Natalizumab for Multiple Sclerosis: Understanding Treatment Options

Written by Editor

Disclaimer: This article is for informational and educational purposes only and should not be regarded as medical advice, diagnosis or a recommendation for any particular treatment. Multiple sclerosis is highly individual, and treatment decisions depend on the type and activity of MS, MRI findings, previous therapies, blood-test results, other medical conditions and the patient’s own circumstances. Anyone considering changing or starting a disease-modifying therapy should discuss the benefits and risks with their neurologist or specialist MS team.

When MS Breaks Through Treatment

Understanding JC Virus, PML Risk and Other High-Efficacy Treatment Options.

When MS Remains Active Despite Treatment: What Patients Need to Know About Natalizumab, JC Virus, PML, Alternative Disease-Modifying Therapies and Stem Cell Transplantation

Modern disease-modifying therapies have transformed the treatment of multiple sclerosis (MS), but unfortunately no medication can guarantee that the disease will remain completely inactive.

A person may have very few obvious symptoms, yet an MRI scan can reveal new or enlarging lesions. This is sometimes described as radiological disease activity or breakthrough disease activity.

Where new lesions appear despite treatment with a high-efficacy disease-modifying therapy such as alemtuzumab (Lemtrada), the MS team may reconsider whether the existing treatment is still providing sufficient control.

This does not necessarily mean that the previous treatment was a failure. Alemtuzumab works by substantially changing the immune-cell population and can provide long periods of disease control for many people. However, MS can become active again, and continued MRI activity can be a reason to consider switching treatment or escalating therapy. The MS Trust states that new MRI activity despite treatment can indicate that the disease remains active and may lead the MS team to discuss another disease-modifying therapy.

One treatment that may be considered for highly active relapsing MS is natalizumab.

What Is Natalizumab?

Natalizumab is a monoclonal antibody used to treat very active relapsing multiple sclerosis.

The original brand is Tysabri, while Tyruko is a natalizumab biosimilar.

Rather than broadly destroying immune cells, natalizumab works by blocking a molecule involved in helping certain immune cells cross from the bloodstream into the brain and spinal cord. By limiting the movement of these inflammatory immune cells into the central nervous system, natalizumab can reduce the inflammatory attacks responsible for MS lesions.

It is considered a high-efficacy disease-modifying therapy.

Clinical trial evidence indicates that natalizumab can reduce MS relapses by around two-thirds to 70%, while MRI studies have shown substantial reductions in new inflammatory lesions.

Natalizumab is generally given every four weeks. Depending on the product and NHS arrangements, treatment may be given intravenously by infusion or through subcutaneous injections.

Importantly, updated NICE guidance published in January 2026 expanded access to natalizumab for certain adults with highly active relapsing-remitting MS after previous disease-modifying treatment.

Why Might Natalizumab Be Suggested After Another Treatment?

One of natalizumab’s advantages is that it acts relatively quickly.

When MRI scans show substantial ongoing inflammatory activity, neurologists may want a treatment capable of rapidly suppressing further MS activity rather than waiting many months to determine whether another therapy is working.

NICE experts noted during the 2026 appraisal that natalizumab’s relatively rapid action can make it particularly relevant for people with very active disease where further inflammatory attacks could result in additional disability.

This is one reason natalizumab may enter the conversation where another disease-modifying treatment has not prevented new lesions.

However, natalizumab has a particular safety concern that patients need to understand before treatment begins: progressive multifocal leukoencephalopathy, or PML.

What Is JC Virus?

The JC virus, usually abbreviated to JCV, is extremely common.

It is named after the initials of the patient in whom the virus was first identified and has nothing specifically to do with multiple sclerosis.

The MS Trust estimates that somewhere between 40% and 90% of the general population has been exposed to JC virus. Most people never know they have encountered it because it normally causes no symptoms and remains controlled by the immune system.

Therefore:

Being JC virus positive does not mean someone has PML.

It usually means that antibodies showing previous exposure to JC virus have been detected in their blood.

For most people, JC virus remains harmless.

The problem can arise when certain treatments alter immune surveillance sufficiently for the virus to reactivate in the central nervous system.

That can lead to PML.

What Is PML?

Progressive multifocal leukoencephalopathy (PML) is a rare but potentially life-threatening infection of the brain caused by reactivation of JC virus.

