If you can reach modern rheumatology
If you have access to modern rheumatology, you are being diagnosed in the best-treated era ankylosing spondylitis has ever had. Twenty-five years ago, AS treatment was essentially painkillers, physiotherapy, and stoicism. Today the guideline toolkit includes NSAIDs, TNF inhibitors, IL-17 inhibitors, and JAK inhibitors, with the newest UK guideline explicitly listing TNFi, IL-17i, and JAKi as licensed targeted options for axial spondyloarthritis [1], [3]. Bimekizumab — the first dual IL-17A/F inhibitor with FDA approval for active AS and non-radiographic axSpA — entered the AS toolkit in 2024 [4].
Read this in five ways
- Newly diagnosed
start with the treatment pyramid.
- NSAIDs not enough
jump to biologics and JAK inhibitors.
- Drug stopped working
jump to switching.
- Uveitis, IBD, psoriasis, pregnancy
jump to treatment choice.
- Appointment tomorrow
jump to the 10-question script.
Get the AS Treatment Kit
Use the article, but do not make your tired future self hunt for the practical bits. These plain-text tools are built to paste into Notes, print, or bring to clinic.
| Term | Plain translation | Why it matters |
|---|---|---|
| TermAS | Plain translationAnkylosing spondylitis, usually meaning radiographic axial disease where sacroiliac or spinal changes are visible on X-ray. | Why it mattersOlder labels and many patients still use AS as the umbrella word. |
| TermaxSpA | Plain translationAxial spondyloarthritis, the broader family that includes radiographic AS and non-radiographic disease. | Why it mattersModern guidelines often use axSpA because inflammation can be real before X-ray damage appears. |
| Termnr-axSpA | Plain translationNon-radiographic axial spondyloarthritis: symptoms plus objective inflammation, often MRI or CRP, without definite X-ray sacroiliitis. | Why it mattersSome drugs have specific nr-axSpA label language. Access rules may differ from AS. |
This article is the map. It is the medical backbone of the AS set: read it with Move or Fuse for the movement plan, and with the community piece for the parts guidelines do not capture. By the end you should be able to walk into any rheumatologist's office and have an informed, two-way conversation about your treatment — not just receive instructions.
Where we were, where we are
For about a hundred years, AS treatment was three things: aspirin or other anti-inflammatory pain control, physiotherapy, and surgery for the worst spinal deformities. Patients fused. Patients lost height. Patients could lose the ability to lift their gaze to the world in front of them. There was no targeted immune therapy for the axial inflammation itself.
- 2003 · TNFThe first TNF-alpha inhibitors reached AS care in the early biologic era. For the first time, treatment could target an upstream inflammatory cytokine rather than only suppress pain downstream [2], [15].
- 2015 · IL-17Secukinumab opened the IL-17 era. It gave patients with active axial disease a mechanistically different option, including people who had not done well enough on TNF blockade [7].
- 2019–22 · JAKJAK inhibitors entered the axSpA conversation as oral targeted synthetic DMARDs. Upadacitinib showed ASAS40 benefit in both biologic-naive and biologic-refractory axial disease programs, but its safety label is different from a biologic label [9]-[11].
- 2024 · dual IL-17Bimekizumab blocks IL-17A and IL-17F together. In BE MOBILE 1 and 2 it improved ASAS responses, function, pain, MRI inflammation, quality of life, and spinal mobility versus placebo across non-radiographic and radiographic axSpA [5], [6].
If you have access to modern rheumatology, you are being diagnosed in the best-treated era AS has ever had. That sentence is not a consolation. It is a responsibility to stay in the plan.
The treatment pyramid
Every major guideline recommends a stepped approach: education, exercise and physiotherapy as the base; NSAIDs as initial drug treatment where safe; targeted therapy when active disease remains despite adequate NSAID trials or NSAIDs are contraindicated [1]-[3]. You climb only as high as you need to. Most patients do not need every level.
