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CompletedNCT03286556STRIVE-IPFUpdated Feb 24, 2026Results posted

Autoantibody Reduction for Acute Exacerbations of Idiopathic Pulmonary Fibrosis

A Phase 2 interventional study of Autoantibody Reductive Therapy and Treatment as Usual (TAU) in Idiopathic Pulmonary Fibrosis, Acute Fatal Form, sponsored by University of Alabama at Birmingham. Completed at 7 sites in United States. Open to participants aged 40 Years to 85 Years. Per ClinicalTrials.gov, last updated 2026-02-24.

Sponsored by University of Alabama at Birmingham · Phase 2, Interventional, and Treatment

Phase
Phase 2
Study type
Interventional
Enrollment
82
Allocation
Randomized
Ages
40 Years to 85 Years
Sex
All
01

Study summary

Acute exacerbations (AE) are a dreaded manifestation of idiopathic pulmonary fibrosis (IPF) that presents with rapidly worsening respiratory function over days to weeks. AE account for about 1/2 the deaths in IPF patients, and are refractory to all medical therapies attempted to date.

Considerable preliminary data shows pathological B-cell abnormalities and autoantibodies are present in AE-IPF and associated with disease severity.

The experimental therapy here (therapeutic plasma exchange plus rituximab plus intravenous immunoglobulin) is mechanistically targeted to ameliorate autoantibody-mediated pulmonary injury. Anecdotal pilot studies indicate these treatments have significant benefit for a disease syndrome that has, until now, been almost invariably inexorable. This clinical trial has the potential to profoundly affect current paradigms and treatment approaches to patients with AE-IPF.

Read the detailed description

The primary goal of clinical trial is to determine effects of combined therapeutic plasma exchange (TPE), rituximab, and intravenous immunoglobulin (IVIG) in comparison to effects of treatment as usual (TAU), among AE-IPF patients.

Our central hypothesis is "AUTOANTIBODY REDUCTION IS BENEFICIAL FOR AE-IPF PATIENTS." A corollary of this hypothesis is that antibody-mediated autoimmunity can play an important role in IPF exacerbations.

Following baseline screening assessments, hospitalized AE-IPF patients at the collaborating sites that meet all inclusion/exclusion criteria will be randomly assigned to receive one of the following treatments in a ratio of 2:1:

  • Arm A (n=34) - Experimental Treatment:

Steroids: Prednisone 60 mg (p.o.) on day 1, followed by 20 mg/day on days 2-5, 7-14, and 16-19 (or the i.v. methylprednisolone equivalent). Methyl-prednisolone 100 mg i.v. will be administered on days 6 and 15, as a premedication prior to the rituximab.

Insertion of a dialysis/apheresis catheter into a central vein, and initiation of therapeutic plasma exchange (TPE), rituximab, and intravenous immunoglobulin (IVIG) regimens:

Therapeutic Plasma Exchange (TPE) will consist of 1x estimated plasma volume exchanges for 3 successive days (1-3) and then, after a one day interval to enable equilibration of autoantibodies between intra- and extra-vascular spaces, again on days 5, 6, 9, 11, 13, and 15.

Rituximab: One gm i.v. will be administered on day 6 and day 15 after completion of the TPE on those days.

Intravenous immunoglobulin (IVIG): 0.5 gm/kg/day i.v. on days 16-19

  • Arm B (n=17) - Treatment as Usual (TAU):

The same steroid regimen as described for Arm A, i.e., prednisone 60 mg (p.o.) on day 1, followed by 20 mg/day on days 2-5, 7-14, and 16-19 (or the i.v. methylprednisolone equivalent), and methylprednisolone 100 mg i.v. administered on days 6 and 15.

All patients enrolled in both cohorts at all sites will also receive empiric broad-spectrum antibiotics for 8 days. The empiric antibiotic regimen will be reassessed and tailored based on any subsequent cultures and sensitivity results.

Patients will be monitored carefully for occurrences of adverse events, laboratory test abnormalities, and changes in vital signs.

The respective treatment courses can be finished on an outpatient basis among enrolled patients who are able to be discharged from the hospital, if medically indicated, and if those treatment compliance can be assured.

Patients will be followed for the duration of their hospital admission after enrollment, and then observed as either inpatients or outpatients on days 19, 60, 90, 180, 270, and 365. A telephone contact will occur at monthly intervals, aside from those visits above. The total observation/subject is 365 days.

