2,405 Clinical Trials for Various Conditions
This is a first-in-human, multicenter, open-label, phase 1 study to evaluate the safety, PK, PD and preliminary efficacy of STX-0712 in patients with advanced CMML and AML for whom there are no further treatment options known to confer clinical benefit.
Chronic Myelomonocytic Leukemia, Chronic Myelomonocytic Leukemia (CMML), Chronic Myelomonocytic Leukemia-1, Chronic Myelomonocytic Leukemia-2, Refractory Chronic Myelomonocytic Leukemia, CMML, Acute Myeloid Leukemia, Acute Myeloid Leukemia (AML), Acute Myeloid Leukemia Post Cytotoxic Therapy, Acute Myeloid Leukemias, Refractory Acute Myeloid Leukemia (AML), Acute Monocytic Leukemia
The purpose of this research is to see how personal financial burden (financial toxicity) related to cancer affects the overall health and quality of life by evaluating the impact of systematic financial navigation in addition to standard financial distress interventions during cancer treatment.
Acute Myeloid Leukemia
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.
Acute Myeloid Leukemia
The researchers are doing this study to find out if an allogeneic hematopoietic stem cell transplant (HSCT) or maintenance therapy with azacitidine and venetoclax is more effective at keeping AML from coming back (relapsing).
Acute Myeloid Leukemia
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.
Recurrent Acute Myeloid Leukemia, Refractory Acute Myeloid Leukemia
This Phase 1, multicenter, open-label, dose escalation and dose optimization study is designed to assess the safety, tolerability, pharmacokinetics (PK), pharmacodynamics (PD), and preliminary clinical activity of AUTX-703 administered orally in subjects with advanced hematologic malignancies.
Relapsed Acute Myeloid Leukemia (AML), Refractory Acute Myeloid Leukemia (AML), Relapsed/Refractory AML, Relapsed Myelodysplastic Syndromes, Refractory Myelodysplastic Syndromes, Relapsed/Refractory (R/R) Acute Myeloid Leukemia (AML)
This is a first in human, multi center, open label, phase 1/1b study to evaluate the safety and preliminary efficacy of CER-1236 in patients with relapsed/refractory (R/R), measurable residual disease (MRD) positive acute myeloid leukemia (AML), or TP53mut disease.
AML, Acute Myeloid Leukemia, Refractory Acute Myeloid Leukemia
The goal of this clinical research study is to learn if metal detoxification (with calcium disodium edetate \[Ca-EDTA\] and dimercaptosuccinic acid \[DMSA\]) during standard therapy can help improve outcomes in patients with intermediate-risk, high-risk, or secondary AML compared to standard therapy alone. Researchers think lowering the level of metals found in the blood/bone marrow may help to control the disease and/or improve the response to chemotherapy.
Acute Myeloid Leukemia (AML)
The study is a Phase II clinical trial. Patients will receive intensity-modulated total marrow irradiation (TMI) at a dose of 9 Gray (Gy) with standard myeloablative fludarabine intravenous (IV) and targeted busulfan (FluBu4) conditioning prior to allogeneic hematopoietic stem cell transplant (HSCT). Graft-versus-host disease (GVHD) prophylaxis will include Cyclophosphamide on Day +3 and +4, tacrolimus, and mycophenolate mofetil.
Acute Myeloid Leukemia, Relapsed, Adult, Acute Myeloid Leukemia Refractory, Chronic Myeloid Leukemia - Accelerated Phase, Myelodysplastic Syndromes
This is a phase 1 dose escalation study to determine the safety of anti-FLT3 CAR-T in subjects with R/R AML. The primary objective is to assess safety. Up to 18 evaluable subjects will be enrolled. Evaluable subjects are defined as those who have received an infusion of HG-CT-1. Primary clinical objectives: i. Determine the safety of HG-CT-1 based on the proportion of subjects infused with HG-CT-1 who experience a dose limiting toxicity (DLT). Secondary clinical objectives: i. Estimate the efficacy of HG-CT-1 according to standard clinical response criteria for AML. ii. Estimate overall survival of evaluable subjects. iii. Estimate progression-free survival of evaluable subjects. iv. Estimate duration of response in evaluable subjects who achieve a response. Secondary scientific objectives: i. Describe the persistence and trafficking of HG-CT-1. ii. Describe HG-CT-1 bioactivity and its predictors.
