Adalimumab_Launch.ppt

1. ADALIMUMAB 40 mg SC

3. Common Sites Of Musculoskeletal Pain
(Bursa)
(Enthesis)
(Tendons)
(Tendons &
Synovium)
(Synovium)
(ligament))

4. Parts of Skeletal system & Inflammation
• Membrane covering the ends of bones having
fibres, proteoglycan & water to facilitate gliding
between bone ends & absorb mechanical impact.
Cartilage
• Covering over the joint, holds the bones together
Joint Capsule
• Anchors muscles to bone for providing flexibility,
covered by fibrous sheath.
• Inflammation can lead to Tenosynovitis
Tendon
• Fibrous tissue through which cartilages are
connected to form a bone joint.
Ligament
• Ligaments and tendons attach to bones through a
site which is enthesis
Enthesis

5. Human Vertebral Column

6. Sacro-iliac joint

7. Rheumatoid Arthritis
 Rheumatoid arthritis (RA) is a
symmetric, chronic, inflammatory,
autoimmune disease of unknown
etiology
 The hallmark feature of this
condition is persistent symmetric
polyarthritis (synovitis) that affects
the hands and feet, though any joint
lined by a synovial membrane may
be involved.
 Extra-articular involvement of
organs such as the skin, heart, lungs,
and eyes can be significant

8. American College of Rheumatology Recommendations Update for
the Treatment of Established Rheumatoid Arthritis, 2012

9. Established RA who becomes
intolerant or nonresponsive
to MTX and TNF-inhibitor
therapy

10. Diagnostic Values
Elements SDAI CDAI DAS28
No of Swollen
joints
Yes Yes Yes
No of tender
counts
Yes Yes Yes
Acute Phase
reactants (ESR/
CRP)
CRP Level - ESR/CRP
Patient Global
Health
VAS
Overall global
assessment
Yes Yes -

11. Cutoff values
Index Value Disease activity state
SDAI Remission <3.3
Low disease <11
Moderate disease <26
High disease >26
CDAI Remission <2.8
Low disease <10
Moderate disease <22
High disease >22
DAS28 Remission <2.6
Low disease <3.2
Moderate disease <5.1
High disease >5.5

12. What is ACR criteria of testing DMARDs?
ACR 20/50/70 response includes following criteria:
≥20, 50 or 70% improvement in swollen joint counts
≥20, 50 or 70% improvement in tender joint count
≥20, 50 or 70% in atleast 3 of the following parameters
o Patients global assessment of RA
o Physicians global assessment of RA
o Patients pain assessment
o CRP or ESR levels
o Disability (measured with health assessment questionnaire)

13. What is DAS28 score and how are the scores interpreted?
DAS28 includes assessment of following parameters:
Number of joints tender (out of 28)
Number of joints swollen (out of 28)
Patients general health (VAS scale)
Interpreted as:
DAS28 score >5.1: High level of disease activity
DAS28 score 3.2-5.1: Moderate level of disease activity
DAS28 score 2.6-3.2: Low level of disease activity
DAS28 score <2.6: Disease Remission

14. Psoriatic arthritis
Psoriatic arthritis is an inflammatory arthritis
associated with psoriasis, usually with
negative tests for rheumatoid factor.
It is not a homogeneous clinical entity.
In common with other spondyloarthritides,
the key features are seronegative arthritis,
enthesitis and, in a minority, sacroiliitis or
spondylitis.
It is the only SpA in which small joints of the
hand are frequently affected.
Psoriasis occurs in 5% of most white
populations, and 5 – 15% of sufferers
develop one or another form of associated
arthritis

15. Patterns of psoriatic arthritis
Asymmetrical oligoarthritis (50%); involvement of one to five joints
Predominantly distal interphalangeal joint disease (5 – 10%), distinctive but
unusual form of psoriatic arthritis
Rheumatoid pattern (25%); symmetrical small - joint arthritis particularly
affecting metacarpophalangeal, wrist and proximal interphalangeal joints; may be
indistinguishable from rheumatoid arthritis
Arthritis mutilans (1 – 5%); osteolysis results in destruction of the small joints
Spondyloarthritis (20%); may be isolated sacroiliitis, atypical or typical AS

