- 51% of No Tau / Low Tau Patients Showed
Improved Cognition and Function Over Three Years; Only Lecanemab
Has Clinical Data in No Tau / Low Tau Patient Group
- Clinical Data and Biomarkers Show
Alzheimer's Disease Does Not Stop Progressing After Plaque
Clearance. Lecanemab's Dual Action Supports Neuronal Function by
Clearing Highly Toxic Protofibrils that Continue to Cause Neuronal
Injury and Death After Rapid Plaque Clearance
- Lecanemab Slows Tau Spread Across All Brain
Regions
PHILADELPHIA, July 30,
2024 /PRNewswire/ -- Eisai Co., Ltd. (Headquarters:
Tokyo, CEO: Haruo Naito, "Eisai") and Biogen Inc. (Nasdaq:
BIIB, Headquarters: Cambridge,
Massachusetts, United
States, CEO: Christopher A.
Viehbacher, "Biogen") announced today that the latest
findings for lecanemab-irmb (U.S. brand name: LEQEMBI®),
an anti-amyloid beta (Aβ) protofibril* antibody for the treatment
of early Alzheimer's disease (AD), were presented at the
Alzheimer's Association International Conference (AAIC) 2024, held
in Philadelphia, USA, and virtually. Dual-acting lecanemab is
the only early AD treatment widely available to support neuronal
function by clearing the highly toxic protofibrils that continue to
cause neuronal injury and death even after plaques have been
cleared from the brain. The presentation slides for the two
scientific sessions on lecanemab at the AAIC will be available on
the Eisai Co. Ltd. Investor Page by 7:00 p.m. on July
30th EDT.
Experience the full interactive Multichannel News Release here:
https://www.multivu.com/players/English/9282551-eisai-leqembi-clinical-data-aaic-2024-alzheimers/
Three Years of Continuous Lecanemab Treatment Reduced
Clinical Decline by -0.95 on CDR-SB Showing Continued Clinically
and Personally Meaningful Benefit for Early AD
Patients
Clarity AD was a global Phase 3 placebo-controlled,
double-blind, parallel-group, randomized study in 1,795 people with
early AD (Lecanemab group: 10 mg/kg bi-weekly IV treatment: 898,
placebo group: 897). 95% of patients who completed the core
study (18 months) chose to continue in the open-label
extension study (OLE). In the Clarity AD core study, the mean
change from baseline between the lecanemab treated group and the
placebo group was -0.45 (P=0.00005) on the primary
endpoint of the Clinical Dementia Rating-Sum of Boxes (CDR-SB)
global cognitive and functional scale. Over three years of
treatment across the core study and OLE, lecanemab reduced
cognitive decline on the CDR-SB by -0.95 compared to the expected
decline based on the Alzheimer's Disease Neuroimaging Initiative
(ADNI)** group.1 A change from 0.5 to 1 on the CDR score
domains of Memory, Community Affairs and Home/Hobbies is the
difference between slight impairment and loss of independence, such
as people's ability to be left alone, remember recent events,
participate in daily activities, complete household chores,
function independently and engage in hobbies and intellectual
interests.2,3
Safety Matters
No new safety findings have been
observed with continued lecanemab treatment over three (3) years.
Most Amyloid-related imaging abnormalities (ARIA) occurred in the
first six months of treatment. After the first six months, ARIA
rates are low and similar to ARIA rates on placebo. Most patients
who had ARIA had CDR-SB assessments after the event. Sensitivity
analyses showed ARIA had no impact on cognition or function. From
these results ARIA was not associated with accelerated long-term
progression.1 As stated in the FDA product label,
the incidence and timing of ARIA vary among
treatments.4
More than 50% of Patients Who Started Treatment in the
Earliest Stage of AD Continued to Show Improvement After Three
Years of Lecanemab Treatment
The Clarity AD study included
an optional tau PET substudy and used the tau PET probe MK6240 to
identify patients with no tau or a low accumulation of tau in the
brain. As tau begins to accumulate in the brain, cognition and
function start to decline; therefore, patients with no tau or low
tau in the brain represent an early stage of AD. After three years
of lecanemab treatment, 59% of these patients (24/41) showed
improvement or no decline, and 51% (21/41) showed improvement
from baseline on the CDR-SB. On the ADAS-Cog14 measurement scale,
63% of patients showed improvement or no decline and 61% showed
improvement. On the ADCS MCI-ADL, 63% of patients showed
improvement or no decline and 59% showed improvement. This
suggests that earlier initiation of treatment with lecanemab may
have a significant positive impact on disease progression and may
provide continued benefits to patients with early AD over the
long-term.1
Even After Plaque Clearance, AD Continues to Progress When
Treatment is Stopped
Study 201 is a multicenter,
double-blind, placebo-controlled, Phase 2b trial conducted in 856 patients with early AD.