Relapsed/refractory Acute Myeloid Leukemia (R/R AML)
The purpose of this study is as follows: 1. Determine whether people receiving the combination treatment of olutasidenib, venetoclax, and azacitidine have the same, more, or fewer side effects compared to the usual chemotherapy treatment that people with this condition receive. 2. Determine how well the combination treatment of olutasidenib, venetoclax, and azacitidine works compared to the usual chemotherapy treatment that people with this condition receive.
Acute Myeloid Leukemia, IDH1 Mutation
The purpose of this study is to find out if azacitidine and venetoclax are an effective treatment approach to get rid of or lower measurable residual disease (MRD) in people with acute myeloid leukemia (AML) who have received standard chemotherapy and are planning to have an allogeneic hematopoietic stem cell transplant (HSCT). Allogeneic HSCT, sometimes called a bone marrow transplant, involves receiving healthy blood-forming cells (stem cells) from a donor in order to replace the patient's immune system and lower the chances of the disease returning (relapse).
Acute Myeloid Leukemia (AML)
The goal of this all-oral combination is to deliver safe and effective therapy for the largest portion of AML subtypes (NPM1mt, KMT2Ar, NUP98r \~ 40-45%).
Acute Myeloid Leukemia
Phase I, open-label study to assess the safety, feasibility, pharmacokinetics, and preliminary efficacy of CART123 cells given in combination with ruxolitinib in patients with relapsed or refractory acute myeloid leukemia (AML). All subjects will receive a single infusion of CART123 cells following ruxolitinib administration and lymphodepletion. Ruxolitinib dosing will begin at initiation of lymphodepleting chemotherapy (Day -6 ±1d) and continue for up to 14 days post CART123 administration.
Relapsed AML, Refractory AML
This phase I trial tests safety, side effects, and best dose of AOH1996 alone or in combination with venetoclax with or without azacitidine for the treatment of patients with acute myeloid leukemia (AML) that has come back after a period of improvement (relapsed) or AML that has not responded to previous treatment (refractory). AOH1996 is in a class of medications called PCNA inhibitors. It inhibits cancer growth and induces deoxyribonucleic acid (DNA) damage. This may help keep cancer cells from growing and damage cancer cell DNA. Venetoclax is in a class of medications called B-cell lymphoma-2 (BCL-2) inhibitors. It may stop the growth of cancer cells by blocking BCL-2, a protein needed for cancer cell survival. Azacitidine is in a class of medications called demethylation agents. It works by helping the bone marrow to produce normal blood cells and by killing abnormal cells in the bone marrow. Giving AOH1996 alone or in combination with venetoclax with or without azacitidine may be safe, tolerable and/or effective in treating patients with AML.
Recurrent Acute Myeloid Leukemia, Refractory Acute Myeloid Leukemia
The objective of this study to evaluate the safety, tolerability, pharmacokinetic profile, and preliminary efficacy of BL-M11D1 in patients with relapsed/refractory acute myeloid leukemia.