16. Juvenile Idiopathic/ Rheumatoid Arthritis
 Juvenile idiopathic arthritis (JIA) is the most
likely diagnosis in children with persistent
symptoms and clinical features of arthritis for
at least 6 weeks
 It is not the same disease as rheumatoid
arthritis.
 JIA is an umbrella term that includes at least
seven different conditions, each representing
a unique form of childhood arthritis.
 JIA is characterized by persistent, non -
recurrent, objective joint swelling.
 Joint pain and stiffness are presenting
symptoms in most, but not all, children and
young people with JIA.
 Early diagnosis is the key to optimal
outcome.
 Effective treatment is available and positively
affects long – term outcome
 Peripheral joint arthritis in children is usually
accompanied by joint swelling
Criteria for the diagnosis of juvenile
idiopathic arthritis
All three conditions must be met:
• Arthritis persisting for > 6 weeks
• Onset before age 16 years
• Exclusion of other conditions
associated with or mimicking arthritis

17. Typical symptoms of juvenile idiopathic arthritis
Present in all forms of JIA
•Joint symptoms (pain, dysfunction,
stiffness), particularly after sleep or
prolonged sitting
•Persistent joint swelling, particularly
of the knee, ankle, wrist and small
joints of the hand
•Difficulty chewing, asymmetric
mouth opening
•Muscle atrophy
•Flexion contracture deformity
•Synovial hypertrophy
Constitutional symptoms (dramatic
in children with systemic arthritis but
mild in polyarthritis and Enthesisits
related arthritis [ERA])
•Fever (high in systemic arthritis, low
grade in polyarthritis, no pattern in
ERA)
•Rash (maculopapular, recurrent in
systemic arthritis, nodules in
polyarthritis, rheumatoid factor+,
psoriasis and nail pitting in psoriatic
arthritis)
•Growth failure (almost always severe
in systemic arthritis, mild in
polyarthritis and localized to specific
bones in oligoarthritis)

18. International League of Associations for Rheumatology
classification of juvenile idiopathic arthritis
Systemic arthritis
Oligoarthritis — persistent
Oligoarthritis — extended
Polyarthritis — rheumatoid - factor negative
Polyarthritis — rheumatoid - factor positive
Psoriatic arthritis
Enthesitis - related arthritis
Undifferentiated arthritis
Oligoarthritis, persistent, in a 3 - year - old girl
Symmetric arthritis in a young child with polyarthritis, negative for rheumatoid fa

19. Treatment of JIA
•Ibuprofen 10 mg/kg/dose four times a day
•Piroxicam 0.2 – 0.3 mg/kg/dose once a day
•Naproxen 10 mg/kg/dose twice a day
Non - steroidal anti -
infl ammatory drugs
•Triamcinolone 0.5 mg/kg/joint for medium joint and 1-20.5
mg/kg/joint for large joints
Intra - articular
corticosteroids
•Methylprednisolone 10 – 30 mg/kg/dose daily over 1 – 3
days
•Prednisolone 0.2 – 2 mg/kg/dose once a day
Parenteral
corticosteroids
•0.3 – 1 mg/kg/dose once weekly orally or subcutaneously
Methotrexate
•25 mg/kg/dose twice daily
Sulfasalazine
•0.4 mg/kg/dose twice weekly or 0.8 mg/kg once weekly,
both subcutaneously
Etanercept

20. Spondyloarthritis (or spondyloarthropathy)
 The prefixes “spondyl” and
“spondylo” means “vertebra.
 Spondyloarthritis (or
spondyloarthropathy) is the name
for a family of inflammatory
rheumatic diseases that cause
arthritis.
 It involves the sites where
ligaments and tendons attach to
bones are effected, called as
“entheses”
 Symptoms are present in two
main ways.
 The first is inflammation causing
pain and stiffness, most often of
the spine. Some forms can affect
the hands and feet or arms and
legs.
 The second type is bone
destruction causing deformities of
the spine and poor function of the
shoulders and hips.
•Inflammation and arthritis of
vertebral column and axial skeleton
Ankylosing
Spondylitis
•Affects mainly the spine and pelvic
joints
Axial
spondyloarthritis
•Affecting mostly the arms and legs
Peripheral
spondyloarthritis
•Formerly known as Reiter's
syndrome
Reactive arthritis
•Arthritis associated with Psoriasis
Psoriatic arthritis
•Spondylitis associated with
inflammatory bowel diseases
(ulcerative colitis and Crohn's
disease)
Enteropathic arthritis
•Cannot be diagnosed as any other
spondyloarthritis
Undifferentiated SpA

