Neoplasms

Heart and Blood Diseases

Blood and Lymph Conditions

Immune System Diseases

All Conditions

Rare Diseases

Multiple Myeloma

Neoplasms, Plasma Cell

Neoplasms by Histologic Type

Hemostatic Disorders

Blood Coagulation Disorders

Vascular Diseases

Paraproteinemias

Blood Protein Disorders

Hematologic Diseases

Hemorrhagic Disorders

Lymphoproliferative Disorders

Immunoproliferative Disorders

Lipid Regulating Agents

All Drugs and Chemicals

Fenofibrate

Fenofibric acid

Hypolipidemic Agents

Antimetabolites

Anticholesteremic Agents

Fenofibrate orally daily for each 28 day cycle, per study protocol.

Upon screening, registration and enrollment, all subjects will receive Fenofibrate 160 mg orally daily for at least 2 months and may continue receiving study medication for as long as in the opinion of the investigator there is clinical benefit in doing so. Patients with calculated creatinine clearance \< 50 mL/min will receive a reduced dose of 54 mg orally daily.

Denise Pereria, MD

Multiple myeloma cells are dependent on calcium (Ca2+) for their function. Specifically, Ca2+ is required for the function of the endoplasmic reticulum in which proteins, including immunoglobulins, are folded prior to their release from the cell. Multiple myeloma cells secrete large concentrations of immunoglobulins continuously and as result depend on mitochondria activity to replenish the Ca2+ levels in the endoplasmic reticulum as was shown in vitro in our lab. Fenofibrate has been shown to inhibit mitochondrial function resulting in inhibition of protein folding in the endoplasmic reticulum of multiple myeloma (MM) cells that leads to the induction of a stress signal known as the unfolded protein response and subsequently apoptosis. The effective anti-myeloma concentrations for fenofibrate are attainable in the clinical setting as they are in the same range as the effective concentrations for anti-hyperlipidemic effect. The investigators propose to evaluate fenofibrate therapy in multiple myeloma patients.

Phase II Study to Evaluate Fenofibrate Therapy in Patients With Smoldering or Symptomatic Multiple Myeloma

To determine response rate (Strict Complete Response (sCR), Complete response (CR), Very Good Partial Response (VgPR), and Partial Response (PR)) in multiple myeloma patients receiving oral fenofibrate therapy. Response will be measured by serum and urine protein electrophoresis and immunofixation, as well as by percentage of plasma cells present on bone marrow biopsy.

To evaluate safety and tolerability of fenofibrate therapy in patients with multiple myeloma.

Proportion of participants achieving progression-free survival. Measured from date of initiation of treatment (Day 1) to the earliest occurrence of any of the following events: documented disease progression, or death from any cause. Patients who are alive and progression-free will be censored at the date of last documented progression-free status.

University of Miami

Assistant Professor of Clinical

Fenofibrate orally daily for each 28 day cycle, per study protocol.

Fenofibrate: Upon screening, registration and enrollment, all subjects will receive Fenofibrate 160 mg orally daily for at least 2 months and may continue receiving study medication for as long as in the opinion of the investigator there is clinical benefit in doing so. Patients with calculated creatinine clearance \< 50 mL/min will receive a reduced dose of 54 mg orally daily.

Fenofibrate Therapy

Age, Categorical

Sex: Female, Male

United States

Region of Enrollment

Denise Pereira MD

Strict Complete Response (sCR)

Complete response (CR)

Very Good Partial Response (VgPR)

Partial Response (PR)

No participants achieved response to protocol therapy (Strict Complete Response (sCR), Complete response (CR), Very Good Partial Response (VgPR), or Partial Response (PR)). Two (2) patients had stable disease (SD); one (1) patient achieved Stable Disease/clinical Progressive Disease, and three (3) patients had progressive disease (PD).