It damages the cells responsible for maintaining myelin, the protective covering around nerve fibres.

That makes PML particularly important in MS because some of its neurological symptoms can initially resemble an MS relapse.

Symptoms may include progressive weakness, changes in coordination, visual problems, speech or communication difficulties, cognitive changes and sometimes changes in behaviour or personality.

PML can cause severe permanent neurological disability and can be fatal. However, monitoring has improved considerably, and detecting PML before significant symptoms develop can improve outcomes.

Why Is Natalizumab Associated With PML?

Among MS disease-modifying therapies, natalizumab has the clearest recognised association with PML.

This does not mean that most people taking natalizumab will develop PML. They will not.

Risk varies significantly from one individual to another.

Three important factors are considered when doctors assess natalizumab-associated PML risk:

JC virus antibody status and antibody index, duration of natalizumab treatment, and previous exposure to certain immunosuppressive medicines.

The risk generally rises after approximately two years of natalizumab treatment, particularly in people who are JC virus antibody positive.

The JCV antibody index gives further information about the level of antibodies found in the blood. In appropriate patients, lower index readings are associated with lower PML risk, while an index above approximately 1.5, particularly after more than two years of treatment, can indicate a substantially higher risk.

European Medicines Agency guidance states that for people who are JCV-antibody negative, the estimated PML risk is around 0.1 per 1,000 people, although antibody-negative patients still require repeat testing because JCV status can change over time. https://www.ema.europa.eu/en/medicines/human/EPAR/tysabri

A positive JCV result therefore should not automatically be interpreted as meaning natalizumab cannot be used. It changes the risk calculation and may influence how treatment is monitored, how long it is continued, or whether another therapy is considered.

Monitoring JC Virus and PML Risk

Before natalizumab is started, patients would normally have JCV antibody testing and an MRI scan that can be used as a baseline.

Repeat JCV blood tests are then undertaken during treatment.

People at increased PML risk may undergo MRI scans more frequently. European guidance recommends considering MRI monitoring every three to six months for higher-risk patients.

If doctors suspect PML because of symptoms or an MRI abnormality, natalizumab should be stopped while PML is investigated. Further testing may include specialised MRI sequences and testing cerebrospinal fluid for JC virus DNA using PCR.

There is also evidence that extended-interval natalizumab dosing, approximately every six weeks rather than every four weeks in selected patients, may reduce PML risk. This is a specialist decision and should never be attempted simply by delaying treatment without medical advice.

Advantages and Disadvantages of Natalizumab

Natalizumab has several important advantages. It is a highly effective MS therapy, acts relatively rapidly and can substantially reduce both relapses and new inflammatory MRI lesions. This can be particularly valuable when MS is highly active.

The principal disadvantage is its association with PML, especially in patients who are JCV positive and remain on treatment for longer periods.

Other reported side effects include headaches, dizziness, nausea, urinary tract infections, joint pain, tiredness, allergic or infusion reactions and liver problems. Some people also develop antibodies against natalizumab that reduce its effectiveness.

Natalizumab also requires careful planning if it is stopped. MS disease activity can return after discontinuation, so neurologists generally plan the next treatment rather than simply leaving a prolonged untreated gap.

Are There Alternatives to Natalizumab?

Yes.

Natalizumab is not the only high-efficacy treatment available for active relapsing MS.

Current NICE guidance includes several treatment options for highly active disease where MS continues to show activity despite treatment. These include ocrelizumab, ofatumumab, ublituximab, cladribine and natalizumab, among others, depending on the particular clinical situation.

There is no universal “best” MS drug. The appropriate choice depends on how aggressively the disease is behaving, previous treatments, infection history, immune-system status, pregnancy considerations, MRI findings, JCV status and the patient’s preferences.

Ocrelizumab-Ocrevus

Ocrelizumab is another highly effective monoclonal antibody. Unlike natalizumab, it targets CD20-positive B cells, which are believed to play an important role in the abnormal immune response seen in MS.

Treatment is generally given at approximately six-month intervals.

Its advantages include high efficacy and comparatively infrequent dosing.

The main concerns include increased susceptibility to infections, infusion or injection reactions, herpes infections and reductions in immune protection in some patients.

PML has been reported with ocrelizumab, but it appears considerably less commonly than with natalizumab, and several recorded cases occurred in people who had previously taken another medicine associated with PML.

