JSP191 for Myelodysplastic Syndrome
Recruiting in Palo Alto (17 mi)
+1 other location
Age: 18+
Sex: Any
Travel: May Be Covered
Time Reimbursement: Varies
Trial Phase: Phase 1
Waitlist Available
Sponsor: Jasper Therapeutics, Inc.
No Placebo Group
Trial Summary
What is the purpose of this trial?This trial is testing a new drug called JSP191 to see if it is safe and effective for patients with Low-Risk Myelodysplastic Syndromes who need regular blood transfusions or have low blood cell counts. The goal is to find out if JSP191 can improve their blood cell counts and reduce their need for transfusions.
Do I have to stop taking my current medications for the JSP191 trial?
The trial protocol does not specify whether you need to stop taking your current medications. Please consult with the study team for guidance.
What data supports the idea that JSP191 for Myelodysplastic Syndrome (also known as: JSP191, AMG 191) is an effective treatment?
The available research does not provide specific data on JSP191 for Myelodysplastic Syndrome. Instead, it discusses other treatments and the challenges in developing effective therapies for MDS. The research highlights the need for new therapeutic targets and mentions other drugs like luspatercept and imetelstat that are being tested for MDS. Without specific data on JSP191, we cannot compare its effectiveness to other treatments for this condition.
12345What safety data exists for JSP191 treatment for Myelodysplastic Syndrome?
The provided research does not contain specific safety data for JSP191 or AMG 191 in the treatment of Myelodysplastic Syndrome. The studies focus on other treatments and therapeutic advances for MDS, but do not mention JSP191 or AMG 191.
26789Eligibility Criteria
This trial is for adults over 18 with low to intermediate-risk Myelodysplastic Syndrome (MDS) who have symptoms like anemia or bleeding. Women able to have children must use effective birth control, and men too, during the study and for 3 months after. Participants need to understand and agree to the study's requirements.Inclusion Criteria
I am a man who is either surgically sterile or willing to use contraception.
Women of childbearing potential (WOCBP) must agree to use a specified form of contraception
I have low blood counts causing symptoms.
+4 more
Exclusion Criteria
I am pregnant or nursing and do not want to stop breastfeeding.
I have had a stem cell transplant before.
I have a history of HIV or active hepatitis B or C.
+3 more
Participant Groups
The trial is testing JSP191 (Briquilimab) as a second-line treatment for MDS. It's in Phase 1, which means it's early in testing and focuses on how safe it is and what doses are tolerable when given to people.
1Treatment groups
Experimental Treatment
Group I: JSP191Experimental Treatment1 Intervention
This study will explore up to 5 ascending dose levels (Cohorts 1, 2, 3, 4, and 5) and subjects will receive JSP191 on Day 1 on each 8-week cycle for 4 consecutive cycles.
Find a Clinic Near You
Research Locations NearbySelect from list below to view details:
Memorial Healthcare SystemHollywood, FL
Moffitt Cancer CenterTampa, FL
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Who Is Running the Clinical Trial?
Jasper Therapeutics, Inc.Lead Sponsor
References
Evolving therapies for lower-risk myelodysplastic syndromes. [2020]The development in the therapeutic landscape of myelodysplastic syndromes (MDS) has substantially lagged behind other hematologic malignancies with no new drug approvals for MDS for 13 years since the approval of decitabine in the United States in 2006. While therapeutic concepts for MDS patients continue to be primarily defined by clinical-pathologic risk stratification tools such as the International Prognostic Scoring System (IPSS) and its revised version IPSS-R, our understanding of the genetic landscape and the molecular pathogenesis of MDS has greatly evolved over the last decade. It is expected that the therapeutic approach to MDS patients will become increasingly individualized based on prognostic and predictive genetic features and other biomarkers. Herein, we review the current treatment of lower-risk MDS patients and discuss promising agents in advanced clinical testing for the treatment of symptomatic anemia in lower-risk MDS patients such as luspatercept and imetelstat. Lastly, we review the clinical development of new agents and the implications of the wider availability of mutational analysis for the management of individual MDS patients.
Emerging Therapies for the Myelodysplastic Syndromes. [2023]Despite considerable advances in our understanding of the molecular and epigenetic underpinnings of the myelodysplastic syndromes (MDS), this diverse group of myeloid neoplasms remains a significant clinical challenge. Considerable barriers to timely development of effective therapy include the diverse molecular landscape encountered in MDS patients, the difficulty in translating specific molecular aberration into a clinically meaningful animal model, as well as challenges in patient recruitment into clinical trials. These speak to the need to discover efficacious novel therapeutic targets which would in turn translate into improved patient outcomes in terms of both survival and quality of life. In this review, we outline recently published data pertaining to therapeutic advances in TGF-β pathway inhibition, STAT3, Hedgehog signaling, and additional therapeutic venues being actively explored in MDS.
