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Multiple Sclerosis, Chronic Progressive

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KYV-101

Standard lymphodepletion regimen

Anti-CD20 mAB

Kyverna Therapeutics, Inc.

A Study of Anti-CD19 Chimeric Antigen Receptor T-Cell (CD19 CAR T) Therapy, in Subjects with Refractory Primary and Secondary Progressive Multiple Sclerosis

Multiple sclerosis (MS) is an autoimmune and neurodegenerative disease in which lymphocytes at first attack the myelin sheaths within the central nervous system (CNS), accompanied or later followed by axonal damage. B cells play a central and multifunctional role in the immunopathogenesis of MS. B cells present antigen to T cells in stimulating a pro-inflammatory immune cascade, secrete pathogenic cytokines, moderate T cell and myeloid cell functions, form structural B cell meningeal follicles within the human central nervous system and produce pathogenic antibodies upon evolution to plasma cells.

CD19-targeted chimeric antigen receptor (CAR) T cells harness the ability of cytotoxic T cells to directly and specifically lyse target cells to effectively deplete B cells in the circulation and in lymphoid and potentially non-lymphoid tissues. KYV-101, a fully human anti-CD19 CAR T-cell therapy, will be investigated in adult subjects with refractory primary and secondary progressive multiple sclerosis.

A Study of Anti-CD19 CAR T-Cell Therapy, in Subjects With Refractory Primary and Secondary Progressive Multiple Sclerosis

A Phase 2, Open-Label, Randomized, Multicenter Study of KYV-101, an Autologous Fully Human Anti-CD19 Chimeric Antigen Receptor T-Cell (CD19 CAR T) Therapy, in Subjects With Refractory Primary and Secondary Progressive Multiple Sclerosis (KYSA-7)

Confirmed disability Progression on the EDSS scale. The EDSS scale ranges from 0 to 10 in 0.5- unit increments that represent higher levels of disability. Scoring is based on an examination by a neurologist.

Incidence and severity of adverse events (AEs)

Incidence and severity of adverse events of special interests (AESIs)

Incidence and severity of serious adverse events (SAEs)

Composite Confirmed Disability Progression (CCPD)

Levels of Chimeric antigen receptor positive (CAR-positive) T cell counts

Serum cytokines will be measured by multiplexed mesoscale discovery (MSD) assay and will include cytokines historically associated with potential CAR T toxicity (CRS and ICANS) such as gamma interferon (IFNg) and interleukin 6 (IL-6).

Percentage of participants who develop anti-KYV-101 antibodies by immunoassays)

Kyverna Therapeutics

Disease Susceptibility

Pharmaceutical Solutions

All Drugs and Chemicals

Antineoplastic Agents

Cladribine

Immunosuppressive Agents

Immunologic Factors

Drug: Cladribine at a dose of 1.8 mg/kg of body weight. Cladribine will be given subcutaneously over 6 visits every 5-6 weeks.

Comparator: Placebo matched to the subcutaneous injection of cladribine.

Cladribine subcutaneous injection, 10 mg daily, for 2-3 consecutive days (depending on individual dose)

Cladribine Subcutaneous Injection

0.9% sodium chloride injected subcutaneously, 10 ml daily, for 2-3 consecutive days

0.9% Chloride Injection Sodium

Iwona Kurkowska-Jastrzebska, MD, PhD

Łukasz Smolinski, MD, PhD

Beata Błażejewska-Hyżorek, MD, PhD

Łukasz Smoliński, MD, PhD

The purpose of the study is to evaluate the efficacy and safety of subcutaneously administered cladribine versus placebo to stop inflammation and treat disease progression of non-active secondary progressive multiple sclerosis.