For somebody particularly concerned about natalizumab and JCV, ocrelizumab is therefore one of the high-efficacy alternatives worth discussing with an MS specialist, although it has its own immune-related risks.

Ofatumumab-Kesimpta

Ofatumumab also targets CD20-positive B cells.

Unlike ocrelizumab, it is generally administered as a monthly subcutaneous injection, which can be self-administered after appropriate training.

It is considered a highly effective treatment and may offer greater independence for patients who would prefer not to regularly attend an infusion clinic.

Common issues include injection reactions, respiratory infections, urinary infections, herpes infections and reduced immunoglobulin levels.

PML has not been reported in MS clinical trials using the licensed MS dose, although a theoretical risk remains because of its effect on the immune system.

Ublituximab-Briumvi

Ublituximab is another B-cell-depleting anti-CD20 treatment.

It is administered by intravenous infusion, with maintenance treatment approximately every six months.

NICE recommended ublituximab for relevant patients in England and Wales in late 2024, and NHS guidance now includes it among high-efficacy treatment options.

The principal side effects are infusion-related reactions and infections. Because it suppresses B cells, patients are screened and monitored for immune-related complications.

As of the available safety data cited by the MS Trust, no PML cases had been reported in people receiving ublituximab for MS up to February 2025, although a theoretical risk remains.

Cladribine-Mavenclad

Cladribine differs significantly from the antibody treatments.

It is given as tablets in short treatment courses rather than continuously. Treatment is normally given during two periods separated by approximately twelve months, with the intention of providing longer-term disease control after immune-system reconstitution.

This can be attractive for people who prefer not to have continuous injections or infusions.

However, cladribine reduces lymphocyte numbers and can increase susceptibility to infections, particularly shingles. Blood monitoring is therefore required.

For extremely active disease, the speed and expected degree of disease suppression required may influence whether a neurologist favours natalizumab or an anti-CD20 treatment instead.

What About Stem Cell Therapy for MS?

One of the most important developments in aggressive MS treatment is autologous haematopoietic stem cell transplantation, usually abbreviated to AHSCT or HSCT.

This needs an important clarification.

AHSCT does not involve injecting stem cells into the brain to repair damaged nerves.

It is primarily an immune-system treatment.

Doctors first collect the patient’s own haematopoietic stem cells, the cells capable of rebuilding the blood and immune system.

Chemotherapy is then used to suppress or partially destroy the existing immune system responsible for attacking myelin.

The patient’s own previously collected stem cells are subsequently returned to the bloodstream, allowing a new immune system to develop.

The aim is effectively to reset the immune system and stop it from launching further inflammatory attacks against the central nervous system.

AHSCT cannot currently regrow nerves that have already been permanently damaged and should not be confused with experimental regenerative stem-cell treatments marketed by some private clinics.

The MS Society describes AHSCT as the only proven stem-cell treatment currently used for MS, while other forms of regenerative stem-cell treatment remain experimental.

Who May Benefit Most From AHSCT?

Evidence suggests AHSCT works best in carefully selected people with highly active inflammatory relapsing MS, particularly when they continue to experience relapses or new MRI lesions despite high-efficacy treatment.

Current European guidance particularly supports AHSCT in people who have ongoing inflammatory disease despite highly effective therapies such as alemtuzumab, natalizumab, ocrelizumab, ofatumumab or other appropriate high-efficacy DMTs.

The evidence is strongest among people who are relatively young, have had MS for a shorter period, remain below a certain level of disability and continue to show active inflammation on MRI or through relapses.

The MS Society notes that the evidence is strongest for patients with an EDSS of 5.5 or below, preferably aged below approximately 45 and with MS of less than around ten years’ duration, although individual specialist assessments are required.

People in Wales who meet the criteria can potentially be referred to specialist AHSCT services in England, although access remains limited and decisions are made by specialist multidisciplinary teams.

Is AHSCT Better Than Natalizumab or Ocrelizumab?

This question is still being researched.

Observational studies suggest that AHSCT can provide extremely strong suppression of inflammatory MS activity in appropriately selected people.

However, it is not possible to conclude that AHSCT is universally superior to high-efficacy treatments such as natalizumab or ocrelizumab.

A large observational comparison found AHSCT and ocrelizumab had broadly similar relapse and disability outcomes over the shorter follow-up available, while AHSCT showed some advantages compared with other treatments. Because this was not a randomised head-to-head trial, the results require careful interpretation.