Targeting the Myeloid Lineages and the Immune Microenvironment in Myelodysplastic Syndromes: Novel and Evolving Therapeutic Strategies. [2022]To discuss the recent and emerging data for novel targeted therapies in myelodysplastic syndromes (MDS).
Meeting report: myelodysplastic syndromes at ASH 2007. [2018]Myelodysplastic syndromes (MDS) remain challenging to both clinicians and biologists. This year's edition of the Annual Meeting of the American Society of Hematology has provided several breakthroughs in the biology and therapeutics of MDS, such as uncovering of the molecular genetics of the 5q- syndrome and clear evidence of a survival advantage with a hypomethylating agent in high-risk MDS. We summarize those advances and delineate some perspectives for these diseases.
New strategies in myelodysplastic syndromes: application of molecular diagnostics to clinical practice. [2021]An increasingly complete compendium of recurrently mutated genes in myelodysplastic syndromes (MDS) has been defined, and the application of massively parallel sequencing to identify mutations in clinical practice now promises to improve the care of patients with this disease. More than 25 recurrent MDS-associated somatic mutations have been identified, involving biologic pathways as diverse as chromatin remodeling and pre-mRNA splicing. Several of these mutations have been shown to have prognostic implications that are independent of existing risk stratification systems based on clinical and pathologic parameters. Application of these recent discoveries to diagnosis, prognosis, risk stratification, and treatment selection for patients with MDS has the potential to improve patient outcomes. Here, we review recent advances in MDS and discuss potential applications of these discoveries to clinical practice.
Novel agents for myelodysplastic syndromes. [2022]There have been several advances in the field of myelodysplastic syndromes over the past year, yielding two new US Food and Drug Administration drug approvals. The pharmacology, pharmacokinetics, clinical trials, therapeutic use, adverse effects, clinical use controversies, product description, and upcoming trials for myelodysplastic syndromes novel agents luspatercept-aamt and decitabine/cedazuridine are reviewed.
Myelodysplastic syndromes in children. [2019]Myelodysplastic syndromes (MDSs) are rare disorders in children, showing peculiar clinical manifestations and biological features. This review will summarize biological, genetic and clinical features of childhood MDS and will provide an update of the algorithm of treatment of the different disease variants.
Immunosuppressive Therapy: Exploring an Underutilized Treatment Option for Myelodysplastic Syndrome. [2021]Immunosuppressive therapy (IST) in low risk myelodysplastic syndrome (MDS) is known to achieve hematologic improvement but remains an underutilized treatment option. We report our experience using antithymocyte globulin (ATG) and cyclosporine A (CSA) to explore clinical predictive response factors.
Phase II pilot study of oral dasatinib in patients with higher-risk myelodysplastic syndrome (MDS) who failed conventional therapy. [2015]Given evidence for the role of Src family kinases, especially Lyn kinase, in myeloblast proliferation and the in vitro inhibitory activity of dasatinib on Src and Lyn, we conducted a phase II study to assess overall response to 100mg/day dasatinib in patients with higher-risk myelodysplastic syndrome (MDS), chronic myelomonocytic leukemia, or acute myeloid leukemia arising from MDS and who had failed prior treatment with azanucleoside analogs. Among 18 patients treated, 3 responded, 4 had stable disease, and 10 experienced disease progression. Toxicities were limited and consistent with previous reports. Dasatinib appears to be safe but with limited efficacy.
[Clinical analysis of 28 cases of pediatric myelodysplastic syndrome]. [2013]To explore the clinical features, diagnosis and treatment of pediatric myelodysplastic syndrome (MDS).
Genome-wide analysis of myelodysplastic syndromes. [2019]Myelodysplastic syndromes (MDS) are heterogeneous hematopoietic neoplasms characterized by ineffective hematopoiesis and a risk for progression to acute myeloid leukemia. A number of cytogenetic changes have been described that are characteristic to MDS and of clinical relevance; the specific gene targets of these alterations were largely unknown. On the other hand, over the past decade, technologies have been dramatically improved to enable high-throughput analysis of entire MDS genomes, leading to identification of frequent copy number neutral events and a number of novel gene targets implicated in the pathogenesis of MDS. In this review, we briefly overview the recent progress in the genetics of MDS, focusing on the newly identified gene targets in MDS.