How the choice is actually made
The most useful treatment conversation is not “which drug is strongest?” It is “which drug best fits this person's disease pattern and risk profile?” The 2025 BSR guideline is blunt on this point: there is no evidence strong enough to recommend one targeted class over another for musculoskeletal symptoms alone, so extra-musculoskeletal manifestations and safety drive many real choices [3].
| If your pattern includes… | Often favored | Why it matters |
|---|---|---|
| If your pattern includes…Recurrent uveitis | Often favoredTNF monoclonal antibody | Why it mattersAdalimumab/infliximab-class drugs have stronger eye-disease experience than etanercept; IL-17 is not usually the first eye-driven choice [2], [3]. |
| If your pattern includes…Crohn's disease or ulcerative colitis | Often favoredTNF monoclonal antibody, sometimes JAK depending on case | Why it mattersIL-17 inhibitors can trigger or worsen IBD and bimekizumab labeling tells clinicians to avoid active IBD [4]. |
| If your pattern includes…Major psoriasis | Often favoredIL-17 inhibitor | Why it mattersIL-17 blockade is often very strong for skin disease, so psoriasis can tilt the decision toward secukinumab, ixekizumab, or bimekizumab [3], [5]-[8]. |
| If your pattern includes…Pregnancy planning | Often favoredCertolizumab or another pregnancy-compatible TNFi | Why it mattersCertolizumab has minimal placental transfer; drug timing should be planned before conception, not after a positive test [19]. |
| If your pattern includes…Failed one biologic | Often favoredSwitch within class or switch mechanism | Why it mattersPrimary non-response and secondary loss of response are different problems; modern guidelines support reassessment and switching rather than drifting on a failing drug [1], [3]. |
| If your pattern includes…Canadian public-plan coverage | Often favoredOften biosimilar-first where available | Why it mattersHealth Canada authorizes biosimilars as highly similar biologics; interchangeability and switching rules are provincial/territorial decisions [24]. |
What is not a main axial-AS treatment
- systemic steroidsLong-term oral steroids are generally not a core treatment for axial AS inflammation. Short courses may appear in special situations, but they are not the long-term backbone [1], [2].
- MTX / sulfasalazineMethotrexate and sulfasalazine can have a peripheral-joint role, but they are not substitutes for targeted therapy when spinal inflammation is uncontrolled [1], [2].
- opioidsOpioids may blunt pain in selected severe cases, but they do not treat inflammation or prevent structural damage. If pain is the only thing changing, the inflammation plan may still be failing.
- surgeryHip replacement, fracture care or deformity surgery can matter for complications, but surgery is not routine inflammation control.
- fused-spine warningA fused or partly fused spine can fracture after trauma that seems minor. New severe spinal pain after a fall, collision or sudden jolt needs urgent medical assessment.
Drug by drug
Let's go through every class. For each: what it is, how it works, who it may fit, what it does well, what it does not do, and what to watch for. The goal is not to self-prescribe; it is to recognize the logic of the treatment plan your rheumatologist is building [1]-[3].
NSAIDs
The familiar anti-inflammatory pain medicines at AS-appropriate doses — naproxen, ibuprofen, celecoxib, diclofenac, etoricoxib, meloxicam. They block COX enzymes, reducing prostaglandin-driven inflammation. In many systems, inadequate response to at least two NSAIDs at an adequate dose is part of the pathway before targeted therapy, unless NSAIDs are unsafe or contraindicated [1]-[3].
- Often reduce pain and morning stiffness quickly, especially in people with inflammatory back pain [1], [2]
- Cheap, available everywhere, well understood
- Can be used continuously or on-demand depending on disease activity, risk, and clinician advice [1]
- GI side effects — ulcers, bleeding (lower with COX-2 selective options for some patients)
- Cardiovascular and kidney risk with high-dose long-term use, especially with age, hypertension, kidney disease, or other risk factors
- They help symptoms and inflammation, but whether continuous NSAID use reliably slows radiographic progression remains debated [16]
Conventional DMARDs
The older immunosuppressants — sulfasalazine and methotrexate. The honest reality: they are not recommended for purely axial/spinal disease because the evidence does not support meaningful axial benefit. They retain a limited role for some patients with prominent peripheral arthritis (knees, ankles, wrists), but they are not substitutes for targeted therapy when axial inflammation is uncontrolled [1], [2].