02

Conditions studied

  • Idiopathic Pulmonary Fibrosis, Acute Fatal Form

Keywords

  • Acute Exacerbation of Idiopathic Pulmonary Fibrosis
03

Who can participate

Ages eligible
40 Years to 85 Years
Sexes eligible
All
Accepts healthy volunteers
No

Inclusion criteria

  1. Age between 40-85 years old.
  2. A diagnosis of IPF that fulfills ATS/ERS Consensus Criteria.1
  3. Worsening or new development of dyspnea or hypoxemia within the last 30 days.
  4. Ground-glass abnormality and/or consolidation superimposed on a reticular or honeycomb usual interstitial pneumonitis (UIP) pattern on locally read chest CT scan.
  5. Ability and willingness to give informed consent (no surrogates) and adhere to study requirements.

Exclusion criteria

Exclusion Criteria:

  1. Diagnoses of current infection per clinical or microbial assessments.
  2. Diagnoses of an additional or alternative etiology for respiratory dysfunction based upon clinical assessment, including congestive heart failure, sepsis, thromboembolism, etc.
  3. History or serologic evidence of hepatitis B or C infection.
  4. Coagulopathy, defined as a International Normalized Ratio (INR) >1.6, partial thromboplastin time (PTT) > 2x control, fibrinogen \<100 mg/dL, or platelet count \<50 thousand (K) unless these abnormalities can be reversed safely.
  5. Hyperosmolar state or diabetic ketoacidosis to suggest uncontrolled diabetes, or uncontrolled hypertension (systolic BP >160 mm Hg and diastolic BP >100 mm Hg) that would contraindicate use of corticosteroids.
  6. Hemodynamic instability, defined as an inotrope or vasopressor requirement.
  7. History of reaction to blood products or murine-derived products or prior rituximab use.
  8. History of malignancy, excluding basal or squamous cell skin cancer and low-risk prostate cancer, the latter defined as stage T1 or T2a, with prostate specific antigen (PSA) less than 10 ng/dl. The experimental treatments are not known to promote cancer progression, and these criteria are within current guidelines.
  9. Unwillingness to accept blood product transfusion.
  10. Diagnosis of major comorbidities expected to interfere with study participation.
  11. Treatment for >14 days within the preceding month with >20 mg. prednisone (or equivalent) or any treatment during the last month with a cellular immuno-suppressant (e.g., cyclophosphamide, methotrexate, calcineurin inhibitors, mycophenolate, azathioprine, etc.). An exception will be made if the patient has a bronchoalveolar lavage (BAL) negative for pathogens.
  12. Current treatment with an angiotensin converting enzyme inhibitor that cannot be discontinued and/or substituted (to obviate hemodynamic complications during TPE).
  13. Concurrent participation in other experimental trials.
  14. Fertile females who do not agree to contraception or abstinence, or have a positive pregnancy test (urine or blood). IPF is a disease of older adults, and male predominant, so this will not be a frequent consideration.
  15. Presence of positive (abnormal) classical autoimmune tests: anti-nuclear antibody (ANA), rheumatoid factor (RF), Anti- Sjögren's-syndrome-related antigen (SSA) , and Anti-Cyclic Citrullinated Peptide (CCP). This criterion will eliminate patients with confounding classical autoimmune syndromes. Many IPF patients will have already had these tests, which are standard of practice (SOP) at many IPF centers, and these prior results will suffice if the tests were performed within the last year. Otherwise, these tests need to be performed prior to enrollment and they can usually be procured in 1-2 days. Based on experience, we anticipate \~10% of patients who fulfill all other IPF criteria will nonetheless be positive for one of these classical autoantibody tests.
  16. IgA deficiency (IgA level \<7 mg/dL)- to preclude IVIG reactions.
04

Study design

Phase
Phase 2
Primary purpose
Treatment
Allocation
Randomized
Intervention model
Parallel assignment
Masking
None (open label)
Enrollment
82 participants (actual)

Study arms

  • Experimental
    Autoantibody Reductive Therapy

    Therapeutic Plasma Exchange (TPE) consisting of 1x estimated plasma volume exchanges for 3 successive days (1-3) and then, after a one day interval to enable equilibration of autoantibodies between intra- and extra-vascular spaces, again on days 5, 6, 9, 11, 13, and 15. Rituximab: One gm i.v. will be administered on day 6 and day 15 after completion of the TPE on those days. Intravenous immunoglobulin (IVIG): 0.5 gm/kg/day i.v. on days 16-19 All subjects in this trial, including patients in this arm, will receive identical empiric antibiotics and steroids. The steroid dose is: Prednisone 60 mg (p.o.) on day 1, followed by 20 mg/day on days 2-5, 7-14, and 16-19 (or the i.v. methylprednisolone equivalent). Methylprednisolone 100 mg i.v. will be administered on days 6 and 15, as a premedication prior to the rituximab.