The Genetics of Myelodysplastic Syndromes: Clinical Relevance. [2022]Myelodysplastic syndromes (MDS) are a clonal disease arising from hematopoietic stem cells, that are characterized by ineffective hematopoiesis (leading to peripheral blood cytopenia) and by an increased risk of evolution into acute myeloid leukemia. MDS are driven by a complex combination of genetic mutations that results in heterogeneous clinical phenotype and outcome. Genetic studies have enabled the identification of a set of recurrently mutated genes which are central to the pathogenesis of MDS and can be organized into a limited number of cellular pathways, including RNA splicing (SF3B1, SRSF2, ZRSR2, U2AF1 genes), DNA methylation (TET2, DNMT3A, IDH1/2), transcription regulation (RUNX1), signal transduction (CBL, RAS), DNA repair (TP53), chromatin modification (ASXL1, EZH2), and cohesin complex (STAG2). Few genes are consistently mutated in >10% of patients, whereas a long tail of 40-50 genes are mutated in <5% of cases. At diagnosis, the majority of MDS patients have 2-4 driver mutations and hundreds of background mutations. Reliable genotype/phenotype relationships were described in MDS: SF3B1 mutations are associated with the presence of ring sideroblasts and more recent studies indicate that other splicing mutations (SRSF2, U2AF1) may identify distinct disease categories with specific hematological features. Moreover, gene mutations have been shown to influence the probability of survival and risk of disease progression and mutational status may add significant information to currently available prognostic tools. For instance, SF3B1 mutations are predictors of favourable prognosis, while driver mutations of other genes (such as ASXL1, SRSF2, RUNX1, TP53) are associated with a reduced probability of survival and increased risk of disease progression. In this article, we review the most recent advances in our understanding of the genetic basis of myelodysplastic syndromes and discuss its clinical relevance.
TET2 rs2454206, TET2 rs12498609 and ASXL1 rs3746609 single nucleotide polymorphisms in patients with myelodysplastic syndromes. [2021]To study the association between TET2rs2454206, TET2rs12498609 and ASXL1rs3746609 and Myelodysplastic syndromes (MDS), a total of 90 MDS patients and 143 healthy volunteers were included. The clinical data, bone marrow samples of patients and peripheral blood samples of volunteers were obtained. We found TET2rs2454206 G/A genotype, TET2rs12498609 G/C genotype and ASXL1rs3746609 A/G genotype in 13.3%, 11.1%, 10.1% MDS patients and in 42.7%, 22.4%, 23.8% healthy volunteers (P
Molecular analysis of myelodysplastic syndrome with isolated deletion of the long arm of chromosome 5 reveals a specific spectrum of molecular mutations with prognostic impact: a study on 123 patients and 27 genes. [2018]The only cytogenetic aberration defining a myelodysplastic syndrome subtype is the deletion of the long arm of chromosome 5, which, along with morphological features, leads to the diagnosis of myelodysplastic syndrome with isolated deletion of the long arm of chromosome 5. These patients show a good prognosis and respond to treatment such as lenalidomide, but some cases progress to acute myeloid leukemia; however, the molecular mutation pattern is rarely characterized. Therefore, we investigated a large cohort of 123 myelodysplastic syndrome patients with isolated deletion of the long arm of chromosome 5, diagnosed following the World Health Organization classifications 2008 and 2016, by sequencing 27 genes. A great proportion of patients showed no or only one mutation. Only seven genes showed mutation frequencies >5% (SF3B1, DNMT3A, TP53, TET2, CSNK1A1, ASXL1, JAK2). However, the pattern of recurrently mutated genes was comparable to other myelodysplastic syndrome subtypes by comparison to a reference cohort, except that of TP53 which was significantly more often mutated in myelodysplastic syndrome with isolated deletion of the long arm of chromosome 5. As expected, SF3B1 was frequently mutated and correlated with ring sider-oblasts, while JAK2 mutations correlated with elevated platelet counts. Surprisingly, SF3B1 mutations led to significantly worse prognosis within cases with isolated deletion of the long arm of chromosome 5, but showed a comparable outcome to other myelodysplastic syndrome subtypes with SF3B1 mutation. However, addressing genetic stability in follow-up cases might suggest different genetic mechanisms for progression to secondary acute myeloid leukemia compared to overall myelodysplastic syndrome patients.