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Fingolimod for the Abrogation of Interstitial Fibrosis and Tubular Atrophy Following Kidney Transplantation

Phase 2
Conditions
Interstitial Fibrosis
Kidney Transplant; Complications
Kidney Transplant Failure and Rejection
Kidney Transplant Failure
Kidney Transplant Rejection
Kidney Failure, Chronic
Graft Rejection
Interventions
Drug: Placebo
Registration Number
NCT05285878
Lead Sponsor
The Methodist Hospital Research Institute
Brief Summary

This is a randomized, double-blind, placebo-controlled trial in de novo kidney transplant patients to determine if the addition of fingolimod (brand name Gilenya®, candidate name- FTY720) on the background of standard immunosuppression will prevent expansion of the interstitial compartment of the transplanted kidney. Interstitial expansion is the precursor of interstitial fibrosis and graft loss. The study will test the hypothesis that abgrogating the fibrogenic effects of both the RhoA and mTOR pathways with fingolimod will reduce structural damage in transplanted kidneys and possible subsequent transplant failure.

Detailed Description

Prevention of, or slowing the progression of, the development of allograft fibrosis has not been successful in previous efforts. This study will to evaluate the potential of fingolimod (Gilenya®, Novartis Pharmaceuticals, East Hanover, NJ) (1), a sphingosine 1-phosphate receptor modulator and a RhoA inhibitor (2), to abrogate the presence of interstitial fibrosis/tubular atrophy (IF/TA) after kidney transplantation. The study may provide important information for future clinical trials for prevention of IF/TA in kidney transplant recipients.

Interstitial fibrosis and tubular atrophy almost invariably occur together (10) and are present in approximately 45% of kidney allografts by the first year posttransplant (11). Naesens et al (11) demonstrated that any positive chronic interstitial fibrosis score is associated with graft loss after the first year post transplant with a more rapidly declining slope than those without interstitial fibrosis. Furthermore, they demonstrated that a tubular atrophy score of 2-3 was associated with 20% graft loss during the 2nd year posttransplant, \>30% graft loss by 5 years and \~60% graft loss by 10 years posttransplant. Combined, IF/TA contributes to renal graft dysfunction or the decline in kidney function after transplantation and may be a factor in the 20.6% of total grafts lost (including death) by 5 years post-transplant (11,12).

Expansion of the interstitial compartment is a major component of IF/TA. Protocol (12,13) and for-cause (10,11) biopsies have provided evidence of the worsening of IF/TA with time in kidney transplant recipients and demonstrated a direct relationship between interstitial expansion and renal allograft functional decline and graft failure (11-14). Assessing the interstitial expansion by quantifying the fraction of renal cortical volume:interstitial compartment changes over time standardizes the assessment of IF/TA (15,16) and will be used in the current protocol (Section 10.2.1).

Fingolimod was originally intended as a prophylaxis against acute rejection in transplant recipients (17). A full development program was produced beginning with pharmacokinetics of single dose (18) and multiple doses (19) in healthy volunteers and evaluations of the effect of FTY720 on T-lymphocytes to better understand the immunosuppressive properties of the sphingosine 1-phosphate receptor modulator (20). Development proceeded with several studies where fingolimod was compared to standard immunosuppression regimens as an adjunct therapy with calcineurin inhibitors for prevention of kidney transplant acute rejection. After two cardiac events occurred in an open-label trial and lack of efficacy for prevention of acute rejection was demonstrated, the development of fingolimod as a therapeutic agent for rejection prophylaxis in transplantation ceased. Whereas the current study is not proposed to prevent acute rejection and will be using a smaller dose than those evaluated in phase 3 trials for acute rejection prophylaxis, a summary of these studies is important to the understanding of the safety of fingolimod in kidney transplant recipients.

Studies of de novo kidney transplant recipients report a reduction in absolute lymphocyte counts of approximately 25-35% in the lower dose groups (0.25mg and 0.5mg FTY720, respectively) that corrects to within approximately 20% of baseline (day of transplant surgery) level (22-28). Additionally, asymptomatic bradycardia or reduced heart rate was reported and responded to treatment when required or resolved on its own (23-26,28). Prudent exclusion criteria of patients who have heart rate \<50bpm at baseline is warranted for the current study. Macular edema occurred more often in kidney transplant patients taking ≥2.5mg FTY720 (15/667, 2.2%) compared to mycophenolate mofetil (MMF, 5/373, 1.3%; 25,26,28); thus, the current study will exclude patients with a history of macular degeneration or diabetic retinopathy. Only one report indicated that liver enzymes were elevated in participants taking FTY720 (25) and the increase was mild (\<2x upper limit of normal \[ULN\]).