TNF inhibitors
Five established agents, all targeting tumor necrosis factor alpha — a master cytokine of inflammation — by binding it directly or acting as a decoy receptor. With TNF neutralized, downstream inflammation in joints and entheses can fall dramatically. TNF inhibitors remain a common first biologic choice after inadequate NSAID response, especially when uveitis or IBD pushes the decision toward a TNF monoclonal antibody [1]-[3].
| Drug (brand) | Route | Typical frequency | Evidence / label note |
|---|---|---|---|
| Drug (brand)Adalimumab (Humira/biosimilars) | RouteSC injection | Typical frequencyEvery 2 weeks | Evidence / label noteEstablished TNFi option; biosimilars common [2], [24] |
| Drug (brand)Etanercept (Enbrel/biosimilars) | RouteSC injection | Typical frequencyWeekly | Evidence / label noteEstablished TNFi option, but weaker fit for IBD/uveitis-driven choices [2], [3] |
| Drug (brand)Infliximab (Remicade/biosimilars) | RouteIV infusion | Typical frequencyEvery 6-8 weeks | Evidence / label noteEstablished TNFi monoclonal; biosimilars common [2], [24] |
| Drug (brand)Golimumab (Simponi) | RouteSC injection | Typical frequencyMonthly | Evidence / label noteEstablished TNFi option [2] |
| Drug (brand)Certolizumab (Cimzia) | RouteSC injection | Typical frequencyEvery 2-4 weeks | Evidence / label noteTNFi often discussed in pregnancy planning [19] |
- Large evidence base and the longest real-world track record among targeted AS treatments [2], [15]
- Often improve pain, stiffness, function and inflammatory markers within the first months [2]
- TNF monoclonal antibodies are especially important when recurrent uveitis or IBD is part of the picture [2], [3]
- May reduce radiographic progression over time by reducing sustained inflammation, though structural-damage data are more complex than symptom data [15]
- Increased infection risk — TB reactivation is the classic reason for screening before treatment [18]
- Loss of response can happen; real-world persistence is roughly 70–80% at 1 year for TNFi in AS meta-analyses, then falls over time [15]
- Etanercept is not the preferred TNFi when IBD or recurrent uveitis is the dominant problem [2], [3]
- Usually avoided with demyelinating disease, severe heart failure, active serious infection, or untreated latent TB [18]
IL-17 inhibitors
IL-17 is a cytokine family involved in entheseal and axial inflammation. Secukinumab and ixekizumab block IL-17A; bimekizumab blocks IL-17A and IL-17F. The class has strong trial evidence in radiographic and non-radiographic axSpA, and it becomes particularly attractive when psoriasis is prominent [5]-[8].
| Drug (brand) | Target | Typical frequency | Evidence / label note |
|---|---|---|---|
| Drug (brand)Secukinumab (Cosentyx) | TargetIL-17A | Typical frequencyMonthly | Evidence / label noteMEASURE phase 3 evidence [7] |
| Drug (brand)Ixekizumab (Taltz) | TargetIL-17A | Typical frequencyEvery 4 weeks | Evidence / label noteCOAST phase 3 evidence [8] |
| Drug (brand)Bimekizumab (Bimzelx) | TargetIL-17A + F | Typical frequencyEvery 4 weeks | Evidence / label noteFDA-labeled for active AS/nr-axSpA; BE MOBILE evidence [4]-[6] |
- Secukinumab and ixekizumab consistently beat placebo on ASAS responses in phase 3 programs [7], [8]
- Bimekizumab produced ASAS40 responses of roughly 45% at week 16 in radiographic axSpA and sustained responses through week 52 in BE MOBILE [5], [6]
- Often excellent for psoriasis, which can make this class a better whole-person fit than TNFi for some patients [3]
- Can work after TNF failure; prior TNFi exposure does not automatically close the IL-17 door [5], [6], [8]
- Can worsen or trigger IBD; BIMZELX labeling says to avoid use in active IBD and monitor for new or worsening symptoms [4]
- Candida/yeast infections are more common with IL-17 blockade, especially with dual IL-17A/F inhibition [4]
- BIMZELX carries label warnings for suicidal ideation/behavior and liver biochemical abnormalities, which means mood history and liver labs belong in the pre-start conversation [4]
- Less compelling than TNF monoclonals for recurrent uveitis-driven treatment decisions [2], [3]
- Newer than TNFi, so long-term population safety data are still accumulating [3]
JAK inhibitors
Oral pills — not injections — that block Janus kinases, intracellular enzymes that translate multiple inflammatory signals into action. In current U.S. labeling, both tofacitinib and upadacitinib are AS options only after inadequate response or intolerance to TNF blocker therapy; upadacitinib also has a U.S. nr-axSpA indication when objective inflammation is present after TNF blocker therapy [11], [25]. BSR 2025 includes JAK inhibitors among licensed targeted therapies in the UK landscape [3].