Rate of Response in Participants Receiving Fenofibrate Therapy

Number of Subjects Experiencing Adverse Events

6 months

12 months

Proportion of Participants Achieving Progression-Free Survival

Overall Study

Nervous System Diseases

Leukemia

Neuroblastoma

Sarcoma

Lymphoma

Central Nervous System Neoplasms

Nervous System Neoplasms

Neuroectodermal Tumors, Primitive, Peripheral

Neuroectodermal Tumors

Neuroectodermal Tumors, Primitive

Neoplasms, Neuroepithelial

Neoplasms, Germ Cell and Embryonal

Neoplasms, Glandular and Epithelial

Neoplasms, Nerve Tissue

Soft Tissue Sarcoma

Lymphosarcoma

Neuroepithelioma

Anti-Infective Agents

Antineoplastic Agents

Antirheumatic Agents

Anti-Inflammatory Agents

Analgesics

Thalidomide

Etoposide

Cyclophosphamide

Angiogenesis Inhibitors

Etoposide phosphate

Celecoxib

Immunosuppressive Agents

Immunologic Factors

Antineoplastic Agents, Alkylating

Alkylating Agents

Enzyme Inhibitors

Anti-Inflammatory Agents, Non-Steroidal

Analgesics, Non-Narcotic

Cyclooxygenase 2 Inhibitors

Cyclooxygenase Inhibitors

Anti-Bacterial Agents

Growth Inhibitors

Thalidomide: Start at 3 mg/kg (rounded to nearest 50 mg), increasing dose weekly by 50 mg as tolerated to 24 mg/kg (max 1,000 mg); Celecoxib: \< 20 kg at 100 mg; 20-50 kg at 200 mg; \> 50 kg at 400 mg; Fenofibrate: 90 mg/m2 (max 200 mg); Etoposide: 50 mg/m2; Cyclophosphamide: 2.5 mg/kg (max 100 mg); Patients receive oral etoposide once daily on days 1-21 and 43-63 (weeks 1-3 and 7-9) and oral cyclophosphamide once daily on days 22-42 (weeks 4-6). Patients also receive oral thalidomide once daily, oral celecoxib twice daily, and oral fenofibrate once daily in weeks 1-9. Treatment repeats approximately every 9 weeks for at least 3 courses in the absence of disease progression or unacceptable toxicity. Patients receive alternating etoposide and cyclophosphamide pulses (i.e., etoposide-cyclophosphamide-etoposide during courses 1 and 3 and cyclophosphamide-etoposide-cyclophosphamide during course 2).

celecoxib

cyclophosphamide

etoposide

fenofibrate

thalidomide

Mark W. Kieran, MD, PhD

RATIONALE: Drugs used in chemotherapy, such as etoposide and cyclophosphamide, work in different ways to stop the growth of cancer cells, either by killing the cells or by stopping them from dividing. Thalidomide, celecoxib, and fenofibrate may stop the growth of cancer cells by blocking blood flow to the cancer. Celecoxib also may stop the growth of cancer cells by blocking some of the enzymes needed for cell growth. Giving combination chemotherapy together with thalidomide, celecoxib, and fenofibrate may kill more cancer cells.

PURPOSE: This phase II trial is studying how well giving etoposide and cyclophosphamide together with thalidomide, celecoxib, and fenofibrate works in treating young patients with relapsed or progressive cancer.

OBJECTIVES:

Primary

* Evaluate the activity of etoposide, cyclophosphamide, thalidomide, celecoxib, and fenofibrate, in terms of prolonging the time to disease progression, in young patients with relapsed or progressive cancer.

Secondary

* Determine, preliminarily, the biologic activity of this regimen, in terms of tumor response and overall survival, in these patients.
* Determine the toxicity of this regimen in these patients.
* Evaluate different radiographic techniques as markers of tumor response in these patients.
* Evaluate the predictive ability of in vitro correlative studies as markers of tumor response.

STATISTICAL DESIGN: Patients were classified into one of 8 strata according to diagnosis: leukemia/lymphoma, bone tumors, neuroblastoma, high grade glial tumors, low grade glial tumors, ependymoma, medulloblastoma/PNET, and miscellaneous. A two-stage design for each disease stratum was planned. The accrual goal at the end of the two-stage design was 20 subjects for each stratum. A stopping rule was applied after the accrual of the first 10 eligible subjects enrolled in each disease stratum. If 1 or more patients in the first 10 evaluable patients were alive and progression-free at 27 weeks and have tolerated therapy then accrual to stage two would proceed. Among 20 patients within a stratum, if 3 or more patients met primary endpoint then regimen would be considered successful. The probability of concluding the treatment is feasible is 0.95 if true success rate is 30% and 0.07 if true succes rate is 5%. Overall accrual target was 80-160 patients. Please see published manuscript (Robison et al Pediatr Blood Cancer 2014) for results within disease strata.