Controlling hypertension and prevention and treatment of acute rejection are standard approaches to kidney function preservation in kidney transplant recipients. Additionally, the use of calcineurin inhibitor (CNI)-sparing protocols has been reported with various approaches but data are insufficient to equivocally demonstrate consistently lower IF/TA in the approaches reported to date (7). Thus, it is important to examine additional approaches for prevention of IF/TA in this population.

Preliminary data from Chen W et al strongly suggests that fingolimod is able to inhibit chronic rejection of transplanted hearts in a rat and mouse model by inhibiting RhoA and down-regulating mammalian target of rapamycin (mTOR) Complex 2 (mTORC2)/Regulatory Associated Protein Of MTOR Complex 1 Independent Companion Of MTOR Complex 2 (RICTOR; 30,31). Therefore, this study will test the hypothesis that abrogating the fibrogenic effects of both RhoA and mTOR pathways with fingolimod would abrogate IF/TA and that reducing this structural damage in transplanted kidneys would result in improved or preserved kidney function and reduced graft loss.

The purpose of this study is to demonstrate that 0.5mg/day of fingolimod for 3 months administered to de novo kidney transplant recipients will be safe and to examine the course of IF/TA over a 1-year period by testing the ability of 0.5mg/day fingolimod for 3 months to abrogate the development of IF/TA in de novo kidney transplant recipients compared to placebo.

Recruitment & Eligibility

Status
ENROLLING_BY_INVITATION
Sex
All
Target Recruitment
20
Inclusion Criteria
  • Provision of signed and dated informed consent form
  • Stated willingness to comply with all study procedures and availability for the duration of the study
  • Receiving a first or second kidney transplant
  • Male or female, aged ≥18 to ≤65
  • Women of child bearing potential who have a negative serum pregnancy test prior to treatment
  • Women of child bearing potential (including perimenopausal women who have had a menstrual period within the previous 1 year) who agree to use 2 forms of effective birth control regimen (at least one of which is a barrier method) throughout the study period and for 6 weeks following the end of the study or the last dose of mycophenolic acid, whichever comes first.
  • Panel of reactive antibodies <50%
  • Able to take oral medication
  • Agreement to adhere to Lifestyle Considerations throughout study duration: refraining from the consumption of grapefruit or grapefruit juice and stopping any anticoagulation therapy, including ASA, one week prior and one week post kidney biopsy procedure
Exclusion Criteria
  • Transplantation of any organ other than kidney
  • History or presence of second degree AV block, third degree AV block, symptomatic bradycardia, or an arrhythmia requiring current treatment with Class Ia or III antiarrhythmic drugs.
  • Heart rate <60 beats per minute
  • Presence of an increased QTc interval > 500 ms on screening ECG.
  • Presence of a cardiac pacemaker.
  • History of any major cardiac events, including heart attack within the last six months of enrollment, unstable angina, congestive heart failure, or any severe cardiac disease as determined by investigator
  • Known macular degeneration
  • Diagnosed with any significant coagulopathy or medical condition requiring long-term systemic anticoagulation after transplantation, which would interfere with obtaining biopies.
  • Diagnosed with chronic immune system disease
  • Diagnosed with acute pulmonary disease
  • Diagnosed with severe liver disease, including abnormal liver enzymes or total bilirubin greater than three times upper limit of normal.
  • Diagnosed with any past or present malignancies except squamous or basal cell carcinoma of the skin excised at least two years prior to randomization.
  • Diagnosed with active acute or chronic infection, or febrile illness within two weeks prior to randomization.
  • Recent history of strokes in the preceding 6 months
  • Use of ketoconazole for more than 2 weeks
  • Use of any investigational drug during the 4 weeks prior to enrolling in this study
  • Women of child bearing potential who are breastfeeding
  • Women of childbearing potential not practicing reliable methods of contraception. Reliable methods for contraception include surgical sterilization (hysterectomy, bilateral tubal ligation), double-barrier method (such as condom and diaphragm). To be considered as post-menopausal and not of childbearing potential, female participants must have experienced 12 consecutive months of amenorrhea.
  • Known allergic reactions to components of Gilenya®, specifically fingolimod, gelatin, magnesium stearate, mannitol, titanium dioxide, and/or yellow iron oxide
  • Presence of any medical or psychosocial condition, which the investigator believes, would hinder adherence to the study requirements.