Multiple sclerosis is an inflammatory disease of the central nervous system. In most patients, it starts with a relapsing course (RMS) which is caused by acute inflammatory lesions in the brain and spinal cord. RMS transforms at later stages into progressive disease (secondary progressive MS). Currently approved disease-modifying treatments are effective in reducing clinical relapses and brain and spinal lesions visible in MR, but they perform poorly in preventing disease progression and overall disability accumulation. The growing evidence shows that disease progression partially depends on chronic inflammation present in the CNS. Drugs, which may cross the blood-brain barrier and reach inflammatory cells residing in the CNS might be effective in this stage of the disease. Cladribine is one of the DMT approved for RMS. It is a synthetic purine analog with selective lymphocyte toxicity, which enter the CNS and is found in cerebrospinal fluid. In patients treated with cladribine, the oligoclonal bands tend to disappear proving that neuroinflammation is diminished.

The participants of this clinical trial with the later non-active stage of MS are enrolled to be treated with cladribine subcutaneously or a non-active comparator (placebo) for 6 months and followed for the next 2 years, with an MRI scan and clinical evaluation every 6 months. The main questions it aims to answer are if in the non-active stage of MS cladribine is potent to lessen brain volume loss and if it is potent to attenuate inflammation in the CNS.

This is a randomized, placebo-controlled, double-blind, multi-center, phase 2 study of subcutaneous cladribine in non-relapsing, secondary progressive multiple sclerosis. Eligible patients will be randomly allocated in a 1:1 ratio to receive either placebo or subcutaneous cladribine at a dose of 1.8 mg/kg of body weight. The study will consist of three periods: screening, treatment, and follow-up. During the screening, the investigators will assess patient eligibility. During the treatment, cladribine will be given over 6 visit every 5-6 weeks. During the follow-up of 96 weeks, safety and efficacy assessments will be carried out on five visits: the first visit will take place 4 weeks after the last cladribine dose, and the remaining visits will take place every 24 weeks.

There will a rescue option of unblinding and treatment with a full dose of cladribine (cladribine arm) or approved medications (placebo arm) for patients with a severe relapse or ≥ 2 non-severe relapses after enrolment or with a substantial neuroimaging disease activity ≥ 4 Gd+ lesions in any scan, ≥ 3 Gd+ lesions in any two scans, ≥ 2 Gd+ lesions in any three scans, or ≥ 9 new/enlarging T2 lesions on any scan compared with baseline).

All raters will be blinded to treatment allocation. All neuroimaging examinations will be evaluated at a central neuroimaging unit by investigators blinded to treatment allocation.

Study type: interventional (clinical trial) Planned enrolment: 188 patients Allocation: randomized Masking: Double (Participant, Investigator) Primary purpose: Treatment Start Date: October 2022

Study design: The study aims to assess the safety and efficacy of subcutaneous cladribine in patients with SPMS who have not experienced relapses over a year and with or without active lesions on neuroimaging. The study will be randomized, placebo-controlled, and double blind. Because no treatment is approved for inactive SPMS, placebo was chosen as the comparator. Patients receiving other treatments for SPMS or immunosuppressant will not be included.

The study will consist of the following phases:

1. Screening phase (about 4 weeks)
2. Treatment phase, patients will be randomized 1:1 ratio of either cladribine 1,8mg/kg or placebo (30 weeks)
3. Follow-up phase , patients will be followed every 24 weeks for up to 122 weeks for safety and efficacy of the treatment;

Patients: The group of 188 patients fulfilling inclusion criteria and not-fulfilling exclusion criteria will enrolled to the study. All patient has to sign written informed consent form approved by Ethics Committee.

Blinding: Randomization and blinding will be done by "dual assessor" approach . Every site will have two teams of blinded and blinded investigators . The blinded investigators include Principal or treating investigators and rating investigators, as well as blinded treating nurse. The unblinded team includes: Randomizing investigator responsible also for laboratory assessment and unblinded nurse/pharmacist responsible for preparing drugs.

Intervention:

Experimental arm Drug: Cladribine at a dose of 1.8 mg/kg of body weight. Cladribine will be given subcutaneously over 6 visits every 5-6 weeks.