Etoposide, Cyclophosphamide, Thalidomide, Celecoxib, and Fenofibrate in Relapsed or Progressive Cancer

Anti-Angiogenic Chemotherapy: A Phase II Trial of the Oral 5-Drug Regimen (Thalidomide, Celecoxib, Fenofibrate, Etoposide and Cyclophosphamide) in Patients With Relapsed or Progressive Cancer

Proportion of patients alive at 27 weeks without progressive disease (PD) and having tolerated therapy. As appropriate for tumor type and location, gadolinium-enhanced MRI and other imaging modalites were used to assess response. Progressive disease was defined as \>/=25% increase in product of diameters, development of new areas of disease, or disease-attributable clinical deterioration or death, progressive disease. For patients with leukemia PD was defined as \>/=25% or \>/=5,000 cells/mm3 increase in number of circulating cells, development of extramedullary disease, or other clinical evidence of progression.

27-week progression-free survival is the probability of patients remaining alive and progression-free at 27-weeks from study entry estimated using Kaplan-Meier methods. As appropriate for tumor type and location, gadolinium-enhanced MRI and other imaging modalites were used to assess response. Progressive disease was defined as \>/=25% increase in product of diameters, development of new areas of disease, or disease-attributable clinical deterioration or death, progressive disease. For patients with leukemia PD was defined as \>/=25% or \>/=5,000 cells/mm3 increase in number of circulating cells, development of extramedullary disease, or other clinical evidence of progression.

27-week overall survival is the probability of patients remaining alive at 27-weeks from study entry estimated using with Kaplan-Meier methods.

As appropriate for tumor type and location, gadolinium-enhanced MRI and other imaging modalites were used to assess response. Best response was regarded as best response at any single assessment. Response was defined as follows: complete resolution of all demonstrable tumor, complete response (CR); \>/=50% decrease in the product of the 2 maximum perpendicular diameters relative to the baseline evaluation, partial response (PR); \<50% decrease and \<25% increase in product of diameters, stable disease (SD); and \>/=25% increase in product of diameters, development of new areas of disease, or disease-attributable clinical deterioration or death, progressive disease (PD). For patients with leukemia PD was defined as \>/=25% or \>/=5,000 cells/mm3 increase in number of circulating cells, development of extramedullary disease, or other clinical evidence of progression.

National Cancer Institute (NCI)

Boston Children's Hospital

Dana-Farber Cancer Institute

Principal Investigator

5-drug Metronomic Antiangiogenic Regimen

5-drug Metronmic Antiangiogenic Regimen

Age, Continuous

High Grade Glioma

Ependymoma

Low Grade Glioma

Bone Tumors

Medulloblastoma/PNET

Leukemia/Lymphoma

Miscellaneous CNS Tumors

Miscellaneous non-CNS Tumors

Patients were stratified within 7 disease strata and an 8th 'miscellaneous' stratum.

Disease Group

The analysis population represents patients who started treatment.

Mark Kieran

The analysis dataset is comprised of all treated patients.

Therapy Completion Rate

27-Week Progression-Free Survival

27-Week Overall Survival

Complete Response

Partial Response

Stable Disease

Progressive Disease

Not Evaluable

Best Response

Urinary Tract, Sexual Organs, and Pregnancy Conditions

Uterine Cervical Neoplasms

Carcinoma

Carcinoma in Situ

Uterine Cervical Dysplasia

Uterine Cervical Diseases

Uterine Diseases

Genital Diseases, Female

Genital Diseases

Urogenital Diseases

Female Urogenital Diseases

Pregnancy Complications

Female Urogenital Diseases and Pregnancy Complications

Precancerous Conditions

Cervical Intraepithelial Neoplasia

Participants with high-grade dysplasia will receive 200mg of Fenofibrate starting on the day of enrollment and will continue the drug administration daily for 2-4 weeks +/- 7 days until their excisional procedure

Participants with invasive cervical cancer will receive 200mg of Fenofibrate starting on the day of enrollment and will continue the drug administration daily for 2-4 weeks +/- 7 days until their definitive hysterectomy or chemoradiation

Fenofibrate is an FDA approved drug for cardiovascular indications and have decades of data supporting a favorable safety profile event with chronic use.