| Drug | U.S. AS status | U.S. nr-axSpA status | Key caution |
|---|---|---|---|
| DrugTofacitinib (Xeljanz) | U.S. AS statusActive AS after inadequate response or intolerance to one or more TNF blockers [25] | U.S. nr-axSpA statusNot a main U.S. nr-axSpA option in the label checked for this article [25] | Key cautionJAK boxed warning; infection/TB screening, CBC and lab monitoring, malignancy/MACE/thrombosis risk discussion [25] |
| DrugUpadacitinib (Rinvoq) | U.S. AS statusActive AS after inadequate response or intolerance to one or more TNF blockers [11] | U.S. nr-axSpA statusActive nr-axSpA with objective signs of inflammation after inadequate response or intolerance to TNF blocker therapy [11] | Key cautionBoxed warning; CBC/liver/lipid monitoring, shingles discussion, thrombosis/MACE/malignancy risk discussion [11] |
- Oral — no injections, no refrigeration, no needle anxiety
- Upadacitinib reached ASAS40 in 45% vs 18% on placebo at week 14 among bDMARD-refractory AS patients in SELECT-AXIS 2 [9]
- Open-label extension data show sustained clinical responses through 1-2 years in trial populations [10]
- Potentially useful when multiple cytokine pathways or comorbid immune disease make a broader intracellular approach attractive [3], [11]
- FDA boxed warnings cover serious infections, mortality, malignancy, major adverse cardiovascular events, and thrombosis [11], [25]
- Elevated shingles risk — recombinant zoster vaccination is commonly discussed before JAK therapy [11], [20], [25]
- Lab monitoring needed: CBC, liver enzymes, and lipids are typical [11], [25]
- Risk-benefit is especially careful in older patients, smokers, and people with prior cardiovascular events, clots, or malignancy [11], [25]
The numbers
This is the chart most patients have never seen. The bars are ASAS40 response rates — the proportion of patients achieving at least a 40% improvement across multiple disease-activity domains, usually measured around week 14-16 in phase 3 programs. ASAS40 is stringent, much harder to hit than ASAS20, and still not the same thing as remission [5], [7]-[10].
| Bar tag | How to read it |
|---|---|
| Bar tagTNF / IL-17 / JAK | How to read itDrug class, not a ranking. A class with a lower-looking bar may still be the right first choice for uveitis, IBD, pregnancy, infection history or access. |
| Bar tagAS / nr-axSpA | How to read itRadiographic AS and non-radiographic axSpA trials are related but not identical populations. |
| Bar tagbio-naive / refractory | How to read itPeople who have never used a biologic and people who already failed one are not the same trial population. |
| Bar tagweek 14 vs week 16 | How to read itA two-week difference does not explain everything, but mixed timepoints are another reason not to treat the chart like a leaderboard. |
- cross-trial cautionEach drug was tested against placebo in its own trial design. Different entry criteria, prior-biologic exposure, CRP/MRI requirements and rescue rules make naive ranking misleading [5], [7]-[10].
- the curve keeps risingA week-16 partial responder is not automatically a forever non-responder. BE MOBILE and SELECT-AXIS extension data show that some responses deepen over longer follow-up [6], [10].
- real-world persistenceTrial response is not the same as staying on treatment. A 2024 real-world cohort notes TNFi drug survival around 76% at 1 year in a prior AS meta-analysis, with persistence declining over time [15].
- work is an outcomeIn a meta-analysis of workers starting b/tsDMARDs, baseline overall work-productivity impairment averaged 52.1%, with presenteeism near 48.8%; treatment studies generally show improvement, but not magic erasure of disease burden [13], [14].
| Number patients ask for | Best honest answer | Citation |
|---|---|---|
| Number patients ask forChance of a strong early response | Best honest answerMany modern targeted agents land around the 35-50% ASAS40 range by week 14-16, depending on drug and population; placebo is often meaningful too. | Citation[5], [7]-[10] |
| Number patients ask forChance of needing a switch | Best honest answerSwitching is common enough that every plan should have Plan B. Real-world drug survival is useful because it captures effectiveness, side effects, access and patient preference together. | Citation[3], [15] |
| Number patients ask forHow long diagnosis takes | Best honest answerA systematic review/meta-analysis estimated mean diagnostic delay at about 6.7 years globally, with higher estimates in some health systems. | Citation[12] |
| Number patients ask forWhether treatment helps work | Best honest answerBiologic/targeted therapy improves work outcomes on average, but people often start with major work impairment. | Citation[13], [14] |
| Number patients ask forWhether NSAIDs stop fusion | Best honest answerNSAIDs are first-line symptom/inflammation tools; radiographic-progression prevention from continuous NSAID use remains uncertain. | Citation[1], [16] |
| Number patients ask forWhether inflammation affects heart risk | Best honest answeraxSpA is associated with excess cardiovascular burden; controlling inflammation, moving regularly, treating blood pressure/lipids and not smoking all matter. | Citation[17] |
Real lives
These are composites — synthesized from typical clinical pathways and guideline logic, not specific individuals. They illustrate patterns: a clear responder, a switcher, and someone whose diagnosis came late enough that structural damage became part of the story [1]-[3], [12].