    Drug: Autoantibody Reductive Therapy

  • Active comparator
    Treatment as Usual (TAU)

    The same steroid regimen as described for the experimental arm, i.e., prednisone 60 mg (p.o.) on day 1, followed by 20 mg/day on days 2-5, 7-14, and 16-19 (or the i.v. methylprednisolone equivalent), and methylprednisolone 100 mg i.v. administered on days 6 and 15, as well as empiric antibiotics.

    Drug: Treatment as Usual (TAU)

Interventions

  • DrugAutoantibody Reductive Therapy

    TPE x 9, rituximab x 2, IVIG x 4. See arm/group descriptions for additional details.

  • DrugTreatment as Usual (TAU)

    Antibiotics and steroids

    Also known as: Antibiotics and steroids

05

What researchers measure

Primary outcomes

  1. %Survival

    Actuarial survival

    Time frame: 6 months

Secondary outcomes

  1. Percentage of Participants With a Change in Oxygen Requirements to Maintain Adequate SaO2

    Changes in amount of supplemental oxygen, as liters/min or % fractional inspired oxygen concentration, required to maintain arterial oxygen concentration (SaO2) \>/=93%

    Time frame: before and immediately after hospital treatment

  2. Walk Distance

    6 minute walk distance using standardized American Thoracic Society/European Respiratory Society (ATS/ERS) protocols.

    Time frame: 6 months

06

Results

Posted Feb 24, 2026

Participant flow

Participant flow — Overall Study
MilestoneAutoantibody Reductive TherapyTreatment as Usual (TAU)
Started3318
Completed3118
Not completed20
Withdrew: Withdrawal by subject10
Withdrew: Lost to follow-up10

Outcome measures

Primary%Survival

Actuarial survival

Time frame:
6 months
Reported as:
Mean · percentage of participants
%Survival
percentage of participantsAutoantibody Reductive TherapyTreatment as Usual (TAU)
%Survival44 ± 97 ± 6
SecondaryPercentage of Participants With a Change in Oxygen Requirements to Maintain Adequate SaO2

Changes in amount of supplemental oxygen, as liters/min or % fractional inspired oxygen concentration, required to maintain arterial oxygen concentration (SaO2) \>/=93%

Time frame:
before and immediately after hospital treatment
Reported as:
Number · % participants with O2 reductions
Percentage of Participants With a Change in Oxygen Requirements to Maintain Adequate SaO2
% participants with O2 reductionsAutoantibody Reductive TherapyTreatment as Usual (TAU)
Percentage of Participants With a Change in Oxygen Requirements to Maintain Adequate SaO25022
SecondaryWalk Distance

6 minute walk distance using standardized American Thoracic Society/European Respiratory Society (ATS/ERS) protocols.

Time frame:
6 months
Reported as:
Mean · feet
Walk Distance
feetAutoantibody Reductive TherapyTreatment as Usual (TAU)
Walk Distance245 ± 347133 ± 216

Adverse events

Collected over 180 days. Non-serious events are listed at a 5% frequency threshold.

Adverse event summary by group
GroupDeathsSeriousOther
Autoantibody Reductive Therapy18/33 (54.5%)5/33 (15.2%)6/33 (18.2%)
Treatment as Usual (TAU)16/18 (88.9%)0/18 (0%)2/18 (11.1%)
Most frequent serious events
Most frequent serious events
EventAutoantibody Reductive TherapyTreatment as Usual (TAU)
Hematoma at plasma exchange catheter siteBlood and lymphatic system disorders1/330/18
Transient ischemic attackNervous system disorders1/330/18
Pulmonary EdemaRespiratory, thoracic and mediastinal disorders1/330/18
TransaminitisHepatobiliary disorders1/330/18
Subcortical Cerebral IschemiaNervous system disorders1/330/18
Drug ReactionRespiratory, thoracic and mediastinal disorders1/330/18
Most frequent other events
Most frequent other events
EventAutoantibody Reductive TherapyTreatment as Usual (TAU)
LeukocytosisBlood and lymphatic system disorders6/332/18
RashSkin and subcutaneous tissue disorders4/331/18
WeaknessNervous system disorders3/330/18
HypotensionCardiac disorders2/331/18

