Neoplasms

All Conditions

Skin and Connective Tissue Diseases

Digestive System Diseases

Gland and Hormone Related Diseases

Respiratory Tract (Lung and Bronchial) Diseases

Urinary Tract, Sexual Organs, and Pregnancy Conditions

Rare Diseases

Carcinoma

Breast Neoplasms

Pancreatic Neoplasms

Melanoma

Carcinoma, Non-Small-Cell Lung

Stomach Neoplasms

Carcinoma, Squamous Cell

Head and Neck Neoplasms

Carcinoma, Renal Cell

Lung Neoplasms

Carcinoma, Hepatocellular

Kidney Neoplasms

Colorectal Neoplasms

Squamous Cell Carcinoma of Head and Neck

Neoplasms, Glandular and Epithelial

Neoplasms by Histologic Type

Respiratory Tract Neoplasms

Thoracic Neoplasms

Lung Diseases

Respiratory Tract Diseases

Carcinoma, Bronchogenic

Bronchial Neoplasms

Intestinal Neoplasms

Gastrointestinal Neoplasms

Digestive System Neoplasms

Gastrointestinal Diseases

Colonic Diseases

Intestinal Diseases

Rectal Diseases

Neoplasms, Squamous Cell

Stomach Diseases

Pancreatic Cancer

Renal Cell Carcinoma

Stomach Cancer

Clear Cell Renal Cell Carcinoma

Antineoplastic Agents

All Drugs and Chemicals

Trastuzumab

Antibodies

Antibodies, Monoclonal

Cetuximab

Immunomodulating Agents

Immunoglobulins

Mitogens

Antineoplastic Agents, Immunological

FATE-NK100 as a monotherapy in subjects with advanced solid tumor malignancies.

FATE-NK100 in combination with trastuzumab in subjects with human epidermal growth factor receptor 2 positive (HER2+) advanced breast cancer, HER2+ advanced gastric cancer or other advanced HER2+ solid tumors.

Regimen C: FATE-NK100 in combination with cetuximab in subjects with advanced colorectal cancer (CRC) or head and neck squamous cell cancer (HNSCC), or other epidermal growth factor receptor 1 positive (EGFR1+) advanced solid tumors.

FATE-NK100 is a donor-derived NK cell product comprised of ex vivo activated effector cells with enhanced anti-tumor activity

FATE-NK100

Epidermal growth factor receptor inhibitor antineoplastic agent

Jeff Chou, MD

This is a Phase 1, single-dose, open-label, dose-escalation study. The study will be conducted in three parts (i.e. regimens) in an outpatient setting as follows:

* Regimen A: FATE-NK100 as a monotherapy in subjects with advanced solid tumor malignancies.
* Regimen B: FATE-NK100 in combination with trastuzumab in subjects with human epidermal growth factor receptor 2 positive (HER2+) advanced breast cancer, HER2+ advanced gastric cancer or other advanced HER2+ solid tumors.
* Regimen C: FATE-NK100 in combination with cetuximab in subjects with advanced colorectal cancer (CRC) or head and neck squamous cell cancer (HNSCC), or other epidermal growth factor receptor 1 positive (EGFR1+) advanced solid tumors.

FATE-NK100 as Monotherapy and in Combination With Monoclonal Antibody in Subjects With Advanced Solid Tumors

The incidence of dose-limiting toxicity (DLT) within each dose cohort within the first 28 days after FATE-NK100 administration (ie, Day 1 through Day 29).

Objective-response rate (ORR): defined as the proportion of patients who achieve partial response (PR) or complete response (CR) per Response Evaluation Criteria in Solid Tumors (RECIST) 1.1 at any time on study.

The PK of FATE-NK100, as assessed by the proportion of lymphocytes in peripheral blood that are of donor/product origin at the specified time points.