Relapsed/Refractory Acute Myeloid Leukemia
This clinical trial evaluates the effects of hemoglobin threshold-specific packed red blood cell (PRBC) transfusions on quality of life and functional outcomes in patients who have undergone chemotherapy or an allogeneic hematopoietic stem cell transplant for a high-grade myeloid neoplasm, acute myeloid leukemia, or B acute lymphoblastic lymphoma/leukemia. Some types of chemotherapy and stem cell transplants can induce low platelet counts and/or anemia that requires PRBC transfusions. Given critical shortages in blood supply, and risks associated with transfusion of PRBC, there has been much investigation into the "minimum" hemoglobin level that effectively balances safety and toxicity in patients. This clinical trial evaluates the effects of giving PRBC transfusions based on a more restrictive hemoglobin threshold (\> 7 gm/dL) compared to a more liberal hemoglobin threshold (\> 9 gm/dL) on quality of life and functional outcomes. A more restrictive threshold may be just as effective at maintaining patient quality of life and function while decreasing side effects from blood transfusions and helping to conserve blood supply resources.
Acute Myeloid Leukemia, B Acute Lymphoblastic Leukemia, B Lymphoblastic Lymphoma, Myeloid Neoplasm
This is a Phase 2 study of the study drug, ivosidenib (a mutant IDH1 inhibitor), compared to placebo, given to patients with IDH1-mutant acute myeloid leukemia (AML) after hematopoietic stem cell transplantation (HCT).
IDH1 Mutation, Acute Myeloid Leukemia (AML), Hematopoietic Stem Cell Transplant (HSCT)
This is a multicenter randomized controlled trial that assesses the efficacy of a decisional intervention \[University of Rochester-Geriatric Oncology assessment for Acute myeloid Leukemia (UR-GOAL)\] compared to an attention control.
Oncology, Myeloid Leukemia, Acute, Cancer
This is a phase I/2, interventional, open-label, multicenter study to assess the safety and efficacy of ARD103 in patients with relapsed or refractory acute myeloid leukemia or myelodysplastic syndrome.
Acute Myeloid Leukemia, in Relapse, Acute Myeloid Leukemia Refractory, MDS (Myelodysplastic Syndrome)
This trial will evaluate whether luveltamab tazevibulin is well tolerated and active against a rare form of AML carrying a particular genetic abnormality called CBFA2T3::GLIS2 that arises in infants and children. To be treated in this trial children must have a leukemia which did not respond or recurred after prior treatment. Luveltamab tazevibulin is an antibody-drug conjugate, which brings tazevibulin, an anticancer drug, to a molecule called FOLR1, present on the surface of CBFA2T3::GLIS2 AML cells.
Acute Myeloid Leukemia (AML)
This phase II MyeloMATCH treatment trial studies how well ASTX727 and venetoclax plus enasidenib works compared to ASTX727 and venetoclax alone for the treatment of older patients with newly diagnosed acute myeloid leukemia (AML) or younger patients who are considered unfit for standard treatment, and who have an abnormal change (mutation) in the IDH2 gene. This gene mutation can cause AML to grow and spread. This trial is being done to see if adding enasidenib to the usual treatment can help more patients with the IDH2 gene get rid of AML. Cedazuridine is in a class of medications called cytidine deaminase inhibitors. It prevents the breakdown of decitabine, making it more available in the body so that decitabine will have a greater effect. Decitabine is in a class of medications called hypomethylation agents. It works by helping the bone marrow produce normal blood cells and by killing abnormal cells in the bone marrow. Venetoclax is in a class of medications called B-cell lymphoma-2 (BCL-2) inhibitors. It may stop the growth of cancer cells by blocking Bcl-2, a protein needed for cancer cell survival. Enasidenib works by stopping the growth and spread of tumor cells that have the IDH2 mutation. Giving ASTX727 and venetoclax plus enasidenib may work better in treating AML patients with the IDH2 mutation.
Acute Myeloid Leukemia
This multicenter, open-label phase II study combines CLAG-based therapy with or without venetoclax in patients with relapsed or refractory (R/R) acute myeloid leukemia (AML) in order to improve measurable residual disease (MRD) clearance and event-free survival. Investigators hypothesize that the addition of venetoclax to CLAG-M in patients with relapsed or refractory AML is safe, and superior to CLAG-M alone in improving patient outcomes.