Baseline characteristics

Age, Categorical
Age, Categorical(Participants)Autoantibody Reductive TherapyTreatment as Usual (TAU)Total
<=18 years000
Between 18 and 65 years000
>=65 years331851
Age, Continuous
Age, Continuous(years)Autoantibody Reductive TherapyTreatment as Usual (TAU)Total
Mean70 ± 770 ± 870 ± 7
Sex: Female, Male
Sex: Female, Male(Participants)Autoantibody Reductive TherapyTreatment as Usual (TAU)Total
Female13215
Male201636
Ethnicity (NIH/OMB)
Ethnicity (NIH/OMB)(Participants)Autoantibody Reductive TherapyTreatment as Usual (TAU)Total
Hispanic or Latino101
Not Hispanic or Latino311849
Unknown or Not Reported101
Race (NIH/OMB)
Race (NIH/OMB)(Participants)Autoantibody Reductive TherapyTreatment as Usual (TAU)Total
American Indian or Alaska Native000
Asian011
Native Hawaiian or Other Pacific Islander000
Black or African American101
White321749
More than one race000
Unknown or Not Reported000
Region of Enrollment
Region of Enrollment(participants)Autoantibody Reductive TherapyTreatment as Usual (TAU)Total
United States331851
07

Study locations

7 sites
  • University of Alabama at Birmingham
    Birmingham, Alabama 35233, United States
  • Dan Dilling
    Chicago, Illinois 60611, United States
  • Thomas Jefferson University Medical Center
    Philadelphia, Pennsylvania 19107, United States
  • Temple University Hospital
    Philadelphia, Pennsylvania 19140, United States
  • University of Pittsburgh Medical Center
    Pittsburgh, Pennsylvania 15213, United States
  • Baylor University Medical Center
    Houston, Texas 77030, United States
  • University of Utah Medical Center
    Salt Lake City, Utah 84112, United States
08