Fate Therapeutics

Blood and Lymph Conditions

Immune System Diseases

Symptoms and General Pathology

Leukemia

Leukemia, Lymphoid

Leukemia, Lymphocytic, Chronic, B-Cell

Neoplasm, Residual

Hematologic Diseases

Lymphoproliferative Disorders

Lymphatic Diseases

Immunoproliferative Disorders

Leukemia, B-Cell

Chronic Disease

Disease Attributes

Neoplastic Processes

Chronic Graft Versus Host Disease

Chronic Lymphocytic Leukemia

Acute Graft Versus Host Disease

This group comprises patients who are diagnosed with CLL, but are asymptomatic and not receiving anti-CLL treatments (e.g. watch-and-wait disease).

This group comprises patients who are diagnosed with CLL, have symptomatic disease, and are undergoing anti-CLL treatments (e.g. chemo-immunotherapy).

This group comprises patients who were diagnosed with CLL, but are considered to be in either complete or partial remission following anti-CLL treatment for at least 6-months.

Participants will perform a supervised acute bout of aerobic exercise over 20-30 minutes, corresponding to a target power output at an intensity +10 to 15% above ventilatory threshold.

Exercise trial

John P Campbell, PhD

Chronic lymphocytic leukaemia (CLL) is the most common adult blood cancer in the United Kingdom. CLL means that many cancer cells appear in the blood, bone marrow and other tissues, for example, the spleen where some blood cells reside. Most patients with CLL have been diagnosed by chance, have no symptoms as a result of CLL, and do not need urgent treatment. However, when the cancer cells build up, people experience symptoms of CLL, and treatment is required. One of the current treatments for CLL is chemo-immunotherapy, that targets and kills cancer cells in the blood. However, this treatment does not kill all cancer cells. Some cancer cells survive by 'hiding' in the bone marrow and tissues, like the spleen, where the treatment cannot get to, this is called minimal residual disease (MRD). MRD eventually builds up and patients experience symptoms of CLL again. New approaches to detect and treat MRD are needed. Research has shown, that the number of blood cells, increases after exercise and that many of these blood cells come from the bone marrow and other tissues.

This study will investigate if exercise can move CLL cancer cells that are 'hiding' in the bone marrow and other tissues into the blood, thus improving the detection of MRD. By moving cancer cells into blood, the investigators also think this will improve the way chemo-immunotherapy works. In this study, the investigators will investigate the number of cancer and natural killer (NK) cells in the blood after exercise, in three different groups of people with CLL: before treatment; during treatment; and after treatment has finished.

Whilst repeated cycles of anti-cluster of differentiation (CD)20 immunotherapy are effective at killing large numbers of chronic lymphocytic leukaemia (CLL) cells, in the peripheral blood circulation, minimal residual disease (MRD) persists diffusely in the bone marrow and secondary lymphoid organs such as the lymph nodes and spleen. This is thought to be for a number of reasons. Firstly, malignant cells sequestered in lymphoid compartments receive protection from their stromal microenvironment. For example, T cells, dendritic cells and macrophages release pro-proliferative and apoptosis-inhibiting signalling pathways, that prolong CLL survival. Consequently, CLL cells in lymphoid tissues are much less susceptible to anti-CD20 immunotherapy, than CLL cells trafficking in the blood. This may be because the circulating CLL cells are not embedded into a protective stromal microenvironment. Secondly, to exert antibody-dependent cellular cytotoxicity (ADCC; i.e., the primary mechanism of action elicited by anti-CD20 immunotherapy against CLL cells) NK cells need to express CD16, a molecule expressed by CD56dim NK cells. However, these potent NK cells are unable to traffic from blood, where NK cells are more abundant, to secondary lymphoid tissues, because NK cells lack lymphoid homing markers. Thus, CLL cells are able to 'hide' from NK cells in lymphoid tissue, ensuring their ongoing survival. In light of the pro-survival features of the CLL microenvironment, new approaches to detect and treat MRD are sought.