Comparator: Placebo matched to the subcutaneous injection of cladribine.

Follow-up: Patients will be assessed and baseline visit, and every 24 weeks over 24 months since the last dose of the interventional drug. The evaluations include:

1. Medical history, concomitant medication, relapse history
2. Physical examination, neurological examination
3. Clinical assessment: EDSS, T25FWT, 9-HPT,
4. MsQoL and CSSR scale
5. MRI of head and spinal cord (baseline, every 6 months for head and every 12 months for spinal cord)
6. Laboratory and biomarkers evaluation (hematology, coagulation, HIV serology, Hepatitis virus B and C serology, tuberculosis tests (Quantiferron test if necessary), ,

The primary end point will be percentage brain volume change between the last dose (week 24) and end of study (week 122). The primary endpoint was selected based on the widely discussed indications for designing studies in the SPMS. The main secondary clinical end points will assess the change in neurological function on the Expanded Disability Status Scale, Timed 25 Foot Walk, and 9-Hole Peg Test, which measures upper limb function. The change in cognitive function will be assessed with various neuropsychological tests. The main secondary neuroimaging end points will include change in the number of contrast-enhancing lesions, the number of T1-hypointesne lesions ("black holes"), and the volume of T2 lesions. The main exploratory end point will be the change in QSM rim+ lesions on brain neuroimaging; these lesions are markers of chronic, smoldering neuroinflammation that may take place behind an intact blood-brain barrier. Change in the concentrations of neurofilament light chain and glial fibrillary acidic protein, which are markers of brain tissue damage, will be main laboratory end points. An exploratory analysis of inflammatory protein biomarkers will be carried out in serum and cerebrospinal fluid of a selected patients (Luminex). The study will assess the safety of cladribine and its effect on quality of life.

The proposed intervention is well supported by the current evidence. Cladribine is among the few drugs that penetrate an intact blood-brain barrier, which allows action on lymphocytes resident in the central nervous system. The study will assess whether cladribine slows down disease progression clinically and it will use the best currently available indicators of disease progression: brain and cervical cord atrophy and the number of demyelinating lesions. Additionally, it will be assessed whether the presence of QSM rim+ lesions is associated with disease course and the therapeutic effect of cladribine. For example, a reduction in the number of these lesions during cladribine treatment would supports an action of the drug behind the blood-brain barrier. An association between QSM rim+ lesions and the therapeutic effect of cladribine could help select a subgroup of patients most likely to benefit from anti-inflammatory treatments. The measurement of serum biomarkers will enable an assessment of the activation of the peripheral immune system (cytokine, chemokines) and of the therapeutic effect of cladribine (NfL, GFAP). The positive results of the current project will allow the design of a phase 3 trial. A practical benefit of the proposed study is that patients with SPSM, who are currently not eligible for any treatment options, will have a choice to receive a potentially effective therapy, which costs substantially less compared to other therapies in MS.

