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to untangle the story

If you’re interested in hearing
more about the ST2/IL-33 pathway,
scan the QR code or speak to
a Roche representative.

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EXACERBATIONS

Explore
INFLAMMATION

Explore
The ST2/IL-33
PATHWAY

Reducing
exacerbations
is still a major
challenge in
the treatment
of COPD^1,2

COPD is a chronic
respiratory disease
characterised by
progressive airway
inflammation...

...yet traditional therapies,
such as bronchodilators
and corticosteroids,
do little to target the
underlying biology.^3–5

Every exacerbation
causes lasting lung damage,
contributing to disease
progression…

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...increasing a patient's risk of hospitalisation or death,
and significantly impacting a patient's ability to live their life.^6-9

In addition, each exacerbation increases
the risk of the next exacerbation.⁹

31%

21%

41%

51%

What percentage of
patients with a history of
exacerbations continue to
suffer from exacerbations?

Select from the
options shown

TRY AGAIN

COPD is a
heterogeneous
disease^4,11,12

…with the presence of both
neutrophilic (Types 1 & 3)
and eosinophilic (Type 2)
inflammation.^5,11–17

What do you currently believe to be
the predominant type of inflammation
in the majority of people with COPD?

A Eosinophilic inflammation (Type 2)

B Neutrophilic inflammation (Type 1, Type 3)

C Both in equal measure

Neutrophilic inflammation is the
predominant type, with the vast
majority of patients (up to 92%)
having airway neutrophilia.^4,13,15-18

Neutrophilic inflammation contributes to extracellular matrix
degradation, fibrosis, emphysema and mucus hypersecretion,
leading to airflow obstruction and exacerbations.^4,13

With its central role in
pathogenesis, it remains the
greatest unmet need in COPD
treatment.^4,5,15-17

Pinch the threads
and pull them together
to continue

Understanding how we could address
neutrophilic inflammation as well as
eosinophilic inflammation…

...could be key to reducing
exacerbations across a broader
population of patients.^5,13

ST2/IL-33 works
upstream to drive
both eosinophilic
and neutrophilic
inflammation^12,19

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thread

Following exposure to tobacco smoke, bacteria
and viruses, damaged lung epithelial cells release
a number of different alarmins, one of which is
IL-33 - an ST2 receptor-mediated cytokine.^12,19

Pull the thread

Binding of IL-33 to the
ST2 receptor, expressed
across a broad range of
immune cells

initiates and amplifies
multiple downstream
inflammatory pathways

that contribute to both
neutrophilic (Type 1 and 3)
and eosinophilic (Type 2)
inflammation^12,19

Studies are investigating
the impact of targeting
the ST2 / IL-33 pathway
in a broad population of
COPD patients.^27-33

Pull the thread

Pull a thread
to untangle the story

If you’re interested in hearing
more about the ST2/IL-33 pathway,
scan the QR code or speak to
a Roche representative.

Reducing
exacerbations
is still a major
challenge in
the treatment
of COPD^1,2

COPD is a chronic
respiratory disease
characterised by
progressive airway
inflammation...

...yet traditional therapies,
such as bronchodilators
and corticosteroids,
do little to target the
underlying biology.^3–5

Every exacerbation
causes lasting lung damage,
contributing to disease
progression…

...increasing a patient's risk of hospitalisation or death,
and significantly impacting a patient's ability to live their life.^6-9

In addition, each exacerbation increases
the risk of the next exacerbation.⁹

What percentage of
patients with a history of
exacerbations continue to
suffer from exacerbations?

Even with current
therapies, up to 51% of
patients with a history
of exacerbations
continue to suffer from
exacerbations^10*

COPD is a
heterogeneous
disease^4,11,12

…with the presence of both
neutrophilic (Types 1 & 3)
and eosinophilic (Type 2)
inflammation.^5,11–17

What do you currently believe to be
the predominant type of inflammation
in the majority of people with COPD?

Neutrophilic inflammation is the
predominant type, with the vast
majority of patients (up to 92%)
having airway neutrophilia.^4,13,15-18

Neutrophilic inflammation contributes to extracellular matrix
degradation, fibrosis, emphysema and mucus hypersecretion,
leading to airflow obstruction and exacerbations.^4,13

With its central role in
pathogenesis, it remains the
greatest unmet need in COPD
treatment.^4,5,15-17

Understanding how we could address
neutrophilic inflammation as well as
eosinophilic inflammation…

...could be key to reducing
exacerbations across a broader
population of patients.^5,13

ST2/IL-33 works
upstream to drive
both eosinophilic
and neutrophilic
inflammation^12,19

Following exposure to tobacco smoke, bacteria
and viruses, damaged lung epithelial cells release
a number of different alarmins, one of which is
IL-33 - an ST2 receptor-mediated cytokine.^12,19

Binding of IL-33 to the
ST2 receptor, expressed
across a broad range of
immune cells

initiates and amplifies
multiple downstream
inflammatory pathways

that contribute to both
neutrophilic (Type 1 and 3)
and eosinophilic (Type 2)
inflammation^12,19

Studies are investigating
the impact of targeting
the ST2 / IL-33 pathway
in a broad population of
COPD patients.^27-33

Touch the screen
to begin

Pull a threadto untangle the story

If you’re interested in hearing more about the ST2/IL-33 pathway, scan the QR code or speak to a Roche representative.