It has been repeatedly shown, in one of the most reproduced findings in human physiology, that immune cell frequency in the peripheral blood increases profoundly, by approximately 50-100%, during a bout of aerobic exercise of moderate to vigorous intensity. This response reflects a redistribution of immune cells from marginal pools in the blood vessels, as well as from lymphoid organs, such as the spleen, bone marrow and lymph nodes into the blood, driven by increased haemodynamic forces and increased levels of catecholamines during exercise. In response to increased levels of exercise-induced catecholamines, beta-2 adrenergic receptors on the cell surface of lymphocytes, induce detachment from the vascular endothelium, thus promoting the mobilisation of lymphocytes into the peripheral blood circulation, during a bout of exercise, returning to pre exercise values in the 1 hour following exercise. The migration of immune cells into blood is comprised of all major immune cell types, including neutrophils, monocytes and lymphocytes. Due to the adrenergic mechanisms responsible there is a preferential mobilisation of the subtypes with the highest expression of beta-2 adrenergic receptors on the cell surface. NK cells are the most exercise responsive T lymphocyte population, followed by CD8+ T cells, B cells and CD4+ T cells. B cells express beta-2 adrenergic receptors and are therefore susceptible to mobilisation via exercise-induced catecholamines. In healthy persons, B cell frequency is increased in blood by approximately 50-100% during various different types of exercise including, cycling, running, rowing and resistance exercise. Furthermore, a rodent model of acute psychological stress - which induces similar adrenergic responses as exercise - demonstrated a similar B cell mobilisation pattern. An additional rodent model observed that acute stressors appear to redirect B cells from the bone marrow, suggesting that the B cells mobilised in response to exercise may have been mobilised from lymphoid tissue. Given these changes to immune cell kinetics, exercise may be an effective means of mobilising CLL cells from diffuse lymphoid tissues into the peripheral blood circulation, which may, in turn, facilitate the detection of MRD in CLL.

This exercise-induced mobilisation of CLL cells from lymphoid tissues may also increase the efficacy of anti-CD20 immunotherapy. Indeed, this process may facilitate the removal of CLL cells from protective, pro-survival microenvironments into the blood circulation. CLL cells survive in lymphoid tissue receiving external signals from the microenvironment promoting growth and survival. Furthermore, CD16+ NK cells, the primary effector cell in ADCC, do not express lymphoid homing markers on their cell surface, and cannot traffic to the lymphoid tissue to elicit potent ADCC responses. Therefore, in order to improve the depth and efficacy of treatment with anti-CD20 monoclonal antibodies (mAb), strategies need to be explored that remove CLL cells from their protective stromal microenvironment within lymphoid tissues, and mobilise into the blood circulation where CLL cells will encounter NK cells capable of eliciting ADCC. Exercise has the potential to redistribute B cells, and exercise has also been shown to increase the frequency of CD16+ NK cells, by over 500% into the blood circulation. Therefore, exercise may mobilise both CLL cells from their protective microenvironment and large numbers of effector NK cells capable of ADCC into the blood circulation, simultaneously. Thus, this process has the potential to improve the depth and efficacy of anti-CD20 mAb treatment.

It is of importance to examine the effects of exercise on CLL and CD16+ NK cells at different stages of the CLL survivorship. For instance, people with watch and wait CLL, who have not yet received anti-CLL therapy, enables investigations into the impact of exercise on both CLL tumour cell and immune cell kinetics, without the presence of confounding variables like anti-CLL treatments, or disease associated morbidities. Indeed, people with watch and wait CLL have no disease symptoms and are thus likely to have fewer contra-indications to exercise than CLL patients later in the CLL survivorship continuum.

Investigating the impact of exercise in people receiving anti-CLL treatments is also warranted, as those likely to benefit from the adjuvant effects of exercise on immunotherapy are, by reason, patients undergoing cycles of immunotherapy treatment. Thus, it is essential to explore how acute exercise is tolerated in people undergoing cycles of treatment, and assessment of the safety and acceptability of exercise is warranted. Moreover, chemoimmunotherapy induces immune-suppression which may nullify the immune changes induced by exercise. Accordingly, investigation of the effects of exercise on immune cell kinetics, as well as residual CLL tumour cells, is warranted in people receiving anti-CLL chemoimmunotherapy.