Three years of progressive low-back pain and morning stiffness. MRI showed bilateral sacroiliitis; HLA-B27 positive; CRP elevated; BASDAI 6.4.
- Month 0Diagnosed. Started naproxen 500 mg twice daily; referred to rheumatology.
- Month 3Partial relief, BASDAI still 5.2. Switched to celecoxib — no better. TB screening begun.
- Month 4Started adalimumab biosimilar, every 2 weeks.
- Week 16BASDAI 1.8. ASAS40 achieved; inflammatory markers normalized.
- Year 2Sustained remission on adalimumab plus daily exercise. Back to her life.
Takeaway · Priya is the clean pathway: adequate NSAID trial, persistent active disease, then a first biologic with a strong response. This is the path everyone hopes for, and a substantial minority achieve it in trials [5], [7]-[10].
Diagnosed in his early thirties after years of dismissed back pain. Responded to infliximab for four years, then faded — anti-drug antibodies confirmed.
- Year 4Switched to adalimumab. Good for 18 months, then progressive loss of efficacy.
- Year 5.5Switched to secukinumab (IL-17). Mild oral thrush; BASDAI 5.6 → 2.4.
- Year 7New bloody diarrhea — Crohn's-like inflammation. Secukinumab stopped (IL-17 can worsen IBD).
- Year 8Switched to upadacitinib (JAK) — oral, covers axial AS and helps the IBD. Stable.
Takeaway · Mark is the switch pathway. Each switch is a planned decision, not a personal failure; modern guidelines expect reassessment when the current drug is not meeting target [1], [3].
Misdiagnosed for over a decade as “fibromyalgia” and “degenerative back disease.” By diagnosis at 44, she already had significant spinal fusion.
- EarlyAdalimumab, then etanercept — both reduced symptoms but radiographic progression continued.
- LaterSecukinumab — better control, but ongoing limitation from existing damage.
- NowBimekizumab, with deep remission of inflammation — but fused segments cannot be reversed.
Takeaway · Sarah's case is the most important argument in this article: diagnostic delay changes the ceiling. Modern drugs can control inflammation; they cannot rebuild a spine segment that has already fused [12].
The treatment journey
What does a typical AS pathway actually look like, from first symptom to good control? The steps vary by country and insurance system, but the broad path is recognizable: symptoms, diagnosis, NSAID trial if safe, objective disease assessment, targeted therapy if active disease persists, then monitoring and switching if needed [1]-[3].
The most striking thing about this timeline isn't the medical steps — it's the gap between first symptoms and diagnosis. A systematic review estimated a mean delay of roughly 6-7 years globally. Cut that gap and you change the rest of the trajectory [12].
— the most actionable bottleneck in the whole pathway
What's coming next
The pipeline is active, but this section needs discipline. “Coming next” does not mean “ask your doctor for this tomorrow.” It means three different things: approved drugs spreading through access systems, mechanisms with trial evidence in axSpA, and speculative immune-reset ideas that are not AS treatments yet [21]-[23].
- Dual IL-17Bimekizumab is not “experimental” anymore for AS in the US; the next question is how its long-term safety, persistence and switching role compare in real-world practice [4]-[6], [15].
- JAK refinementsUpadacitinib has phase 3 AS data and a boxed-warning safety frame. Filgotinib showed phase 2 AS efficacy in TORTUGA but is not a US AS option; the class is promising and risk-sensitive at the same time [9]-[11], [21].
- IL-23 negative lessonRisankizumab failed to show clinically meaningful AS benefit in a phase 2 proof-of-concept trial. That negative result matters because it keeps the field honest about psoriasis mechanisms not automatically translating to axial disease [22].