21. Axial spondyloarthritis
 Axial spondyloarthritis (axSpA) is a chronic inflammatory disease
predominantly affecting the axial skeleton (sacroiliac joints and spine)
 Axial Spondyloarthritis refers to inflammatory disease where the main
symptom is back pain, and where the x-ray changes of sacroiliitis may
or may not be present
 In fact some of these patients may never show any inflammation on an
MRI even if this is repeated later on in life.
 If definite sacroiliitis is absent on radiography, the disease is classified
as axial undifferentiated spondyloarthritis.
 Axial spondyloathritis and undifferentiated spondyloarthropathy are
two different conditions.
 If definitive sacroilitis is absent on radiography but the patient shows
evidence of inflammation on MRI or their clinical features correlate,
the disease is classified as non-radiographic axial SpA.
Ankylosin
g
Spondyliti
s (AS)
X-ray changes are clearly present
Non-
radiographi
c axial
spondyloart
hritis (nr-
axSpA)
X-ray changes are not present but
clinical symptoms may occur.
Inflammation or spine Damage may
be detected with MRI

22. Ankylosing spondylitis
 AS is a progressive, chronic, rheumatic, ,
multisystem inflammatory disorder
involving primarily the sacroiliac (SI)
joints and the axial skeleton.
 The inflammation produced can lead to
new bone formation on the spine,
causing the spine to fuse in a fixed,
immobile position, sometimes creating a
forward-stooped posture.
 The main clinical features are back pain
and progressive stiffness of the spine.
 Ankylosing spondylitis is a major
subtype of a group of chronic
inflammatory diseases known as
spondyloarthropathies
“Spondylitis” is inflammation of
the spinal vertebrae.
“Ankylosing” means “fusing
together” and refers to the loss of
flexibility of the back and the neck
that can result from the
inflammation.

23. Spectrum of disease in patients with chronic
back pain (≥3 months) aged <45 years at
onset

24. Prevalence
It affects young adults with the peak age of onset between 20 and 30 years.
Men are more often affected than women, with a ratio of approximately 3:1.
About 80% of patients with AS develop the first symptoms before their third
decade of life and < 5% present in the fourth decade of life.
Patients with juvenile-onset AS become symptomatic at or before 16 years of age.
The prevalence of AS is 0.1-1.4%
Up to 15% of children with juvenile idiopathic arthritis are classifi ed as having
juvenile - onset spondyloarthritis.
Prevalence is dependent on
The ethnicity
The prevalence of HLA-B27
The selection of patients for evaluation
The screening criteria used for diagnosis

25. Clinical signs and progression
 The first symptom of AS is usually inflammatory back pain
 Onset of low back pain and/or buttock pain that persists for more than 3 months, awakens the patient from
sleep is a typical sign of AS
 It is accompanied by early morning stiffness and is typically improved by exercise.
 Fatigue often accompanies inflammatory back pain, although it may also be present in fibromyalgia and other
conditions.
 Inadequately controlled inflammation leads to persistent stiffness and progressive loss of spinal mobility
 Peripheral enthesitis and arthritis
 Constitutional and organspecific extraarticular manifestations
 Stiffness of the spine and kyphosis resulting in a stooped posture are characteristic of advanced stage AS.

26. Modified New York Criteria for the diagnosis of AS
Radiographic criteria:
Sacroiliitis grade ≥2 bilaterally or sacroiliitis grade 3–4 unilaterally.
Clinical criteria:
Low back pain and stiffness for >3 months which improves with exercise but is not
relieved by rest.
Limitation of motion of the lumbar spine in both the sagittal and frontal planes.
Limitation of chest expansion to 1 inch relative to normal values corrected for age and
sex.

27. AS Treatment
 DMARDS should not be considered
conventional therapy for Ankylosing
Spondylitis and non-radiographic axial
SpA. DMARDS can be recommended for
the treatment of peripheral disease only
according to axial SpA clinical
guidelines
 The current ASAS/EULAR guidelines
for the management of AS mention that
“Sulfasalazine may be considered in
patients with peripheral arthritis
Nonsteroidal
antiinflammatory drugs
Used a first line agent
for Pain in AS
Eg. Ibuprufen,
Diclofenac
Sulfasalazine
Not methotrexate but
sulfasalazine is a
treatment option for AS
TNF-Alpha Inhibitors
Eg. Infliximab,
etanercept,
adalimumab.
Improvement may
occur within a few
weeks of starting the
drugs.
Glucocorticoids (steroids)
Injection is
administered into
painful or swollen
joints
Early diagnosis of AS and
non-radiographic axial SpA
is essential for effective
treatment