Study & Design

Study Type
INTERVENTIONAL
Study Design
PARALLEL
Arm && Interventions
GroupInterventionDescription
PlaceboPlaceboParticipants will take a placebo capsule daily for 3 months. Placebo will be methylcellulose encapsulated into an opaque closed gelatin capsule for blinding. Capsules will be placed in a labeled bottle, with the contents only identifiable by a code on the package label and only the compounding pharmacy and the unblinded pharmacist at Houston Methodist Investigational Drug Service will know the code definition.
FingolimodFingolimodParticipants will take a 0.5 mg fingolimod capsule each day for 3 months. The fingolimod capsule will be placed inside an opaque closed gelatin capsule without transformation of the manufacteror's fingolimod capsule. The fingolimod blinded product and the placebo capsule will be identical in size, color, appearance, and weight.
Primary Outcome Measures
NameTimeMethod
Emergent and Adverse EventsBaseline (day of kidney transplant surgery); 3, 14, 30, 90, 180, 270, and 365 days after starting study drug or placebo

The difference in the proportion of cumulative treatment-emergent (TE) adverse events (AE) determined to be ≥ grade 3 severity that occur during 12 months from the first dose of FTY720 compared to the placebo group.

Secondary Outcome Measures
NameTimeMethod
TGF-beta BiomarkerBaseline, 90 days, and 1 year after the first dose of fingolimod or placebo

Measurement of Transforming Growth Factor beta

Procollagen 3 Peptide BiomarkerBaseline, 90 days, and 1 year after the first dose of fingolimod or placebo

Measurement of Procollagen 3 Peptide

Urinary Albumin:Creatinine RatioBaseline; 3, 14, 30, 90, 180, 270, and 365 days after starting study drug or placebo

The ratio of albumin to creatinine in a urine sample from the patient

Change in Estimated Glomerular Filtration RateBaseline; 3, 14, 30, 90, 180, 270, and 365 days after starting study drug or placebo

Estimated glomerular filtration rate relative to the baseline value or previous endpoints

Causes of End-Stage Renal DiseaseUp to 1 year after taking the first dose of the study drug or placebo

Recording the cause of end-stage renal disease, if it develops

Biopsy-Proven Acute RejectionBaseline, 3 months after kidney transplant, 1 year after kidney transplant

Biopsy-proven acute rejection as diagnosed by a qualified pathologist

Patient SurvivalBaseline; 3, 14, 30, 90, 180, 270, and 365 days after starting study drug or placebo

Whether the patient is deceased or alive

RhoA of Blood MonocytesBaseline, 90 days, and 1 year after the first dose of fingolimod or placebo

Measurement of Ras homolog family member A protein

RICTOR BiomarkerBaseline, 90 days, and 1 year after the first dose of fingolimod or placebo

Measurement of RPTOR Independent Companion Of MTOR Complex 2

Fraction of Renal Cortical Volume Occupied by InterstitiumBaseline, 3 months after kidney transplant, 1 year after kidney transplant

A doubling of the fraction of renal cortical volume occupied by interstitium (VvInt/cortex) compared to the baseline biopsy in participants taking 0.5mg/day fingolimod (experimental group) or placebo (control group) for 3 months

Graft SurvivalBaseline; 3, 14, 30, 90, 180, 270, and 365 days after starting study drug or placebo

Whether the patient required a new kidney graft or the patient is deceased

MCP1 BiomarkerBaseline, 90 days, and 1 year after the first dose of fingolimod or placebo

Measurement of Monocyte Chemoattractant Protein-1

BMP-7 Protein BiomarkerBaseline, 90 days, and 1 year after the first dose of fingolimod or placebo

Measurement of Bone Morphogenetic Protein 7

Trial Locations

Locations (1)

Houston Methodist Research Institute

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Houston, Texas, United States

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