About this trial
QH101 is an allogeneic TCR-enhanced Vδ2 T cell therapy product engineered to express BTN protein-specific binding elements on the cell surface. This innovative approach harnesses the natural cytotoxic capabilities of Vδ2 T cells while augmenting their ability to recognize BTN proteins, thereby significantly improving tumor cell elimination efficiency. Notably, QH101 is designed without co-stimulatory signal domains or the CD3ζ domain, which prevents T cell exhaustion from overactivation and effectively enhances in vivo persistence.
Patients with R/R AML face particularly poor prognoses, with conventional chemotherapy and targeted therapies achieving suboptimal complete remission rates and long-term survival below 10%. Similarly, R/R MDS patients typically demonstrate median overall survival of less than one year (with TP53-mutated cases showing even poorer outcomes of 3-6 months), making clinical trial participation the most viable therapeutic option.
The development of effective treatments for R/R AML/MDS presents significant challenges due to:1)The paucity of disease-specific molecular targets;2)The slow progress in drug development. Allogeneic γδ T-cell therapy featuring enhanced TCR functionality and multi-mechanism tumoricidal activity represents a promising investigational approach for addressing R/R AMLMDS. This innovative strategy combines the advantages of: 1)Improved target recognition through TCR enhancement; 2)Multi-faceted tumor-killing mechanisms; 3)Potential for better safety and persistence profiles.
Eligibility criteria
Qualifiers
Age ≥ 14 years, no gender restrictions;
Relapsed: Leukemic cells reappear in the peripheral blood after complete remission, or Leukemic blasts≥5% in the bone marrow (excluding other causes such as bone marrow regeneration after consolidation chemotherapy), or leukemic cell infiltration in extramedullary sites;
Relapsed: Patients who have achieved hematologic improvement or CR but subsequently experience hematologic decline (e.g., hemoglobin <10 g/dL, platelets <50×10⁹/L, neutrophils <1.0×10⁹/L), or an increase in the proportion of blast cells in the bone marrow (≥5%), or the emergence of new cytogenetic abnormalities or molecular progression (e.g., increased TP53 mutation burden);
Refractory: No hematologic or bone marrow improvement after ≥4-6 cycles of hypomethylating agent (HMA) therapy (e.g., azacitidine or decitabine), or low-risk MDS resistant to erythropoietin or immunomodulatory agents (e.g., lenalidomide).
Disqualifiers
Patients with a history of severe central nervous system disorders, such as uncontrolled epileptic seizures, stroke, severe brain injury with aphasia, paralysis, dementia, Parkinson's disease, or mental disorders;
New York Heart Association (NYHA) Class III or IV heart failure;
Undergone coronary angioplasty, coronary stent implantation, or coronary artery bypass surgery; or experienced thrombotic or embolic events (e.g., cerebrovascular events [including transient ischemic attacks, but excluding lacunar cerebral infarction], deep vein thrombosis [excluding deep vein thrombosis caused by PICC catheter placement], pulmonary embolism, etc.);
Presence of disseminated intravascular coagulation;
Trial design
Treatments tested in this trial
- Allogeneic TCR-enhanced γδ T cell(QH101)
- Fludarabine (FLU)
- Cyclophosphamide (CTX)