28. Assessment of Ankylosing spondylitis
Type Clinical Parameter Definition Range
Overall functional
ability
Bath AS
Functional Index
(BASFI)
Functional instrument based on the patient’s assessment of
his/her ability to perform 10 selected activities
0-10
Disease activity
Bath AS Disease
Activity Index
(BASDAI)
Summary of 6 self-assessments (fatigue, spinal pain, joint pain,
enthesitis, overall level of morning stiffness, and duration of
morning stiffness).
0-10
ESR or CRP level The erythrocyte sedimentation rate and C - reactive protein are
typically elevated, but levels do not usefully indicate
inflammatory activity of spinal disease.
-
ASAS 20%
response (ASAS20)
Improvement of 20% and an absolute improvement of ≥1 unit (on
a scale of 0 to 10) from baseline in ≥3 of the following 4 domains:
patient’s global assessment, total back pain, function (BASFI), and
inflammation (questions 5 and 6 of BASDAI) with an absence of
deterioration from baseline in the potential remaining domain
-
Spinal mobility Bath Ankylosing
Spondylitis
Metrology Index
(BASMI)
A composite score derived from measurements of spinal mobility. -
Radiological
progression
Modified Stoke AS
Spinal Score
(mSASSS)
This uses lateral radiographs of the cervical and lumbosacral spine
and can detect change over 2 years. It evaluates the anterior part of
the lumbar spine and cervical spine and assesses chronic changes
at each level with a score of 0 to 3 (0 = normal; 1 = erosion,
sclerosis or squaring; 2 = syndesmophyte; 3 = bridging
syndesmophyte).
0-3

29. Pathophysiology: Above mentioned Autoimmune
conditions
 An autoimmune reaction is triggered at the site-
 Synovial Joints: RA
 Spine & axial Joints: Ankylosing Spondylosis
 Skin & Joints: Psoariasis Arthritis
 Arthritis in Children: Juvenile idiopathic arthritis
 Trigger in the Immune system first will trigger the second line of defense comprising of Dendritic cells, fibroblasts, Macrophages,
Neutrophils.
 As the nature of all such cells is Phagocytosis, they will try to kill the auto-antigen (body’s own cell) through aforementioned
process
 While trying to kill the auto-antigen, these cells will secrete certain CYTOKINES which will enable them to communicate with other
cells & undergo the required processes.
 Major cytokines which are being released TNF-α, Interleukines (Inflammatory ones)
 The secretion of these cytokines will trigger an inflammatory process at the attack site and will also trigger the third line of defense
i.e T & B cell

30. Pathophysiology (Cont.)
 T cells will again secrete certain cytokines (Interferons, Interleukines) which will activate Prostaglandins and
other Inflammatory markers to produce more inflammation
 B cells on the other hand will start producing Antibodies against that particular self antigen which will
enhance the killing of self cells and spread the killing in other organs through circulation of antibodies in
blood
 Any autoimmune condition will be characterized by inflammation and further degeneration of the target
tissue.
 During the whole process, Cytokines play a major role in producing the characteristic signs of the disease. As
TNF-α is a major cytokine being produced by macrophages, disease can be controlled effectively by not only
stopping the inflammation but also will stop the activation of T & B cells to prevent further damage
 In Autoimmune arthritis (RA, AS, Psoriatic Arthritis) the disease is governed by collective role of all immune
cells.

31. Activation of Innate Immunity
(macrophages, dendritic cells,
B- cells) by antigen (self or non-
self)
Autoantigen
Macrophages are the
source of TNF-α (Pro-
inflammatory cytokine),
IL-16 & IL-1
Pathogenesis
TNF-α
IL-16
IL-1
Secretion of IL-1, 16 &
TNF- α, activation of B-cell
and T-cell
Antibodies
T-cell
Activated T-cells
secret IL-2 & IFN-γ
Activation of B-cells & T-cells forms
an IMMUNE COMPLEX
T-cells, B-cells secrete
PG & MMP
MMP
PG
Destruction of
Cartilage
Together activity of Macrophages, T cells, B cells leads to
cartilage and bone destruction
B-cell
IL-2
IFN-γ
Activated B-cells produce
antibodies

32. Role of TNF-Alpha
TNF-α is a potent pro-
inflammatory cytokine
exerting effects on
various immune cells
and plays a critical role
in the pathogenesis of
several chronic
inflammatory
disorders
It is produced by
macrophages or
monocytes
Activated by mast
cells, fibroblasts,
neurons, glial cells, and
T cells by variety of
infectious stimuli
Functions
of
TNF-α
Antitumor and antiviral activity
The mediation of systemic
inflammatory responses to
infection and sepsis
As well as a crucial role in the
host response to a variety of
infections
Control and containment of
intracellular pathogens
It stimulates recruitment of
inflammatory cells to the area of
infection
Stimulates the formation and
maintenance of granulomas that
physically contain infection