Lastly, examining the impact of exercise in people in CLL remission, following completion of anti-CLL treatment, is required as any exercise induced mobilisation of CLL cells may also facilitate the detection of MRD following anti-CLL treatment. Several studies have demonstrated that patients who achieved a clinical complete remission (CR) but with detectable MRD, can experience a disease relapse due to expansion of the residual CLL cells. Patients with CLL who achieve undetectable MRD (\<1 CLL cell per 10,000 leukocytes in blood or bone marrow), following anti-CLL treatment have better clinical outcomes than those with detectable MRD. A meta-analysis of eleven international studies with a total of 2457 patients observed that undetectable MRD status after treatment with chemotherapy or chemoimmunotherapy in newly diagnosed CLL is associated with overall and progression free survival. Therefore, MRD is a robust post-treatment prognostic biomarker of tumour burden, required for predicting disease recurrence. However, due to the multicompartmental nature of CLL, the bone marrow and secondary lymphoid tissue may serve as reservoirs for residual disease. Therefore, exercise may be utilised to facilitate the detection of MRD by mobilising CLL cells from diffuse sites into the blood circulation, thus potentially accelerating the identification of disease progression in patients following anti-CLL treatment. It is also important to assess immune competency in people in remission following completion of anti-CLL therapy, as any immune suppression at this time may hinder any effects of exercise.

The hypotheses of this pilot study are as follows:

* An acute bout of exercise will increase the frequency of CLL tumour cells in the peripheral blood of people with CLL at different stages of CLL survivorship.
* An acute bout of exercise will increase the frequency of immune cells (e.g., CD16+ NK cells) in the peripheral blood of people with CLL at different stages of CLL survivorship.
* Exercise induced mobilisation of immune cells (e.g., NK cells) will improve the efficacy of anti-CD20 immunotherapy against CLL cells ex vivo.

A pilot, single-centre, Phase I trial containing 3 groups during different phases of CLL survivorship:

* Cohort 1 (Pre treatment) CLL patients with asymptomatic early-stage disease monitored without anti-CLL treatment.
* Cohort 2 (Treatment) Treatment eligible CLL patients receiving first-line anti-CLL treatment or patients receiving anti-CLL maintenance treatment.
* Cohort 3 (Post treatment) CLL patients in complete remission (CR), complete remission with incomplete marrow recovery (CRi) or partial remission (PR) for at least 6 months following the completion of anti-CLL treatment.

All participants will complete the study intervention.

Mobilising Tumour and Immune Cells Via Exercise in Chronic Lymphocytic Leukaemia

Characterising Tumour and Immune Cell Mobilisation Into Blood in Response to Acute Exercise in Chronic Lymphocytic Leukaemia

Ventilatory threshold, in mL/kg/min, will be measured by a submaximal exercise test.

Height, in centimetres, will be measured by a stadiometer.

Weight, in kilograms, will be measured by an electronic weighing scale.

Fat mass, in kilograms, will be measured by Bioelectrical Impedance Analysis (BIA).

Lean mass, in kilograms, will be measured by BIA.

Physical activity, in hours per day, will be measured by the International Physical Activity Questionnaire.

Stress, in a scale of 0-4, will be measured by the Perceived Stress Scale.

Fatigue, in a 5-point scale of 'not at all' to 'very much', will be measured by the Functional Assessment of Chronic Illness Therapy (FACIT) Fatigue Scale.

Sleep, in a scale of 0-3, will be measured by the Pittsburgh Sleep Quality Index.

Quality of life, in a scale of 1-4, will be measured by the Health-Related Quality of Life questionnaire.

Blood pressure, in mmHg, will be measured by an automated blood pressure cuff.

Viral infection history, in a 4-point scale of 'not at all' to 'very much', will be measured by questionnaire.

Number of CLL cells per microgram of adipose tissue will be measured by flow cytometry.

Quantified by the incidence of adverse events.