A major UK study called StarMS is directly comparing AHSCT with several high-efficacy MS treatments. Recruitment finished in 2024, and results are expected around 2027.

Until stronger comparative evidence is available, AHSCT and modern high-efficacy DMTs should be viewed as different treatment strategies rather than assuming one is automatically better.

The Risks of AHSCT

AHSCT is considerably more intensive than taking a conventional disease-modifying drug.

Because chemotherapy deliberately suppresses the immune system, there is a period when the patient becomes highly susceptible to infection.

Hospital isolation is normally required while the immune system begins rebuilding, and infection precautions may continue for months afterwards.

Chemotherapy can also cause nausea, hair loss, fatigue and other complications.

Another particularly important consideration for younger people is fertility. Chemotherapy used during AHSCT can damage the ovaries or testes, potentially causing infertility or early menopause. Fertility preservation may therefore need to be discussed before treatment.

There is also a small risk of developing secondary autoimmune disorders, cancer and serious complications.

Rarely, AHSCT can be fatal. The MS Society reports that since 2005 the treatment-related death rate has been approximately one in 330 people undergoing HSCT for MS, although safety has improved considerably as patient selection and treatment protocols have improved.

This is why AHSCT is performed only after careful evaluation by specialist neurology and haematology teams.

PML Risk Across Different MS Treatments

Natalizumab has the most established PML risk among currently used MS disease-modifying therapies.

Very rare cases have also occurred with treatments including ocrelizumab, fingolimod and dimethyl fumarate, while PML has not been reported in MS patients receiving some other therapies at their licensed MS doses.

The MS Society notes that PML risk varies enormously between medicines and individuals. With natalizumab, risk can range from around one in 10,000 to considerably higher levels in particular JCV-positive risk groups, depending on JCV status, treatment duration and previous immunosuppression.

Consequently, the relevant question is not simply:

“Can this medication cause PML?”

The more useful question is:

“What is my individual PML risk compared with the risk of allowing highly active MS to remain inadequately controlled?”

That is the balance neurologists and patients need to consider together.

New MRI Lesions Matter, Even Without an Obvious Relapse

One of the most important lessons from modern MS monitoring is that someone does not necessarily need to experience a dramatic clinical relapse for their disease to be active. https://www.abovems.com/en_us/home/what-is-ms/ms-education/understanding-your-ms/monitoring-your-ms.html

MRI scans can detect silent inflammatory disease activity.

New or enlarging lesions show that inflammatory activity has occurred somewhere within the central nervous system, even if the patient has not noticed a corresponding symptom.

The number of lesions alone does not determine how much disability someone will experience. Their location, size, whether they are actively enhancing, whether spinal-cord lesions are present, and whether there has been clinical deterioration are also important.

However, the appearance of multiple new lesions while somebody is already receiving treatment is something an MS specialist would normally take seriously because one objective of disease-modifying treatment is to prevent precisely this form of new inflammatory damage.

Alpha-Lipoic Acid, the OCTOPUS Trial and Parallel Biobanking Research

Another developing area of multiple sclerosis research involves alpha-lipoic acid (ALA), a naturally occurring compound with antioxidant properties that is being investigated for its potential to protect nerve cells from damage.

Alpha-lipoic acid is already available commercially as a dietary supplement, but the formulation and dose being studied in clinical trials should not be confused with over-the-counter supplements. Researchers have specifically warned that commercially available products may differ from the pharmaceutical-grade preparation used in studies and that people with MS should not attempt to reproduce trial treatment themselves.

What Is the OCTOPUS Trial?

OCTOPUS, Optimal Clinical Trials Platform for Multiple Sclerosis, is a major UK clinical trial designed specifically for people with primary progressive and secondary progressive multiple sclerosis.

Rather than investigating one drug at a time through a traditional trial lasting many years, OCTOPUS uses a multi-arm, multi-stage, or MAMS, design. Several potential treatments can be compared against a shared control group, allowing researchers to stop treatments that do not appear promising while continuing those showing signs of benefit. New treatment arms can also be introduced later. Researchers estimate that this approach could identify effective treatments considerably faster than conventional trial designs.

The first treatments investigated were metformin and R/S-alpha-lipoic acid.