Appropriate patients participated in the OLE after an off-treatment
period of 9-59 months (mean: 24 months) following the 18-month core
study. During the off-treatment period lecanemab's clinical
effect was maintained but the rate of decline (slope) in patients
who stopped therapy reverted back to the rate of decline in
patients on placebo as measured by CDR-SB. This indicates that even
after Aβ plaque is removed, AD continues to progress, and reverts
to the placebo rate of decline when treatment is
stopped.1
After Plaque Removal, Dual-Acting Lecanemab Continues to
Positively Impact Biomarkers Over the Course of
Treatment
The key AD fluid biomarkers Aβ42/40, pTau181,
pTau217, and glial fibrillary acidic protein (***GFAP) are more
sensitive indicators of amyloid and tau development than Amyloid
PET and have been shown to re-accumulate at a faster rate when
treatment is discontinued. Modeling data from the Study 201 (Phase
2), Clarity AD (Phase 3) and respective OLE studies showed that the
half-life of the treatment effect on the fluid biomarkers plasma
Aβ42/40 ratio, pTau181, and GFAP are lost within 0.5 year, 1.6
years and 1.7 years, respectively, while the half-life of the
treatment effect on amyloid plaque is gradually lost in 12.1 years.
When lecanemab treatment was resumed in the Study 201 OLE
after off-treatment period, fluid biomarkers Aβ42/40 ratio,
pTau181, pTau217 and GFAP improved. These results suggest
that AD continues to progress when treatment is stopped, even
after plaque has been cleared. Patients continue to benefit by
remaining on treatment as lecanemab maintains improvement in the
fluid biomarkers of amyloid pathophysiology.1
Lecanemab's Dual Action on Protofibrils and Plaques Impacts
Amyloid and Slows Tau Spread, Offering Patients a Continuous,
Long-Term Treatment for this Chronic and Progressive
Disease
Lecanemab is the only widely available early
AD treatment that offers a dual mechanism of action designed to
selectively target highly toxic protofibrils in addition to amyloid
plaques. Protofibrils accumulate early in the AD brain and lead to
nerve cell function loss, abnormal nerve processes, inflammation,
and memory loss. In non-clinical studies, antibodies against
protofibrils prevented protofibril-mediated neuronal dysfunction
and memory loss.5 Lecanemab preferentially binds to
toxic protofibrils with the highest affinity. After rapidly
clearing plaque and existing protofibrils, lecanemab continuously
clears the protofibrils that continue to develop and damage
neurons.1 Protofibrils also play a role in tau
spread.5 In the tau PET substudy, continuous lecanemab
treatment slowed the rate of increase in tau accumulation across
all brain regions as measured by tau PET.6 CSF
MTBR-tau243 has high correlation with tau PET and increases with
the progression of AD pathology. Treatment with lecanemab slows the
increase in CSF MTBR-tau243. Additionally, lecanemab improved
pTau217 and other biomarkers related to neuroinflammation and
neurodegeneration. This indicates a potential disease-modifying
effect on tau pathophysiology.7
Eisai serves as the lead for lecanemab's development and
regulatory submissions globally with both Eisai and Biogen
co-commercializing and co-promoting the product and Eisai
having final decision-making authority.
*Protofibrils are thought to be the most toxic
Aβ species that contribute to brain damage in AD and play a major
role in the cognitive decline of this progressive and devastating
disease. Protofibrils can cause neuronal damage in the brain, which
can subsequently adversely affect cognitive function through
multiple mechanisms.5 The mechanism by which this occurs
has been reported not only by increasing the formation of insoluble
Aβ plaques, but also by directly damaging signaling between neurons
and other cells. It is believed that reducing protofibrils may
reduce neuronal damage and cognitive impairment, potentially
preventing the progression of AD.8
**ADNI is a clinical research project launched
in 2005 to develop methods to predict the onset of AD and to
confirm the effectiveness of treatments. The ADNI observational
cohort represents the exact population of those in Clarity AD
study; matched ADNI participants show similar degree of decline to
placebo group out to 18 months.