Quantified by the percentage difference between the prescribed and achieved exercise per session.

Quantified by the percentage of participants who attend screening.

Quantified by the percentage of participants who complete all trial visits.

Number of CLL cells per microlitre will be measured by flow cytometry.

Number of immune cells per microlitre will be measured by flow cytometry.

The percentage of CD20+ cell lysis will be measured using an ex vivo antibody-dependent cellular cytotoxicity assay.

Immunoglobulins, in ng/mL, measured by enzyme-linked immunosorbent assay (ELISA).

Glucose, in mmol/L, measured by an Abbot blood glucose meter.

Lactate, in mmol/L, measured by a blood lactate meter.

Royal United Hospitals Bath NHS Foundation Trust

University of Southampton

Great Western Hospitals NHS Foundation Trust

University of Bath

Principal Investigator

Anti-Inflammatory Agents

Hydrocortisone

Hydrocortisone 17-butyrate 21-propionate

Hydrocortisone acetate

Hydrocortisone hemisuccinate

Nimotuzumab

Peripheral blood lymphocytes will be collected. The NK cell will be selected and expanded ex vivo, then adaptive transfer back into patients. A total of 5.0 x 10\^8/L NK cells will be infused in one cycle.To avoid allergic reactions, 50 mg hydrocortisone was intramuscularly injected into patient 30 min before cells infusion every time. Best supportive care was also provided for patients. Nimotuzumab will be used 24 hours before infusion. Patients continued receiving treatment unless they had unacceptable adverse effects, or progressive disease confirmed by CT and PET-CT or they withdrew consent.

Nimotuzumab will enhance the ADCC effect of NK Cell adaptive transfer

NK Cell adaptive transfer

Shixiu Wu, Doctor

NK cells can persist and expand in vivo following adoptive transfer and may have a role in the treatment of late stage malignancies. NK also express an activating Fc receptor that mediates antibody-dependent cellular cytotoxicity (ADCC) and production of immune modulatory cytokines in response to antibody-coated targets. Nimotuzumab, an monoclonal antibody against EGFR (epidermal growth factor receptor), may enhance the ADCC effect of NK cell. This study will evaluate the safety of combination of nimotuzumab and NK Cell in treating advanced cancer patients. Blood samples will also be collected for research purposes.

This is a phase I clinical study of expanded NK cells from autologous origin. The NK cell will be selected and expanded ex vivo and infused back into patients. Nimotuzumab will be used 24 hours before infusion. 21 advanced cancer patients are planned to receive two cycles of NK cells and Nimotuzumab treatment. Biomarkers and immunological markers are collected and analyzed as well.

Immunotherapy of Advanced Cancer Using a Combination Nimotuzumab and NK Cells

A Phase I Trial of Combined Nimotuzumab With NK Cells Adoptive Transfer for the Treatment of Advanced Cancer

From date of randomization until the date of first documented progression or date of death from any cause

The time from randomization to death from any cause

Peripheral circuiting tumor DNA is collected at baseline and 6 weeks after last treatment

Number of Patients with Clinical or Biological Treatment-related Adverse Events and/or Dose Limiting Toxicities as a Measure of Safety and Tolerability of a Combination of Nimotuzumab and NK Cell as assessed by CTCAE v4.0

Response will be evaluated according to RECIST v1.1

Shanghai bokang bioengineering co., LTD

Hangzhou Cancer Hospital

President of Hangzhou Cancer Hospital

Esophageal Squamous Cell Carcinoma

Esophageal Neoplasms

Esophageal Diseases

Adenocarcinoma

Urologic Neoplasms

Urogenital Neoplasms

Urogenital Diseases

Female Urogenital Diseases

Pregnancy Complications

Female Urogenital Diseases and Pregnancy Complications

Kidney Diseases

Urologic Diseases

Male Urogenital Diseases

Esophageal Cancer

QEQ278

Novartis Pharmaceuticals

Lisa Zhou

Zev A Wainberg

Erin Finch

Manish Patel

Justin Gainor

To characterize safety, tolerability, pharmacokinetics, pharmacodynamics, and preliminary anti-tumor activity of QEQ278 in adult patients with advanced/metastatic non-small cell lung cancer, esophageal squamous cell carcinoma, renal cell carcinoma, and human papilloma virus associated head and neck squamous cell carcinoma.