In September 2026, researchers announced the first major interim decision from OCTOPUS. The combined MRI and clinical evidence indicated that alpha-lipoic acid showed sufficient evidence of potential benefit to progress into the next stage of the study, while metformin did not, and its trial arm was stopped.

This is an encouraging development, but it is important not to interpret it as proof that alpha-lipoic acid treats progressive MS.

The MS Society described the result as an important checkpoint rather than the final answer. Hundreds more participants will now be needed so researchers can determine whether alpha-lipoic acid genuinely slows disability progression and whether it is sufficiently safe for wider use.

Why Are Researchers Interested in Alpha-Lipoic Acid?

One of the major challenges in progressive MS is that treatments which suppress inflammatory relapses do not necessarily prevent the slower process of neurodegeneration, in which nerve fibres and brain tissue are progressively damaged.

Researchers are therefore looking for treatments with neuroprotective properties.

Earlier research involving people with secondary progressive MS found signs that alpha-lipoic acid might reduce the rate of brain-volume loss, although the studies were relatively small and could not establish that it prevents disability. Other studies have investigated effects on walking, cognition and optic neuritis, with mixed findings.

The hope is that alpha-lipoic acid may help protect vulnerable nerve cells from oxidative damage and other processes involved in progressive MS.

OCTOPUS is now attempting to answer the much more important clinical question:

Does that biological promise translate into meaningful slowing of disability progression?

What Dose Is Being Studied?

The OCTOPUS protocol uses 1,200 mg of R/S-alpha-lipoic acid per day, generally given as 600 mg twice daily after an initial lower-dose period. This is a research dose administered within a controlled clinical trial with medical monitoring.

That distinction is important because purchasing 1,200 mg of a nutritional supplement is not equivalent to receiving the trial medicine.

Supplement quality, formulation, absorption and purity can differ considerably, and clinical-trial participants undergo blood tests and medical monitoring that people taking supplements independently would not receive.

What Are the Possible Side Effects?

Alpha-lipoic acid has generally been reasonably well tolerated in previous MS studies, but it is not risk-free.

Reported problems have included gastrointestinal upset, nausea, vomiting, headache, rash and changes in urine odour. The OCTOPUS protocol also monitors liver and kidney function. There is limited evidence that alpha-lipoic acid may affect blood glucose, particularly in people taking insulin or other diabetes medicines.

This is another reason why the current OCTOPUS findings should not be interpreted as a recommendation for people with MS to start taking high-dose alpha-lipoic acid themselves.

Why Biobanks Matter to MS Research

Clinical trials tell researchers whether a treatment appears to work.

Biobanks can help them understand why it works, who is most likely to benefit and who may be at greater risk of side effects.

Alongside OCTOPUS, researchers are creating an optional biorepository of biological samples, including serum, plasma and DNA from consenting participants.

The stated purpose is to investigate biomarkers associated with disease progression and treatment response, with the longer-term ambition of developing more individualised approaches to MS treatment. Samples from the UK OCTOPUS programme are stored within the Welsh Neuroscience Research Tissue Bank in Cardiff.

Researchers could eventually examine whether particular proteins, immune markers or genetic variations are associated with:

Faster or slower MS progression;
Greater response to alpha-lipoic acid or future OCTOPUS treatments;
Specific MRI changes;
Development of disability;
Treatment side effects; or
Different biological forms of progressive MS.

This is particularly important because two people who both have the diagnosis of MS may have very different disease courses and may respond differently to the same medication.

The ultimate aim of this type of research is therefore not simply to ask:

“Does this drug work for MS?”

It is increasingly to ask:

“Which patients are most likely to benefit from this treatment, and why?”

Parallel Research in Australia: PLATYPUS

OCTOPUS has also expanded internationally.

Its Australian extension is known as PLATYPUS, Platform Adaptive Trial for Remyelination and Neuroprotection in Multiple Sclerosis. PLATYPUS forms part of the same international research programme and began recruiting Australian participants in 2025.

Participants at some Australian centres can also voluntarily donate additional blood samples for future MS research.

These samples are anonymised and stored within the Australian MS Biobank at Monash University, where researchers can investigate genetic and biochemical biomarkers and compare them with information about disease course, disability, relapses, MRI findings and treatment response.

This creates a powerful parallel research resource.

Rather than relying only on MRI scans and disability scores, scientists may eventually be able to combine:

clinical information + imaging + genetics + proteins + immune markers + long-term outcomes.