Background: Multiple sclerosis (MS) is the most common chronic inflammatory, demyelinating disease of the central nervous system, with about 2.5 million patients worldwide, including 45 thousand in Poland. Most patients have relapsing-remitting MS (RRMS) at the start of the disease, in which neurological symptoms appear during relapses and may subside. There is a dozen of disease-modifying treatments for this form of the disease. Several years after the diagnosis of RRMS, the disease progresses into SPMS, in which disability worsens gradually independently of relapses. Patients with SPMS suffer from restricted mobility (need walking aids, wheelchair), cognitive impairment, (difficulties in workplace and in managing everyday life), depression, pain due to spasticity, chronic fatigue, lack of sphincter control, or sexual dysfunction. These patients need more medical help (office visits, rehabilitation, hospitalization), are more often unemployed, and have a lower quality of life than do patients with RRMS. Currently, three disease-modifying treatments are available for patients with SPMS in Europe: interferon beta-1b (low efficacy), mitoxantrone (serious adverse effects), and siponimod. However, these medications can be used only in patients with active disease, i.e., in those with still observed relapses or active brain lesions on magnetic resonance imaging. Therefore, about a half of patients with SPMS cannot receive any disease-modifying treatment. The current understanding of the pathogenesis of MS suggests that there are two types of neuroinflammation since disease onset. Type-1 neuroinflammation is characterized by an acute, focal infiltration of pathogenic lymphocytes and autoantibodies, which is associated with blood-brain barrier disruption. This type of neuroinflammation may be responsible for relapses and contrast-enhancing lesions. Type-2 neuroinflammation is a chronic, smoldering process that takes place behind a closed blood-brain barrier, and it is characterized by slowly expanding lesions and follicle-like lymph structures in the meninges, and diffuse inflammatory changes in white matter and cortex. Other characteristics of type-2 neuroinflammation include microglial and astroglial activation, delayed maturation of oligodendrocytes, and inhibition of remyelination. These processes cause disease progression independently of relapses. Both types of neuroinflammation occur simultaneously since disease onset, but type-2 neuroinflammation is thought to predominate in the secondary progressive phase. Standard neuroimaging methods cannot pinpoint lesions that are specific for type 2 neuroinflammation, but longitudinal brain atrophy and enlargement of lesions can indirectly measure its magnitude. Quantitative susceptibility mapping (QSM), a new imaging technique, can indicate chronic inflammatory lesions that are surrounded by active microglia at the lesion border. Microglia because of iron load form a hypointense rim, and might be thus shown by QSM technique (rim+ lesions). However, QSM is not currently used in clinical practice it is now recommended for use in clinical trials.

The currently available disease modifying-treatments for SPMS act solely or mainly on type-1 neuroinflammation, and because of that they are approved for patients with relapses or active lesions only. Cladribine is approved for the treatment of RRMS. Cladribine substantially decreases the number of contrast-enhancing lesions and relapse frequency in patients with RRMS (an effect on type-1 neuroinflammation). Cladribine may also act on type-2 neuroinflammation i.e. on the autoreactive lymphocytes resident in the central nervous system, including tertiary lymphoid structures, because cladribine penetrates into the central nervous system through an intact blood-brain barrier. The effect on type-2 neuroinflammation is supported by the observation that oligoclonal bands disappear in patients with RRMS and SPMS after cladribine treatment.

Cladribine vs Placebo for Non-active Progressive Multiple Sclerosis (CLASP-MS).

Safety and Efficacy of Subcutaneous Cladribine for Nonrelapsing, Secondary Progressive Multiple Sclerosis (CLASP-MS): a Randomized, Placebo-controlled, Double-blind, Phase 2 Study.

brain volume to total intracranial volume

Time to 24-week confirmed composite progression of disability defined as the occurrence of any of the following events: (1) an increase in the EDSS score of 1 or greater in patients with baseline EDSS ≤ 5.5 or of 0.5 or greater in those with baseline EDSS \> 5.5; (2) an increase of 20% or more in Timed 25-Foot Walk; (3) an increase of 20% or more in the 9-Hole Peg Test.

Cognitive performance assessed with Symbol-Digit Modality Test

Cognitive performance assessed with California Verbal Learning Test \[Polish version 2010\]

The MSQOL-54 is a structured, self-report questionnaire filled by the patient.The 54-item instrument generates 12 subscales along with two summary scores, and two additional single-item measures. The summary scores are the physical health composite summary and the mental health composite summary, each may achieve final score from 0 to 100 points.