Cold knife conization or loop electrosurgical excision to remove cells and tissue in the cervix

Cervical Conization

In a hysterectomy, the uterus, cervix, both ovaries, both fallopian tubes, and nearby tissue are removed.

Hysterectomy

Chemotherapy uses anti cancer (cytotoxic) drugs to destroy cancer cells. The drugs circulate throughout the body in the bloodstream. Radiotherapy uses high energy waves similar to x-rays to kill cancer cells.

Chemoradiation

Lindsay A Ferguson, MD

Lindsay Ferguson, MD

Normally, p53 helps prevent tumors from forming in the body. Early studies have shown that Fenofibrate, a cholesterol-lowering drug, can restore normal function to p53 and can change the metabolism of HPV-positive tumors in a way that stops the growth of tumors. The purpose of this study is to understand how Fenofibrate can be used to treat HPV-positive cervical cancers and cervical dysplasia. Researchers will examine collected tissue samples and investigate various genes and proteins to see whether Fenofibrate has an effect on HPV-positive cervical cancers and cervical dysplasia.

Fenofibrate in Patients With Cervical Intraepithelial Neoplasia and Invasive Cervical Carcinoma

Window of Opportunity Trial of Fenofibrate in Patients With High-grade Cervical Intraepithelial Neoplasia and Invasive Cervical Carcinoma

Changes in p53 levels from initial biopsy to repeat sampling at the time of surgery

Changes in tumor metabolic status from initial biopsy to repeat sampling at the time of surgery evaluated via immunohistochemical testing

Assess tolerability of fenofibrate by comparing lab values at baseline to values at conclusion of treatment

Skin and Connective Tissue Diseases

Symptoms and General Pathology

Substance Related Disorders

Wounds and Injuries

Breast Neoplasms

Cardiotoxicity

Breast Diseases

Skin Diseases

Heart Diseases

Drug-Related Side Effects and Adverse Reactions

Chemically-Induced Disorders

Radiation Injuries

Doxorubicin

Liposomal doxorubicin

Antibiotics, Antitubercular

22 patients which will receive four cycles of AC regimen (doxorubicin and cyclophosphamide; each cycle is given every 21 day) plus placebo tablets once daily.

22 patients which will receive four cycles of AC regimen (doxorubicin and cyclophosphamide; each cycle is given every 21 day) plus Fenofibrate 160 mg once daily.

It is an approved drug for hypercholesterolemia, It lowers lipid levels by activating peroxisome proliferator-activated receptor alpha (PPARα).

Placebo is made to look exactly like a real drug but is made of an inactive substance.

Placebo

Anthracycline derived chemotherapy used in treatment of breast cancer

Alkylating agent used in treatment of breast cancer

Hagar Dewidar, Instructor

Tarek Mostafa, Professor

This study aims at evaluating the possible safety and efficacy of fenofibrate in attenuating doxorubicin related cardiac toxicity in breast cancer patients.

Breast cancer represents the most frequently diagnosed malignancy and the second most common cause of cancer death worldwide (Sung et al., 2021). In Egypt, breast cancer is the most common malignancy in women, accounting for 38.8% of cancers in this population, with the estimated number of breast cancer cases nearly 22,700 in 2020 and forecasted to be approximately 46,000 in 2050 (Ibrahim et al., 2014).

Doxorubicin (DOX) is a cytotoxic agent that is commonly used for treatment of breast cancer. Despite its effectiveness, doxorubicin is associated with cumulative and potential cardiotoxicity (Rawat et al.,2021).

Although the precise mechanisms whereby DOX induces myocardial injury have not been fully elucidated, it is widely accepted that DOX induces cardiac injury via several mechanisms, including activation of nuclear factor- Kabba B (NF-ĸB), the induction of pro-inflammatory cytokines, the generation of free radicals, the promotion of apoptotic cell death, and the suppression of Endothelial progenitor cells (EPC) mobilization and function, which are typical changes observed in DOX-induced cardiotoxcity (Cardinale et al., 2020).