33. Adalimumab
ADA is a recombinant, fully human IgG monoclonal antibody against
TNF-a.
It is composed of heavy and light chain variable regions and IgG1:k
constant regions
Adalimumab is the third immunobiological agent (besides etanercept
and infliximab) directed against TNFalpha
Adalimumab has great therapeutic potential in the treatment of RA

34. Adalimumab approval history

35. Mechanism of action
Adalimumab inhibits TNFalpha binding to both receptors
It blocks TNFalpha-induced cytotoxicity cells
Adalimumab binds to pro-TNFalpha on cell membranes and mediates complement-
dependent cytotoxicity, and also binds to Fc receptors on human cells to mediate
antibody-dependent cytotoxicity
Prevents soluble TNF-a from binding to the natural TNF-a receptors
ADA does not bind to or neutralize lymphotoxin (TNF-b)

36. Dose & Benefits
Indication Indication Inference
Rheumatoid Arthritis (RA)
40 mg every other week
Reducing signs and symptoms,
inducing major clinical
response, inhibiting the
progression of structural
damage, and improving
physical function in adult
patients with moderately to
severely active RA
Psoriatic Arthritis (PsA) Reducing signs and symptoms,
inhibiting the progression of
structural damage, and
improving physical function in
adult patients with active PsA
Ankylosing Spondylitis (AS) Reducing signs and symptoms
in adult patients with active AS
Juvenile Idiopathic Arthritis
(JIA)
10 kg (22 lbs) to < 30 kg (66 lbs):
20 mg every other week
≥ 30 kg (66 lbs): 40 mg every
other week
Reducing signs and symptoms
of moderately to severely active
polyarticular JIA in patients 2
years of age and older.

37. Dosage recommendations in JIA
The recommended dose of Adalimumab for patients 2 years of age
and older with polyarticular juvenile idiopathic arthritis (JIA) is based
on weight as shown below.
MTX, glucocorticoids, NSAIDs, and/or analgesics may be continued
during treatment with adalimumab
Patients (2 years of age and older) Dose
10 kg (22 lbs) to <15 kg (33 lbs) 10 mg every other week (10 mg
Prefilled Syringe)
15 kg (33 lbs) to <30 kg (66 lbs) 20 mg every other week (20 mg
Prefilled Syringe)
≥30 kg (66 lbs) 40 mg every other week

38. Precautions and contraindications
 Injections should occur at separate sites in the thigh or abdomen. Rotate injection sites and do not give
injections into areas where the skin is tender, bruised, red or hard.
 Only administer one dose per vial.
 Concomitant use of Anakinra and Abatacept is not recommended
 Treatment with adalimumab should not be initiated in patients with an active infection, including localized
infections.
 Patients greater than 65 years of age, patients with co-morbid conditions and/or patients taking concomitant
immunosuppressants (such as corticosteroids or methotrexate), may be at greater risk of infection.
 Prior to initiating adalimumab, assess if treatment for latent tuberculosis is needed
 Use of TNF blockers, including adalimumab, may increase the risk of reactivation of hepatitis B virus (HBV)
in patients who are chronic carriers of this virus

39. Efficacy and safety of Adalimumab in patients with active
rheumatoid arthritis on a stable dose of methotrexate: Efficacy
This was a double-blind, comparator-controlled, parallel-group study
Adalimumab from the innovator & Adalimumab were administered
at 40 mg dose as a single subcutaneous injection every other week.
The study duration for individual subjects was up to 37 weeks
The observed reduction in HAQ-DI scores was comparable in both
treatment arms.