Number of Gd+ lesions Number of new/enlarging T2 lesions

Concentration of neurofilament light chain in serum

Presence of oligoclonal bands in cerebrospinal fluid (selected patients who will sign an additional consent)

Nalecz Institute of Biocybernetics and Biomedical Engineering, Polish Academy of Sciences

Mossakowski Medical Research Centre Polish Academy of Sciences

Poznan University of Medical Sciences

Military Institute of Aviation Medicine

Institute of Psychiatry and Neurology, Warsaw

Recurrence

Participants receive masitinib (4.5 mg/kg/day), given orally twice daily.

Participants receive masitinib (4.5 mg/kg/day), given orally twice daily, with a dose escalation to 6 mg/kg/day after 3 months of treatment.

Participants receive placebo given orally twice daily.

Participants receive placebo, given orally twice daily, with a matched dose escalation after 3 months of treatment.

Masitinib

Placebo

Patrick Vermersch, MD, PhD

The purpose of this study is to compare the safety and efficacy of masitinib 6 mg/kg/day versus placebo in the treatment of patients with primary progressive multiple sclerosis or relapse-free secondary progressive multiple sclerosis.

Masitinib is a selective tyrosine kinase inhibitor that is thought to exert a neuroprotective effect through its activity on mast cells and other non-neuronal cells of the central nervous system, with subsequent modulation of inflammatory and neurodegenerative processes. The objective of this study is to compare the efficacy and safety of masitinib at 4.5 mg/kg/day versus matched placebo, or masitinib at 4.5 mg/kg/day with a dose escalation to 6 mg/kg/day after 3 months of treatment versus matched placebo, in the treatment of patients with primary progressive multiple sclerosis or relapse-free secondary progressive multiple sclerosis. Approximately 600 patients will be randomized into four treatment groups with a 2:2:1:1 design. The primary outcome measure is the Expanded Disability Status Scale (EDSS) after 96 weeks of treatment in the overall study population with subgroup analysis performed in stratum (primary progressive multiple sclerosis / secondary progressive multiple sclerosis).

Efficacy and Safety of Masitinib in the Treatment of Progressive Multiple Sclerosis

A 96 Week, Prospective, Multicentre, Randomized, Double-blind, Placebo-controlled, 2 Parallel-groups, Phase 3 Study to Compare Efficacy and Safety of Masitinib 4.5 mg/kg/Day Versus Placebo in the Treatment of Patients With Primary Progressive or Relapse-free Secondary Progressive Multiple Sclerosis

Expanded Disability Status Scale (EDSS) after 96 weeks of treatment

Multiple Sclerosis Quality of Life 54 items (MSQOL-54)

Multiple Sclerosis Functional Composite (MSFC)

AB Science

Micronutrients

Hematinics

Iron

Ferrosoferric Oxide

Parenteral Nutrition Solutions

Subjects will undergo MR imaging of the brain and cervical spine for pre- and post-administration of gadoteridol (0.2 mL/kg), then pre- and post-administration of ferumoxytol (4 mg/kg). Scans will be obtained over the course of two separate imaging visits.

Subjects will receive a single, weighted dose of intravenous ferumoxytol (4 mg/kg) diluted in 50 mL of saline.

Ferumoxytol infusion

Subjects will receive a single, weighted dose of intravenous gadoteridol (0.2 mL/kg).

Gadoteridol

3T MR imaging of the brain and cervical spine pre- and post-administration of gadolinium, then pre- and 96 hours (±24 hours) post-administration of ferumoxytol

MRI Brain and Cervical Spine

M. Mateo Paz Soldan, MD, PhD

This pilot study takes the innovative approach of using ultrasmall superparamagnetic iron oxide (USPIO) nanoparticle enhanced MRI to measure activity of the innate immune system within MS lesions. Activity of innate immunity has been hypothesized as one of the critical pathologic processes underpinning neurologic worsening in progressive MS. As such, in the short term this project proposes to investigate USPIO uptake in SPMS lesions as a promising in vivo imaging biomarker for chronic-active lesions, as distinguished from chronic-inactive lesions.

