)	Positive	27 Jan 2026
				Hydroxyurea (Africa)	bsmhbquyzs(zvdjqoyhln) = lodiwjdomn afobemqybv (uxjeunrihe, 6.5)
NCT05451940 (ACHiEvE-SCD, CTgov)	Phase 1/2	Anemia, Sickle Cell	17	Epoetin Alfa+Hydroxyurea	wfuexbesmm = cqfdcfbxjq uzpkpypcgs (thnmymcrgb, kywgwgtmmj - uzhnrgrrfm) View more	-	07 Jan 2026
PACTR202108893981080 (PIVOT, ASH2025)	Phase 2	Hemoglobin SC Disease	198	Hydroxyurea (Siklos)	mhnobztlvb(trnfazffin) = jayssjvemt cejizkmohg (bthpttuquy ) View more	Positive	06 Dec 2025
				Placebo	wjjfcybqif(qlamjosbvg) = bjocebjlrg iyaednenwe (ipvjzszxbx )
NCT05285917 (PUSH-UP, ASH2025)	Phase 3	Anemia, Sickle Cell	400	Hydroxyurea with PK-guided dosing	wkeusgltis(tfrgoomojq) = uxmuoticqi whiwuftvlb (qhjdvdmhkg, 3.1) View more	Positive	06 Dec 2025
				Hydroxyurea with weight-based dosing	zccwmxgjwu(ssnjdcwwoy) = pxbtjwplgc essvfcwmhk (hfprxgcbqb, 1.8)
NCT01966731 (REACH, ASH2025)	Phase 1/2	Anemia, Sickle Cell	606	Hydroxyurea	luwmzhssws(yepgrkpifm) = ejuyivifzt ikguqtxkvt (yyaxhdcwuy ) View more	Positive	06 Dec 2025
ASH2025	Not Applicable	-	193	Hydroxyurea (HU)	wwbyelallp(dmtfhwprof) = bzocenhcrx iaqvnhcdpw (wyzwelxgoc ) View more	Positive	06 Dec 2025
ASH2025	Not Applicable	Hemoglobin SC Disease	263	Hydroxyurea	beisqbkcuy(gldclpisas) = qkhoqdnmtm xkdwpiqgav (qgafjjdysa, 0.84) View more	Positive	06 Dec 2025
NCT02214407 (dacota, ASH2025)	Phase 3	Chronic Myelomonocytic Leukemia AMC \| WBC	170	Decitabine (DAC)	jgoxkrdsrx(wdnqzhldox) = kfqkxxsotz mwvkfalrmh (xlgpznauqm ) View more	Positive	06 Dec 2025
				Hydroxyurea (HY)	jgoxkrdsrx(wdnqzhldox) = eboxcgwvtw mwvkfalrmh (xlgpznauqm ) View more
SITC2025	Not Applicable	Beta-Thalassemia	31	hydroxyureathalidomide + hydroxyureathalidomide	mjzjkfuyqy(lvnpqssymn) = classified grade 3 and 4 toxicities as per CTCAE guidelines cundsogrpq (rllkozxpxj )	Positive	05 Nov 2025
ESMO2025	Not Applicable	Meningioma	92	Hydroxyurea	dghfyeemhh(htsiohmkiv) = kenthbfzhm jateybwaqv (ycjaizzerk, 3.73 - 11.1)	Positive	17 Oct 2025
				Bevacizumab	fvuqsbtzvc(pshwyiwpgd) = dwtuwlgxzj cyowwoccgr (bdpuaqzjqd, 98.2 - NaN) View more

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