- BiomarkersThe future most likely to arrive soon is not a miracle drug; it is better matching: who should start TNF, who should start IL-17, who should switch class, and who is carrying pain from damage rather than active inflammation [3], [23].
- Immune resetCAR-T-like and tolerogenic-vaccine ideas are scientifically exciting in autoimmunity, but they are not established AS therapies. Put them in the “watch the science” bucket, not the “treatment plan” bucket [23].
Practical considerations
A few things every patient on these drugs should know before the first injection, infusion, or pill. These are not bureaucracy; they are the safety rails that let targeted immune therapy be used well [18]-[20].
- Canadian accessIn Canada, Health Canada authorizes biosimilars as highly similar to reference biologics, but provinces and territories decide interchangeability and switching rules. Ask the clinic nurse or pharmacist what your province requires before the prescription is written [24].
- pre-treatment workupBefore biologic or JAK therapy, expect TB screening, hepatitis screening, baseline bloodwork and a vaccine review; BIMZELX and RINVOQ labels both explicitly include pre-treatment infection/vaccine checks [4], [11], [18], [20].
- when to switchPrimary non-response by roughly 12-16 weeks, secondary loss of response, intolerance, or a new comorbidity can all justify a switch. The important thing is to name the reason, because “never worked” and “worked then faded” are different clinical problems [1], [3], [15].
- pregnancyPregnancy planning should happen before medication changes. BSR pregnancy guidance supports several anti-rheumatic drugs in pregnancy/breastfeeding contexts, with certolizumab often favored when a TNFi is needed because placental transfer is minimal [19].
Vaccinations
- Influenza — annually [20]
- COVID-19 — keep updated according to local guidance [20]
- Pneumococcal — schedule depends on age, risk and local guidance [20]
- Shingles (recombinant zoster vaccine) — especially worth discussing before JAK inhibitors [11], [20]
- Hepatitis B — vaccinate if not already immune and risk/indication fits [18], [20]
- Live vaccines (MMR, varicella, yellow fever) — discuss before starting biologics or JAK inhibitors; avoid live vaccines during many immunosuppressive therapies [20]
Your script
Ten questions that turn an appointment from instructions into a two-way conversation. Bring a one-page symptom log if you can: morning stiffness duration, night waking, BASDAI/ASDAS inputs if you track them, missed work/school days, NSAID use, eye/gut/skin symptoms, infections, vaccines, and what outcome would make treatment “worth it” for you [1], [3], [13].
- 01 · the numbers“What's my BASDAI and ASDAS today, and what are we targeting?” ASDAS low disease activity is <2.1 and inactive disease is <1.3; BASDAI remains common but is less objective because it has no CRP component [1], [3].
- 02 · the pyramid“What stage am I at, and what would step us up?” Forces a clear plan instead of drift.
- 03 · plan B & C“If this drug stops working, what's plan B and plan C?” Map your next two moves before you need them.
- 04 · trials“Am I a candidate for any clinical trials?” Especially after multiple failed lines. ClinicalTrials.gov is your friend, but trial eligibility is strict [23].
- 05 · baselines“What baseline imaging and labs do we have, and when do we repeat them?” Track progression objectively, not just by feel.
- 06 · pregnancy“How does my plan change if I want to conceive in the next 2 years?” Forward planning prevents bad surprises.
- 07 · vaccines“What vaccines am I behind on?” Surprisingly often, the answer is ‘several.’
- 08 · biosimilars“Are there biosimilars I could switch to that lower cost or satisfy coverage rules without changing the expected clinical effect?” In Canada, ask specifically about provincial rules [24].
- 09 · specialist PT“Should I see a physiotherapist who specializes in spondyloarthritis?” Generic PT is fine; AS-specific PT is better.
- 10 · the pipeline“Is there anything in the research pipeline I should know about for my situation?” The useful answer is not hype; it is whether a trial, switch class, biosimilar, or monitoring change is relevant to you [3], [21]-[23].
Keep the AS set together
Treatment is one layer. Pair this guide with the patient/community lessons, movement plan, food experiment, personal story, and practical tools.
Use the toolkit
I started by saying that if you can reach modern rheumatology, you are being diagnosed in the best-treated era AS has ever had. The part I left implicit: that is only true if you stay in the plan.