Novel Imaging Markers in SPMS

Novel Imaging Markers of Innate Immune Activation in Secondary Progressive Multiple Sclerosis

Assess the safety and tolerability of ferumoxytol in Secondary Progressive MS cohort based on Adverse Events

University of Utah

Assistant Professor, Department of Neurology, Division of Neuroimmunology

Disease Progression

Dermatologic Agents

Dimethyl Fumarate

BG00012 120 mg (1 BG00012 120 mg capsule + 1 matching placebo capsule) orally twice daily (BID) for 1 week, followed by BG00012 240 mg orally BID thereafter.

BG00012 120 mg capsule orally once a day supplemented with matching placebo capsules for the first 4 weeks of treatment, as an additional blinding measure. Matched placebo capsules only thereafter.

dimethyl fumarate

Medical Director

The primary objective of the study is to investigate whether treatment with BG00012 (dimethyl fumarate) compared with placebo slows the accumulation of disability not related to relapses in participants with secondary progressive multiple sclerosis (SPMS). The secondary objective of the study is to assess the effect of BG00012 compared with placebo on patient-reported outcomes, brain atrophy, and cognitive function.

BG00012 and Delay of Disability Progression in Secondary Progressive Multiple Sclerosis

A Multicenter, Randomized, Double-Blind, Placebo-Controlled Study of the Efficacy and Safety of BG00012 in Delaying Disability Progression in Subjects With Secondary Progressive Multiple Sclerosis

Time to onset of confirmed progression of disability is defined as 1 or more of the following criteria, confirmed at ≥ 6 months after start of treatment and at Week 108 using 1 or more of the following assessments: Expanded Disability Status Scale (EDSS) score increased from Baseline of ≥ 1 point if baseline EDSS ≤ 5.5, or ≥ 0.5 point if Baseline EDSS ≥ 6.0; Timed 25-Foot Walk (T25FW) ≥ 20% increase from Baseline in the time taken for the 25-foot walk; worsening on the 9-Hole Peg Test (9HPT; ≥ 20% increase from Baseline in the time taken for the 9HPT, confirmed in the same hand). The EDSS measures disability status on a scale ranging from 0 to 10, with higher scores indicating more disability. The T25FW is a quantitative mobility and leg function performance test where the participant is timed while walking for 25 feet. The 9HPT is a quantitative test of upper extremity function that measures the time it takes to place 9 pegs into 9 holes and then remove the pegs.

MSWS-12 is a participant self-assessment of walking limitations due to multiple sclerosis (MS) during the past 2 weeks. It contains 12 items that measure the impact of MS on walking. Items are summed to generate a total score and transformed to a scale with a range of 0 to 100, where high scores indicate greater negative impact on walking.

The ABILHAND Questionnaire measures the participant's perceived difficulty in performing everyday manual activities in the last 3 months. Participants fill in the 56-item questionnaire by estimating their own difficulty or ease in performing each of the 56 activities. Items are summed to generate a total score and transformed to a scale with a range of 0 to 100, where high scores indicate greater impact on manual ability.

Whole brain volume is measured by magnetic resonance imaging (MRI).

The SDMT measures the time to pair abstract geometric symbols with specific numbers. The score is the number of correctly coded items from 0-110 in 90 seconds. A higher score indicates a better outcome.

Biogen

Data summaries of adverse events are descriptive in nature and the comparison between treatment groups might not be appropriate due to the small number of participants and limited study follow-up duration.

BG00012 120 mg capsule orally QD supplemented with matching placebo capsules for the first 4 weeks of treatment. Matched placebo capsules only thereafter for up to 108 weeks.

BG00012 120 mg orally BID for 1 week, followed by BG00012 240 mg orally BID beginning on Day 8 for up to 108 weeks.

Tecfidera 240 mg BID

Total

Age, Continuous

< 20 years

20 to 29 years

30 to 39 years

40 to 49 years

>= 50 years

Age, Customized

Sex: Female, Male

The study was terminated early by the sponsor for business reasons. Efficacy, patient-reported outcomes, and pharmacodynamic data were not analyzed.