This study is an open-label, phase I/Ib, multi-center study of QEQ278 as a single agent, consisting of a dose escalation part followed by a dose expansion part.

In the dose escalation part of the study, patients with non-small cell lung cancer (NSCLC), esophageal squamous cell carcinoma (ESCC), renal cell carcinoma (RCC), or human papilloma virus (HPV)-associated head and neck squamous cell carcinoma (HNSCC) will be treated with QEQ278 single agent until the maximum tolerated dose (MTD) is reached or a lower recommended dose (RD) is established.

The study may enter the dose expansion, after an MTD(s) and/or RD(s) is declared in the dose escalation.

A Study to Investigate the Safety and Tolerability of Intravenous QEQ278 in Patients With Advanced Solid Tumors

A Phase I/Ib, Open-label, Multi-center, Study of QEQ278 in Patients With Advanced Solid Tumors

A DLT is defined as an adverse event or abnormal laboratory value assessed as unrelated to disease, disease progression, inter-current illness, or concomitant medications that occurs within the DLT evaluation period and meets the criteria defined in the study protocol.

Incidence and severity of adverse events (AEs) and serious adverse events (SAEs), including changes in laboratory values, vital signs, and electrocardiograms (ECGs) qualifying and reported as AEs.

Number of dose interruptions of QEQ278 and number of dose reductions of QEQ278

Dose intensity of QEQ278 is defined as the ratio of actual cumulative dose received and actual duration of exposure.

ORR is defined as the proportion of patients with a confirmed BOR of complete response (CR) or partial response (PR) by local investigator review as per RECIST v1.1.

DCR is defined as the proportion of patients with a confirmed best overall response (BOR) of CR or PR or stable disease (SD) by local investigator review as per RECIST v1.1.

DOR is defined as the time form the date of the first documented response (CR or PR) to the date of the first documented progression by local investigator review as per RECIST v1.1 or death due to underlying cancer.

PFS is defined as the time from the date of start of treatment to the date of the first documented progression by local investigator review as per RECIST v1.1, or death due to any cause.

The maximum (peak) serum drug concentration after single dose administration

The AUC from time zero to the last measurable concentration sampling time

The time to reach maximum (peak) serum drug concentration after single dose administration

The elimination half-life associated with the terminal slope of a semi logarithmic concentration-time curve

The total body clearance of drug from the serum

The apparent volume of distribution during terminal phase

Heart and Blood Diseases

Multiple Myeloma

Neoplasms, Plasma Cell

Hematologic Neoplasms

Hemostatic Disorders

Blood Coagulation Disorders

Vascular Diseases

Paraproteinemias

Blood Protein Disorders

Hemorrhagic Disorders

Newly diagnosed MM patients who have minimal residual disease (MRD+) in first remission prior to autologous stem cell transplant (ASCT)

Single dose infusion of CIML NK Cells plus KP1237 followed by low dose IL-2

CIML NK Cells plus KP1237 and low dose IL-2

Chief Medical Officer

Giada Bianchi, MD

This is an open-label single center Phase 1a/1b study with the primary objective of establishing the safety and exploring the efficacy of infusing the ex vivo combination product of cytokine induced memory-like (CIML) NK cells plus KP1237 and low dose IL-2 in newly diagnosed MM patients who have minimal residual disease (MRD+) in first remission prior to autologous stem cell transplant (ASCT).