These drugs work — really work — in a way nothing in 1990 could. They will not cure your AS, and not everyone reaches remission. But modern targeted therapy can reduce inflammation, pain, stiffness, MRI activity, and functional loss for many people, especially when it is paired with movement, monitoring, and timely switching when the current drug is not enough [1]-[15]. The cost is needles or pills, monitoring labs, infection vigilance, and an ongoing relationship with a rheumatologist that becomes part of the architecture of your life.
Use the toolkit. Do not disappear from the plan. If a drug scares you, fails you, costs too much, or causes side effects, bring that problem back to the team. Silent stopping is where treatment plans go to become ghosts.
— the science is on your side now
References
- D. van der Heijde et al.. ASAS-EULAR recommendations for the management of axial spondyloarthritis: 2022 update (Ann. Rheum. Dis., 2023). Accessed: Jul. 9, 2026. [Online]. Available: https://ard.bmj.com/content/82/1/19
- M. M. Ward et al.. 2019 update of the ACR/SAA/SPARTAN recommendations for the treatment of ankylosing spondylitis and nonradiographic axial spondyloarthritis (Arthritis Rheumatol., 2019). Accessed: Jul. 9, 2026. [Online]. Available: https://pmc.ncbi.nlm.nih.gov/articles/PMC6764857/
- S. S. Zhao et al.. The 2025 British Society for Rheumatology guideline for the treatment of axial spondyloarthritis with biologic and targeted synthetic DMARDs (Rheumatology, 2025). Accessed: Jul. 9, 2026. [Online]. Available: https://pmc.ncbi.nlm.nih.gov/articles/PMC12107049/
- DailyMed. BIMZELX (bimekizumab-bkzx) prescribing information (published Jun. 2025). Accessed: Jul. 9, 2026. [Online]. Available: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=26b88358-871f-4c80-9d80-b2fb16477f81
- D. van der Heijde et al.. Efficacy and safety of bimekizumab in axial spondyloarthritis: results of two parallel phase 3 randomized controlled trials (Ann. Rheum. Dis., 2023). Accessed: Jul. 9, 2026. [Online]. Available: https://pmc.ncbi.nlm.nih.gov/articles/PMC10086273/
- X. Baraliakos et al.. Bimekizumab treatment in active axial spondyloarthritis: 52-week efficacy and safety from BE MOBILE 1 and 2 (Ann. Rheum. Dis., 2024). Accessed: Jul. 9, 2026. [Online]. Available: https://ard.bmj.com/content/83/2/199
- M. E. Baeten et al.. Secukinumab, an interleukin-17A inhibitor, in ankylosing spondylitis (N. Engl. J. Med., 2015). Accessed: Jul. 9, 2026. [Online]. Available: https://www.nejm.org/doi/full/10.1056/NEJMoa1505066
- A. Deodhar et al.. Ixekizumab in radiographic axial spondyloarthritis: COAST-V and COAST-W 52-week results (Ann. Rheum. Dis., 2020). Accessed: Jul. 9, 2026. [Online]. Available: https://pmc.ncbi.nlm.nih.gov/articles/PMC7025731/
- A. Deodhar et al.. Upadacitinib for active ankylosing spondylitis refractory to biologic therapy: SELECT-AXIS 2 phase 3 trial (Ann. Rheum. Dis., 2022). Accessed: Jul. 9, 2026. [Online]. Available: https://pmc.ncbi.nlm.nih.gov/articles/PMC9606523/
- A. Deodhar et al.. Upadacitinib in bDMARD-refractory ankylosing spondylitis: 1-year open-label extension (Rheumatol. Ther., 2023). Accessed: Jul. 9, 2026. [Online]. Available: https://pmc.ncbi.nlm.nih.gov/articles/PMC10506267/
- DailyMed. RINVOQ (upadacitinib) prescribing information (published Apr. 2026; major label changes in 2025). Accessed: Jul. 9, 2026. [Online]. Available: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=2966aec7-2ef0-923c-d8ff-fe1a957bf095
- L. M. Macfarlane et al.. Diagnostic delay in axial spondyloarthritis: a systematic review (Rheumatology and Therapy, 2022). Accessed: Jul. 9, 2026. [Online]. Available: https://pmc.ncbi.nlm.nih.gov/articles/PMC9187558/
- M. F. R. Farheen et al.. Work productivity in patients with axial spondyloarthritis initiating b/tsDMARDs: systematic literature review and meta-analysis (RMD Open, 2023). Accessed: Jul. 9, 2026. [Online]. Available: https://pubmed.ncbi.nlm.nih.gov/38035757/
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