Biogen Study Medical Director

BG00012 120 mg capsule orally once a day (QD) supplemented with matching placebo capsules for the first 4 weeks of treatment. Matched placebo capsules only thereafter for up to 108 weeks.

BG00012 120 mg orally twice daily (BID) for 1 week, followed by BG00012 240 mg orally BID beginning on Day 8 for up to 108 weeks.

The limited number of participants enrolled and the early termination of the study resulted in efficacy data not collected, and efficacy outcomes not analyzed, as per the pre-specified plan of analysis.

Time to Disability Progression Independent of Relapse

Change From Baseline to 2 Years on the 12-Item Multiple Sclerosis Walking Scale (MSWS-12)

Change From Baseline to Week 108 in ABILHAND Questionnaire Score

Percentage Change From Baseline to Week 108 in Whole Brain Volume

Change From Baseline to Week 108 in Cognitive Function as Measured by the Symbol Digit Modalities Test (SDMT)

Overall Study

500mg MBP8298 IV every six months for a period of two years

MBP8298

Clyde E Markowitz, MD

This study will assess the efficacy and safety of MBP8298 compared to placebo in subjects with Secondary Progressive Multiple Sclerosis (SPMS)

Efficacy and Safety of MBP8298 in Subjects With Secondary Progressive Multiple Sclerosis

A Double-Blind, Placebo Controlled Multi-Center Study to Evaluate the Efficacy and Safety of MBP8298 in Subjects With Secondary Progressive Multiple Sclerosis

Study title	NCT ID	Conditions	Interventions	Eligibility	Organization
A Study of Anti-CD19 CAR T-Cell Therapy, in Subjects With Refractory Primary and Secondary Progressive Multiple Sclerosis	NCT06384976	Multiple Sclero... Multiple Sclero... Multiple Sclero...	KYV-101 Standard lympho... Anti-CD20 mAB	18 Years - 60 Years	Kyverna Therapeutics
Cladribine vs Placebo for Non-active Progressive Multiple Sclerosis (CLASP-MS).	NCT05961644	Multiple Sclero... Multiple Sclero...	Cladribine Subc... 0.9% Chloride I...	30 Years - 65 Years	Institute of Psychiatry and Neurology, Warsaw
Efficacy and Safety of Masitinib in the Treatment of Progressive Multiple Sclerosis	NCT01433497	Multiple Sclero... Multiple Sclero... Multiple Sclero...	Masitinib Placebo	18 Years - 75 Years	AB Science
Novel Imaging Markers in SPMS	NCT05357833	Secondary Progr... Multiple Sclero... Multiple Sclero...	Ferumoxytol inf... Gadoteridol MRI Brain and C...	35 Years - 65 Years	University of Utah
BG00012 and Delay of Disability Progression in Secondary Progressive Multiple Sclerosis	NCT02430532	Multiple Sclero...	dimethyl fumara... Placebo	18 Years - 58 Years	Biogen
Efficacy and Safety of MBP8298 in Subjects With Secondary Progressive Multiple Sclerosis	NCT00468611	Multiple Sclero...	MBP8298	18 Years - 65 Years	BioMS Technology Corp.
Cladribine vs Placebo for Non-active Progressive Multiple Sclerosis (CLASP-MS).	NCT05961644	Multiple Sclero... Multiple Sclero...	Cladribine Subc... 0.9% Chloride I...	30 Years - 65 Years	Institute of Psychiatry and Neurology, Warsaw
Novel Imaging Markers in SPMS	NCT05357833	Secondary Progr... Multiple Sclero... Multiple Sclero...	Ferumoxytol inf... Gadoteridol MRI Brain and C...	35 Years - 65 Years	University of Utah

Spots Global Cancer Trial Database for multiple sclerosis, secondary progressive