Reducing exacerbations is still a major challenge in the treatment of COPD1,2

COPD is a chronic respiratory disease characterised by progressive airway inflammation...

...yet traditional therapies, such as bronchodilators and corticosteroids, do little to target the underlying biology.3–5

Every exacerbation causes lasting lung damage, contributing to disease progression…

...increasing a patient's risk of hospitalisation or death, and significantly impacting a patient's ability to live their life.6-9

In addition, each exacerbation increases the risk of the next exacerbation.9

What percentage of patients with a history of exacerbations continue to suffer from exacerbations?

Even with current therapies, up to 51% of patients with a history of exacerbations continue to suffer from exacerbations10*

COPD is a heterogeneous disease4,11,12

…with the presence of both neutrophilic (Types 1 & 3) and eosinophilic (Type 2) inflammation.5,11–17

What do you currently believe to be the predominant type of inflammation in the majority of people with COPD?

Neutrophilic inflammation is the predominant type, with the vast majority of patients (up to 92%) having airway neutrophilia.4,13,15-18

Neutrophilic inflammation contributes to extracellular matrix degradation, fibrosis, emphysema and mucus hypersecretion, leading to airflow obstruction and exacerbations.4,13

With its central role in pathogenesis, it remains the greatest unmet need in COPD treatment.4,5,15-17

Understanding how we could address neutrophilic inflammation as well as eosinophilic inflammation…

...could be key to reducing exacerbations across a broader population of patients.5,13

ST2/IL-33 works upstream to drive both eosinophilic and neutrophilic inflammation12,19

Following exposure to tobacco smoke, bacteria and viruses, damaged lung epithelial cells release a number of different alarmins, one of which is IL-33 - an ST2 receptor-mediated cytokine.12,19

Binding of IL-33 to the ST2 receptor, expressed across a broad range of immune cells

initiates and amplifies multiple downstream inflammatory pathways

that contribute to both neutrophilic (Type 1 and 3) and eosinophilic (Type 2) inflammation12,19

Studies are investigating the impact of targeting the ST2 / IL-33 pathway in a broad population of COPD patients.27-33

Touch the screen to begin

Pull a thread
to untangle the story

If you’re interested in hearing
more about the ST2/IL-33 pathway,
scan the QR code or speak to
a Roche representative.

Reducing
exacerbations
is still a major
challenge in
the treatment
of COPD^1,2

COPD is a chronic
respiratory disease
characterised by
progressive airway
inflammation...

...yet traditional therapies,
such as bronchodilators
and corticosteroids,
do little to target the
underlying biology.^3–5

Every exacerbation
causes lasting lung damage,
contributing to disease
progression…

...increasing a patient's risk of hospitalisation or death,
and significantly impacting a patient's ability to live their life.^6-9

In addition, each exacerbation increases
the risk of the next exacerbation.⁹

What percentage of
patients with a history of
exacerbations continue to
suffer from exacerbations?

Even with current
therapies, up to 51% of
patients with a history
of exacerbations
continue to suffer from
exacerbations^10*

COPD is a
heterogeneous
disease^4,11,12

…with the presence of both
neutrophilic (Types 1 & 3)
and eosinophilic (Type 2)
inflammation.^5,11–17

What do you currently believe to be
the predominant type of inflammation
in the majority of people with COPD?

Neutrophilic inflammation is the
predominant type, with the vast
majority of patients (up to 92%)
having airway neutrophilia.^4,13,15-18

Neutrophilic inflammation contributes to extracellular matrix
degradation, fibrosis, emphysema and mucus hypersecretion,
leading to airflow obstruction and exacerbations.^4,13

With its central role in
pathogenesis, it remains the
greatest unmet need in COPD
treatment.^4,5,15-17

Understanding how we could address
neutrophilic inflammation as well as
eosinophilic inflammation…

...could be key to reducing
exacerbations across a broader
population of patients.^5,13

ST2/IL-33 works
upstream to drive
both eosinophilic
and neutrophilic
inflammation^12,19

Following exposure to tobacco smoke, bacteria
and viruses, damaged lung epithelial cells release
a number of different alarmins, one of which is
IL-33 - an ST2 receptor-mediated cytokine.^12,19

Binding of IL-33 to the
ST2 receptor, expressed
across a broad range of
immune cells

initiates and amplifies
multiple downstream
inflammatory pathways

that contribute to both
neutrophilic (Type 1 and 3)
and eosinophilic (Type 2)
inflammation^12,19

Studies are investigating
the impact of targeting
the ST2 / IL-33 pathway
in a broad population of
COPD patients.^27-33

Touch the screen
to begin