Peroxisome proliferator-activated receptor-α (PPARα) has been proposed as a key lipid metabolism modulator and regulator of inflammation. There are three isotypes of PPAR (α, β and ȣ) which have distinct but overlapping functions. Fenofibrate, an important PPAR- α agonist, is widely used in in the treatment for hypercholesterolemia and hypertriglyceridemia (Kim and Kim, 2020). Many studies demonstrated the pleiotropic effects of fenofibrate on the heart that afford direct myocardial protection in addition to the lipid-lowering effects through improvement of vascular endothelial function, reducing oxidative stress and increasing endothelial nitric oxide synthase (eNOS) activation (Walker et al., 2012; Jen et al., 2016).

In addition recent animal study showed that fenofibrate decreased the transactivation of Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), activated endothelial nitric oxide synthase (eNOS) and increased nitric oxide (NO) bioavailability, which in turn suppressed MMP-2 (matrix 4 metalloproteinase-2) and MMP-9 (matrix metalloproteinase-9), a well-recognized mediator of adverse ventricular fibrosis and subsequent remodeling, which established the role of fenofibrate against DOX-induced cardiotoxicity in mice (Huang et al., 2021). In addition, it is known that DOX- increases circulating N-terminal pro-B-type natriuretic peptide (NT- pro-BNP) and B-type natriuretic peptide (BNP) that were attenuated by fenofibrate (Huang et al., 2021)

Evaluation of Possible Safety and Efficacy of Fenofibrate in the Prophylaxis of Doxorubicin Induced Cardiotoxicity in Breast Cancer Patients

Clinical Study to Evaluate the Possible Safety and Efficacy of Fenofibrate in the Prophylaxis of Doxorubicin Induced Cardiotoxicity in Breast Cancer Patients

The primary outcome is to avoid decrease in patients ejection fraction while administrating doxorubicin which is known to cause a declination in cardiac ejection fraction threatening of heart failure

The secondary outcome is decrease in serum levels of the measured biological markers which are brain naturetic peptide and myeloperoxidase

Tanta University

Instructor of clinical pharmacy

Nutritional and Metabolic Diseases

Study title	NCT ID	Conditions	Interventions	Eligibility	Organization
Phase II Study to Evaluate Fenofibrate Therapy in Patients With Smoldering or Symptomatic Multiple Myeloma	NCT01965834	Multiple Myelom...	Fenofibrate	18 Years -	University of Miami
Etoposide, Cyclophosphamide, Thalidomide, Celecoxib, and Fenofibrate in Relapsed or Progressive Cancer	NCT00357500	Central Nervous... Leukemia Lymphoma Neuroblastoma Sarcoma Unspecified Chi...	celecoxib cyclophosphamid... etoposide fenofibrate thalidomide	- 21 Years	Dana-Farber Cancer Institute
Fenofibrate in Patients With Cervical Intraepithelial Neoplasia and Invasive Cervical Carcinoma	NCT06191133	Cervical Intrae... Invasive Cervic...	Fenofibrate Cervical Coniza... Hysterectomy Chemoradiation	18 Years -	Case Comprehensive Cancer Center
Evaluation of Possible Safety and Efficacy of Fenofibrate in the Prophylaxis of Doxorubicin Induced Cardiotoxicity in Breast Cancer Patients	NCT06155331	Breast Cancer S...	Fenofibrate Placebo Doxorubicin Cyclophosphamid...	18 Years - 75 Years	Tanta University
Fenofibrate in Patients With Cervical Intraepithelial Neoplasia and Invasive Cervical Carcinoma	NCT06191133	Cervical Intrae... Invasive Cervic...	Fenofibrate Cervical Coniza... Hysterectomy Chemoradiation	18 Years -	Case Comprehensive Cancer Center
Effects of Fenofibrate on Metabolic and Reproductive Parameters in Polycystic Ovary Syndrome	NCT00884819	Polycystic Ovar...	Fenofibrate Placebo	18 Years - 45 Years	Lawson Health Research Institute

Spots Global Cancer Trial Database for fenofibrate

Every month we try and update this database with for fenofibrate 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 fenofibrate

Every month we try and update this database with for fenofibrate 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 fenofibrate 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.