40. RLS Adalimumab Innovator
456.7
400.67
213.7
137.01
Rf measurement
Rheumatoid Factor value, IU/ml, Baseline
Rheumatoid Factor value, IU/ml, Week 16
Treatments are considered to be clinically equivalent

41. Efficacy and safety of Adalimumab in patients with active
rheumatoid arthritis on a stable dose of methotrexate: Safety
The immunogenicity profiling did not indicate any clinically
significant concerns.
In this study, 72 adverse events were reported.
The safety results of the study show that Adalimumab is safe to
administer in patients with active rheumatoid arthritis on a stable
dose of Methotrexate. The safety profile of Adalimumab is comparable
to reference drug product

42. Guideline Speak
NICE Guideline1
Adalimumab or etanercept are recommended as treatment options for adults with
severe active ankylosing spondylitis and NOT INFLIXIMAB
Prescription of an alternative TNF-α inhibitor is not recommended in patients
who have either not achieved an adequate initial response to treatment with
adalimumab or etanercept
NASS Recommendation2:
Adalimumab is recommended as treatment options for active AS & non-
radiographic axial spondyloarthritis
Infliximab is not recommended for the treatment of AS.
American academy of Dermatology:3
Strongly Recommends the use of Adalimumab for Psoriatic Arthritis with “A”
strength of recommendation
1. NICE Guideline, “Adalimumab, etanercept and infliximab for ankylosing spondylitis”, May 2008
2. http://nass.co.uk/campaigning/working-with-nice
3. https://www.aad.org/education/clinical-guidelines/psoriasis-guideline/psoriatic-arthritis/adalimumab

43. Adalimumab effectiveness for the treatment of ankylosing spondylitis: The
ATLAS trial
 Treatment with adalimumab significantly
reduced the signs and symptoms of AS at
weeks 12 and 24.
 The magnitude of improvement was
sustained through 2 years of adalimumab
exposure.
 The percentage of patients achieving
ASAS20, ASAS40, ASAS 5/6 and ASAS
partial remission responses was sustained
from week 24 to up to 2 years of
adalimumab exposure
BASDAI BASFI
6.3
5.2
2.4
2.9
Response of Adalimumab in AS
Adalimumab Therapy
Baseline
Adalimumab treatment led to sustained improvements in
physical function, mobility & health related quality of life of
patient during long term treatment
Adalimumab reduced the signs and symptoms of AS and
induced partial remission for up to 2 years
Ann Rheum Dis 2009;68:922–929

44. Joint-protective effects: Protection beyond disease control by adalimumab plus methotrexate.
 Adalimumab provides better joint protection
than methotrexate in individual joints with
pre-existing damage, irrespective of the
presence of synovitis.
 ADA+MTX reduces the progression of both
JE and JSN in a manner that is independent of
disease activity.
 JSN played a more prominent role in patient-
reported outcomes than JE. Preventing the
onset or worsening of JSN probably
represents a critical aspect of effective disease
management of early rheumatoid arthritis
patients
Changes in joint erosion (JE) by time-averaged 28-joint
disease activity score (TA-DAS28(C-reactive protein (CRP)
tertiles over 52 weeks and 104 weeks
ADA+MTX inhibited both JE and JSN progression
independently of disease activity.
Ann Rheum Dis 2013;72:1156–1162

45. Antidrug antibodies towards adalimumab in peripheral spondyloarthritis: no association with clinical
response to treatment or with disease relapse upon treatment discontinuation
At the end of treatment (2 weeks
after the last injection),
antiadalimumab antidrug antibodies
(ADAbs) in patients who used
concomitant DMARDs was
comparable to patients who did not
use any DMARDs
Clinical response to treatment is independent of the presence of antiadalimumab antidrug antibodies.
Antiadalimumab antidrug
antibodies (ADAbs) at the end of
treatment, 2 weeks after the last
injection, were not different
between patients treated with 12
vs. 24 weeks of
adalimumab (A) or between
responders vs. nonresponders (B).
The effect of disease-modifying antirheumatic drugs on
antiadalimumab antidrug antibodies
Arthritis Res Ther. 2014; 16(4): R160.

46. Salient Features
 Adalimumab is the third immunobiological agent directed against TNFalpha and has been intensively investigated in the treatment of
Rheumatoid diseases with great success.
 It is the first fully human anti-TNFalpha antibody
 Structure promises lower antigenic properties as compared with other murine, chimeric antibodies and recombinant proteins
 Adalimumab's onset of improvement is faster than etanercept
 Weekly injections of 40 mg adalimumab alone, or bi-weekly injections of 40 mg against an MTX background, promise optimal results.
 This dosing regime totals 320 mg (160 mg plus MTX) over 8 weeks, which compares with 200 to 400 mg of infliximab
 Studies show that the anti-human antibody associated with Adalimumab were clinically non-significant
 Broadest clinical utility of the anti-TNF mAbs
 Can be used as a monotherapy or in combination with methotrexate
 Perceived best-in-class efficacy profile for psoriasis and RA
 Convenient self administration once every two weeks with prefilled