References and documents

Publications

  • Feghali-Bostwick CA, Tsai CG, Valentine VG, Kantrow S, Stoner MW, Pilewski JM, Gadgil A, George MP, Gibson KF, Choi AM, Kaminski N, Zhang Y, Duncan SR. Cellular and humoral autoreactivity in idiopathic pulmonary fibrosis. J Immunol. 2007 Aug 15;179(4):2592-9. doi: 10.4049/jimmunol.179.4.2592. PubMed 17675522 ↗
  • Gilani SR, Vuga LJ, Lindell KO, Gibson KF, Xue J, Kaminski N, Valentine VG, Lindsay EK, George MP, Steele C, Duncan SR. CD28 down-regulation on circulating CD4 T-cells is associated with poor prognoses of patients with idiopathic pulmonary fibrosis. PLoS One. 2010 Jan 29;5(1):e8959. doi: 10.1371/journal.pone.0008959. PubMed 20126467 ↗
  • Xue J, Gochuico BR, Alawad AS, Feghali-Bostwick CA, Noth I, Nathan SD, Rosen GD, Rosas IO, Dacic S, Ocak I, Fuhrman CR, Cuenco KT, Smith MA, Jacobs SS, Zeevi A, Morel PA, Pilewski JM, Valentine VG, Gibson KF, Kaminski N, Sciurba FC, Zhang Y, Duncan SR. The HLA class II Allele DRB1*1501 is over-represented in patients with idiopathic pulmonary fibrosis. PLoS One. 2011 Feb 23;6(2):e14715. doi: 10.1371/journal.pone.0014715. PubMed 21373184 ↗
  • Kahloon RA, Xue J, Bhargava A, Csizmadia E, Otterbein L, Kass DJ, Bon J, Soejima M, Levesque MC, Lindell KO, Gibson KF, Kaminski N, Banga G, Oddis CV, Pilewski JM, Sciurba FC, Donahoe M, Zhang Y, Duncan SR. Patients with idiopathic pulmonary fibrosis with antibodies to heat shock protein 70 have poor prognoses. Am J Respir Crit Care Med. 2013 Apr 1;187(7):768-75. doi: 10.1164/rccm.201203-0506OC. PubMed 23262513 ↗
  • Xue J, Kass DJ, Bon J, Vuga L, Tan J, Csizmadia E, Otterbein L, Soejima M, Levesque MC, Gibson KF, Kaminski N, Pilewski JM, Donahoe M, Sciurba FC, Duncan SR. Plasma B lymphocyte stimulator and B cell differentiation in idiopathic pulmonary fibrosis patients. J Immunol. 2013 Sep 1;191(5):2089-95. doi: 10.4049/jimmunol.1203476. Epub 2013 Jul 19. PubMed 23872052 ↗
  • Vuga LJ, Tedrow JR, Pandit KV, Tan J, Kass DJ, Xue J, Chandra D, Leader JK, Gibson KF, Kaminski N, Sciurba FC, Duncan SR. C-X-C motif chemokine 13 (CXCL13) is a prognostic biomarker of idiopathic pulmonary fibrosis. Am J Respir Crit Care Med. 2014 Apr 15;189(8):966-74. doi: 10.1164/rccm.201309-1592OC. PubMed 24628285 ↗
  • Donahoe M, Valentine VG, Chien N, Gibson KF, Raval JS, Saul M, Xue J, Zhang Y, Duncan SR. Autoantibody-Targeted Treatments for Acute Exacerbations of Idiopathic Pulmonary Fibrosis. PLoS One. 2015 Jun 17;10(6):e0127771. doi: 10.1371/journal.pone.0127771. eCollection 2015. PubMed 26083430 ↗
  • Collard HR, Moore BB, Flaherty KR, Brown KK, Kaner RJ, King TE Jr, Lasky JA, Loyd JE, Noth I, Olman MA, Raghu G, Roman J, Ryu JH, Zisman DA, Hunninghake GW, Colby TV, Egan JJ, Hansell DM, Johkoh T, Kaminski N, Kim DS, Kondoh Y, Lynch DA, Muller-Quernheim J, Myers JL, Nicholson AG, Selman M, Toews GB, Wells AU, Martinez FJ; Idiopathic Pulmonary Fibrosis Clinical Research Network Investigators. Acute exacerbations of idiopathic pulmonary fibrosis. Am J Respir Crit Care Med. 2007 Oct 1;176(7):636-43. doi: 10.1164/rccm.200703-463PP. Epub 2007 Jun 21. PubMed 17585107 ↗
  • Kulkarni T, Criner GJ, Kass DJ, Rosas IO, Scholand MB, Dilling DF, Summer R, Duncan SR. Design of the STRIVE-IPF trial- study of therapeutic plasma exchange, rituximab, and intravenous immunoglobulin for acute exacerbations of idiopathic pulmonary fibrosis. BMC Pulm Med. 2024 Mar 20;24(1):143. doi: 10.1186/s12890-024-02957-3. PubMed 38509495 ↗
  • Kulkarni T, Criner GJ, Kass DJ, Rosas IO, Scholand MB, Dilling DF, Summer R, Duncan SR. Design of the STRIVE-IPF Trial- Study of Therapeutic Plasma Exchange, Rituximab, and Intravenous Immunoglobulin for Acute Exacerbations of Idiopathic Pulmonary Fibrosis. Res Sq [Preprint]. 2024 Feb 28:rs.3.rs-3962419. doi: 10.21203/rs.3.rs-3962419/v1. PubMed 38464052 ↗

Study documents

  • Protocol and statistical analysis plan · May 7, 2020

Documents are hosted by the registry — open the source record to download them.

Individual participant data

Plan to share: No

09

Registry details

Key details

Study ID
NCT03286556
Lead sponsor
University of Alabama at Birmingham
Collaborators
National Heart, Lung, and Blood Institute (NHLBI), Brigham and Women's Hospital, Temple University, University of Pittsburgh
Responsible party
Steven R. Duncan, MD (Prinicpal Investigator, University of Alabama at Birmingham) — Principal investigator
First posted
Sep 18, 2017
Start date
Sep 4, 2018
Primary completion
Aug 1, 2024
Completion
Aug 1, 2024
Results posted
Feb 24, 2026
Last update
Feb 24, 2026

Oversight

Data monitoring committee
Yes
FDA-regulated drug
Yes
FDA-regulated device
No
View the source record on ClinicalTrials.gov ↗

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