*** Glial fibrillary acidic protein (GFAP), a
marker of astroglia activation, has been proposed as a biomarker of
Alzheimer's disease (AD). GFAP expression correlates with Aβ
plaque density and cerebrospinal fluid (CSF) concentration is
elevated in symptomatic disease.
Please see full Prescribing Information for
LEQEMBI, including Boxed WARNING.
U.S. INDICATION
LEQEMBI® [(lecanemab-irmb)
100 mg/mL injection for intravenous use] is indicated for the
treatment of Alzheimer's disease (AD). Treatment with LEQEMBI
should be initiated in patients with mild cognitive impairment
(MCI) or mild dementia stage of disease, the population in which
treatment was initiated in clinical trials.
IMPORTANT SAFETY INFORMATION
WARNING:
AMYLOID-RELATED IMAGING ABNORMALITIES (ARIA)
- Monoclonal antibodies directed against
aggregated forms of amyloid beta, including LEQEMBI, can cause
ARIA, characterized as ARIA with edema (ARIA-E) and ARIA with
hemosiderin deposition (ARIA-H). Incidence and timing of ARIA vary
among treatments. ARIA usually occurs early in treatment and is
asymptomatic, although serious and life-threatening events,
including seizure and status epilepticus, rarely can occur. Serious
intracerebral hemorrhages >1 cm, some fatal, have been observed
with this class of medications.
- Apolipoprotein E ε4 (ApoE ε4) Homozygotes:
Patients who are ApoE ε4 homozygotes (~15% of patients with AD)
treated with this class of medications have a higher incidence of
ARIA, including symptomatic, serious, and severe radiographic ARIA,
compared to heterozygotes and noncarriers. Testing for ApoE ε4
status should be performed prior to initiation of treatment to
inform the risk of developing ARIA. Prescribers should discuss with
patients the risk of ARIA across genotypes and the implications of
genetic testing results. Prescribers should inform patients that if
genotype testing is not performed, they can still be treated with
LEQEMBI; however, it cannot be determined if they are ApoE ε4
homozygotes and at higher risk for ARIA.
- Consider the benefit of LEQEMBI for the
treatment of AD and the potential risk of serious ARIA events when
deciding to initiate treatment with LEQEMBI.
|
CONTRAINDICATION
LEQEMBI is contraindicated in
patients with serious hypersensitivity to lecanemab-irmb or to any
of the excipients of LEQEMBI. Reactions have included angioedema
and anaphylaxis.
WARNINGS AND PRECAUTIONS
AMYLOID-RELATED IMAGING ABNORMALITIES
LEQEMBI can
cause ARIA-E and ARIA-H, which can occur together. ARIA-E can be
observed on magnetic resonance imaging (MRI) as brain edema or
sulcal effusions and ARIA-H as microhemorrhage and superficial
siderosis. ARIA can occur spontaneously in patients with AD. With
this class of medications, ARIA-H generally occurs in association
with ARIA-E. Reported ARIA symptoms may include headache,
confusion, visual changes, dizziness, nausea, and gait difficulty.
Focal neurologic deficits may also occur. Symptoms usually resolve
over time.
Incidence of ARIA
Symptomatic ARIA occurred in 3%
(29/898) and serious ARIA symptoms in 0.7% (6/898) with LEQEMBI.
Clinical ARIA symptoms resolved in 79% (23/29) of patients during
the period of observation. ARIA, including asymptomatic
radiographic events, was observed: LEQEMBI, 21% (191/898); placebo,
9% (84/897). ARIA-E was observed: LEQEMBI, 13% (113/898); placebo,
2% (15/897). ARIA-H was observed: LEQEMBI, 17% (152/898); placebo,
9% (80/897). No increase in isolated ARIA-H was observed for
LEQEMBI vs placebo.