Relapsed or Refractory Acute Myeloid Leukemia (AML)
A multi-center, open-label, dose-finding study of five dose levels of APVO436 in combination with venetoclax and azacitidine (ven/aza) in adult patients with newly diagnosed, CD123+ AML.
Acute Myeloid Leukemia (AML)
This clinical research study is being done to answer questions about how to treat cancer. To clear cancer cells from the body, the immune system needs the action of proteins called Type 1 interferons. The protein STING (for STimulator of INterferon Genes) stimulates the body to make Type 1 interferons. Type 1 interferons activate key molecules in cancer immunity to kill cancer cells. CRD3874 is a synthetic drug that activates STING, and STING stimulates the immune system to kill cancer cells. In experiments on blood from humans, CRD3874 makes blood cells produce molecules responsible for anti-cancer activity. CRD3874 was tested in mice with cancers including leukemia, head and neck cancer, lung cancer, pancreatic cancer and sarcoma. In these mice, CRD3874 made tumors shrink or disappear, and some mice developed long-lasting immunity against cancer. Also, when CRD3874 was given with other anti-cancer treatments, it increased their anti-cancer effects.
Acute Myeloid Leukemia
A non-randomized phase Ib study of PC14586 (PMV therapeutics) in patients diagnosed with TP53Y220C-mutant myeloid malignancies, including AML and MDS.
Myelodysplastic Syndrome, Acute Myeloid Leukemia
This is a dose-finding study of oral zelenirstat (PCLX-001) in patients with R/R AML. There are two parts to the study: Dose Escalation and Dose Expansion.
Relapsed Adult AML
This phase I trial tests the safety, side effects, and best dose of FH-FOLR1 chimeric antigen receptor (CAR) T cells in treating pediatric patients with FOLR1+ acute myeloid leukemia (AML) that has come back after a period of improvement (recurrent) or has not responded to previous treatment (refractory). CAR T-cell therapy is a type of treatment in which a patient's T cells (a type of immune system cell) are changed in the laboratory so they will attack cancer cells. T cells are taken from a patient's blood. Then the gene for a special receptor that binds to a FOLR1 on the patient's cancer cells is added to the T cells in the laboratory. The special receptor is called a chimeric antigen receptor. Large numbers of the CAR T cells are grown in the laboratory and given to the patient by infusion for treatment of certain cancers. Chemotherapy drugs, such as fludarabine and cyclophosphamide, are given to a patient before the manufactured FH-FOLR1 CAR T cells are infused back into the patient to assist in the CAR T cell activity in the patient. The trial is evaluating if giving FH-FOLR1 CAR T cell therapy is safe and tolerable for pediatric patients with recurrent or refractory AML.
Recurrent Childhood Acute Myeloid Leukemia, Refractory Childhood Acute Myeloid Leukemia
This is a Phase I dose finding study of GTB-3650 (anti-CD16/IL-15/anti-CD33) Tri-Specific Killer Engager (TriKE®) for the treatment of select CD33-expressing refractory/relapsed myeloid malignancies in adults ≥ 18 years of age who are not a candidate for potentially curative therapy, including hematopoietic stem cell transplantation, and are refractory to, intolerant of, or ineligible for therapy options that are known to provide clinical benefit. The hypothesis is GTB-3650 TriKE will induce natural killer (NK) cell function by targeting malignant cells, as well as, CD33+ myeloid derived suppressor cells (MDSC) which contribute to a tumor induced immunosuppression. Because CD16 is the most potent activating receptor on NK cells, this single agent may induce a targeted antiCD33+ tumor response
Myeloid Malignancy, Acute Myeloid Leukemia, Myelodysplastic Syndromes
The purpose of this research is to see how certain genetic variations relate to side effects and outcomes experienced while receiving treatment with azacitidine and venetoclax.
Leukemia, Myeloid, Acute