Autologous Memory-like NK Cell Therapy With BHV-1100 (Formerly KP1237), Low Dose IL-2 in Multiple Myeloma Patients

A Phase 1 Study of Autologous Memory-like Natural Killer (NK) Cell Immunotherapy With BHV-1100 (Formerly KP1237) and IVIG Followed by Low Dose IL-2 as Early Post-Autologous Transplant Consolidation in Minimal Residual Disease Positive, Multiple Myeloma (MM) Patients in First or Second Remission

Study title	NCT ID	Conditions	Interventions	Eligibility	Organization
FATE-NK100 as Monotherapy and in Combination With Monoclonal Antibody in Subjects With Advanced Solid Tumors	NCT03319459	HER2 Positive G... Colorectal Canc... Head and Neck S... EGFR Positive S... Advanced Solid ... HER2-positive B... Hepatocellular ... Non Small Cell ... Renal Cell Carc... Pancreatic Canc... Melanoma	FATE-NK100 Cetuximab Trastuzumab	18 Years -	Fate Therapeutics
Mobilising Tumour and Immune Cells Via Exercise in Chronic Lymphocytic Leukaemia	NCT05093192	Chronic Lymphoc... Minimal Residua...	Exercise trial	18 Years -	University of Bath
Immunotherapy of Advanced Cancer Using a Combination Nimotuzumab and NK Cells	NCT03554889	Advanced Cancer ADCC NK Cell Mediate... Nimotuzumab Adaptive Transf...	NK Cell adaptiv... Nimotuzumab	18 Years - 75 Years	Hangzhou Cancer Hospital
A Study to Investigate the Safety and Tolerability of Intravenous QEQ278 in Patients With Advanced Solid Tumors	NCT05462873	Carcinoma, Non-... Carcinoma, Rena... Esophageal Squa... Squamous Cell C...	QEQ278	18 Years -	Novartis
Immunotherapy of Advanced Cancer Using a Combination Nimotuzumab and NK Cells	NCT03554889	Advanced Cancer ADCC NK Cell Mediate... Nimotuzumab Adaptive Transf...	NK Cell adaptiv... Nimotuzumab	18 Years - 75 Years	Hangzhou Cancer Hospital
Mobilising Tumour and Immune Cells Via Exercise in Chronic Lymphocytic Leukaemia	NCT05093192	Chronic Lymphoc... Minimal Residua...	Exercise trial	18 Years -	University of Bath
Autologous Memory-like NK Cell Therapy With BHV-1100 (Formerly KP1237), Low Dose IL-2 in Multiple Myeloma Patients	NCT04634435	Multiple Myelom...	CIML NK Cells p...	18 Years - 75 Years	Biohaven Pharmaceuticals, Inc.
Safety, Tolerability, and Anti-Tumor Activity of AFM24 in Combination With SNK01 in Subjects With Advanced/Metastatic EGFR-Expressing Cancers	NCT05099549	Squamous Cell C... Carcinoma, Non-... Colorectal Neop... Advanced Solid ... Refractory Tumo... Metastatic Tumo...	AFM24 SNK01	18 Years -	NKGen Biotech, Inc.
Safety, Tolerability, and Anti-Tumor Activity of AFM24 in Combination With SNK01 in Subjects With Advanced/Metastatic EGFR-Expressing Cancers	NCT05099549	Squamous Cell C... Carcinoma, Non-... Colorectal Neop... Advanced Solid ... Refractory Tumo... Metastatic Tumo...	AFM24 SNK01	18 Years -	NKGen Biotech, Inc.

Spots Global Cancer Trial Database for adcc

Every month we try and update this database with for adcc cancer trials from around the world to help patients and their families find trials that might be right for them.
We offer this 100% free of charge and do not endorse any of the trials listed here, we hope it helps you or a loved one.

Spots Global Cancer Trial Database for adcc

Every month we try and update this database with for adcc cancer trials from around the world to help patients and their families find trials that might be right for them. We offer this 100% free of charge and do not endorse any of the trials listed here, we hope it helps you or a loved one.

Every month we try and update this database with for adcc cancer trials from around the world to help patients and their families find trials that might be right for them.
We offer this 100% free of charge and do not endorse any of the trials listed here, we hope it helps you or a loved one.