That kind of integrated research could help move MS treatment closer to precision medicine, where therapies are selected partly according to an individual’s biological profile rather than diagnosis alone.

Could Alpha-Lipoic Acid Replace Disease-Modifying Therapy?

At present, no.

The current OCTOPUS research concerns primarily progressive MS and neuroprotection. Alpha-lipoic acid has not yet been proven to prevent relapses or new inflammatory lesions in the way established high-efficacy disease-modifying therapies such as natalizumab, ocrelizumab or ofatumumab are designed to do.

Indeed, participants in OCTOPUS can continue appropriate existing MS standard-of-care treatment while receiving the trial intervention.

That distinction is particularly important.

Future MS treatment may ultimately involve two complementary strategies:

controlling inflammatory immune activity to prevent new lesions, while also protecting nerves and encouraging repair to reduce long-term progression.

If alpha-lipoic acid eventually proves successful, its importance may therefore lie not in replacing modern disease-modifying therapies, but potentially in becoming part of a broader strategy to address an aspect of MS that current treatments do not fully control.

A Cautiously Encouraging Development

The September 2026 OCTOPUS announcement represents genuine progress, particularly because treatments capable of slowing progressive neurodegeneration remain one of the greatest unmet needs in multiple sclerosis.

However, the research is not finished.

Alpha-lipoic acid has passed an important early test. It has not yet passed the final one.

The next stage of OCTOPUS will determine whether the early biological signals translate into a meaningful difference to people’s lives.

Meanwhile, the biobanks being developed alongside these international trials may prove almost as valuable as the treatment studies themselves, because the blood and DNA donated today could help researchers understand which treatments work for which patients tomorrow.

Questions Patients Can Ask Their Neurologist

When significant new MRI activity has appeared despite previous high-efficacy treatment, useful questions may include:

What does the latest MRI show compared with the previous scan, and are any lesions currently active or gadolinium-enhancing? Has the spinal cord also been assessed? What is my current JC virus antibody status and, if positive, what is my JCV antibody index? How would my previous treatment history affect my individual PML risk? Why is natalizumab being considered rather than ocrelizumab, ofatumumab, ublituximab or another high-efficacy treatment? How quickly does treatment need to be started to reduce the risk of further inflammatory activity? What blood tests and MRI surveillance would be required? If natalizumab is selected, could extended-interval dosing ever become appropriate? What would the planned treatment be if my JCV index increased? Would I meet the criteria for discussion or referral for AHSCT, either now or if another high-efficacy DMT failed to control the disease? What is the longer-term treatment strategy rather than simply the next medication?

Patients have every right to understand not simply what drug is being proposed, but why it is being proposed and how its risks compare with the alternatives.

Conclusion

The development of new MS lesions despite disease-modifying treatment can understandably be frightening, but it also provides important information that allows clinicians to reassess treatment before further inflammatory damage occurs.

Natalizumab remains one of the most effective treatments available for highly active relapsing MS. Its ability to suppress relapses and new MRI lesions can be substantial, and its relatively rapid action can be particularly valuable when disease activity needs to be brought under control quickly.

Its principal concern is PML.

Understanding JC virus, JCV antibody testing, the antibody index, duration of treatment and MRI surveillance allows PML risk to be assessed much more precisely than simply describing natalizumab as a “dangerous drug”.

At the same time, natalizumab is no longer the only high-efficacy choice.

Ocrelizumab, ofatumumab, ublituximab and other treatments provide alternative ways of controlling highly active MS, each with different advantages, risks and monitoring requirements.

For carefully selected people whose MS continues to produce relapses or new MRI lesions despite powerful disease-modifying therapies, AHSCT is also an increasingly important specialist option.

Medicine cannot yet undo every lesion or repair every damaged nerve caused by multiple sclerosis. But the treatment landscape has changed enormously.

The objective is increasingly ambitious: stop inflammatory disease activity as early and as completely as possible, preserve neurological function and prevent tomorrow’s disability rather than waiting for it to develop.

For anyone facing evidence that their MS is still active, the appropriate conversation is therefore not simply about accepting the next drug offered.

It is about making an informed decision with the specialist team after comparing the available high-efficacy therapies, understanding personal risk factors, and asking whether the chosen treatment offers the strongest reasonable opportunity to prevent further disease activity.