ApoE ε4 Carrier Status and Risk of ARIA
Of the
patients taking LEQEMBI, 16% (141/898) were ApoE ε4 homozygotes,
53% (479/898) were heterozygotes, and 31% (278/898) were
noncarriers. With LEQEMBI, the incidence of ARIA was higher in ApoE
ε4 homozygotes (LEQEMBI: 45%; placebo: 22%) than in heterozygotes
(LEQEMBI: 19%; placebo: 9%) and noncarriers (LEQEMBI: 13%; placebo:
4%). Symptomatic ARIA-E occurred in 9% of ApoE ε4 homozygotes vs 2%
of heterozygotes and 1% of noncarriers. Serious ARIA events
occurred in 3% of ApoE ε4 homozygotes and in ~1% of heterozygotes
and noncarriers. The recommendations on management of ARIA do not
differ between ApoE ε4 carriers and noncarriers.
Radiographic Findings
The majority of ARIA-E
radiographic events occurred within the first 7 doses, although
ARIA can occur at any time, and patients can have >1 episode.
Maximum radiographic severity of ARIA-E with LEQEMBI was mild in 4%
(37/898), moderate in 7% (66/898), and severe in 1% (9/898) of
patients. Resolution of ARIA-E on MRI occurred in 52% of patients
by 12 weeks, 81% by 17 weeks, and 100% overall after detection.
Maximum radiographic severity of ARIA-H microhemorrhage with
LEQEMBI was mild in 9% (79/898), moderate in 2% (19/898), and
severe in 3% (28/898) of patients; superficial siderosis was mild
in 4% (38/898), moderate in 1% (8/898), and severe in 0.4% (4/898)
of patients. With LEQEMBI, the rate of severe radiographic ARIA-E
was highest in ApoE ε4 homozygotes (5%; 7/141) vs heterozygotes
(0.4%; 2/479) or noncarriers (0%; 0/278). With LEQEMBI, the rate of
severe radiographic ARIA-H was highest in ApoE ε4 homozygotes
(13.5%; 19/141) vs heterozygotes (2.1%; 10/479) or noncarriers
(1.1%; 3/278).
Intracerebral Hemorrhage
Intracerebral hemorrhage
>1 cm in diameter was reported in 0.7% (6/898) with LEQEMBI vs
0.1% (1/897) with placebo. Fatal events of intracerebral hemorrhage
in patients taking LEQEMBI have been reported.
Concomitant Antithrombotic
Medication:
In Clarity AD, baseline use of antithrombotic
medication (aspirin, other antiplatelets, or anticoagulants) was
allowed if the patient was on a stable dose. The majority of
exposures to antithrombotic medications were to aspirin.
Antithrombotic medications did not increase the risk of ARIA with
LEQEMBI. The incidence of intracerebral hemorrhage was 0.9% (3/328)
in patients taking LEQEMBI with a concomitant antithrombotic
medication at the time of the event vs 0.6% (3/545) in those who
did not receive an antithrombotic. Patients taking LEQEMBI with an
anticoagulant alone or combined with an antiplatelet medication or
aspirin had an incidence of intracerebral hemorrhage of 2.5% (2/79)
vs none in patients receiving placebo. Caution should be exercised
when considering the administration of anticoagulants or a
thrombolytic agent (e.g., tissue plasminogen activator) to a
patient already being treated with LEQEMBI.
Other Risk Factors for Intracerebral
Hemorrhage:
Patients were excluded from enrollment in
Clarity AD for findings on neuroimaging that indicated an increased
risk for intracerebral hemorrhage. These included findings
suggestive of cerebral amyloid angiopathy (prior cerebral
hemorrhage >1 cm in greatest diameter, >4 microhemorrhages,
superficial siderosis, vasogenic edema) or other lesions (aneurysm,
vascular malformation). The presence of an ApoE ε4 allele is also
associated with cerebral amyloid angiopathy. Caution should be
exercised when considering the use of LEQEMBI in patients with
factors that indicate an increased risk for intracerebral
hemorrhage and in patients who need to be on anticoagulant
therapy.
ARIA Monitoring and Dose Management Guidelines
Obtain
a recent baseline brain MRI prior to initiating treatment with
LEQEMBI and prior to the 5th, 7th, and 14th infusions. Enhanced
clinical vigilance for ARIA is recommended during the first 14
weeks of treatment with LEQEMBI. Depending on ARIA-E and ARIA-H
clinical symptoms and radiographic severity, use clinical judgment
when considering whether to continue dosing or to temporarily or
permanently discontinue LEQEMBI. If a patient experiences ARIA
symptoms, clinical evaluation should be performed, including MRI if
indicated. If ARIA is observed on MRI, careful clinical evaluation
should be performed prior to continuing treatment.
HYPERSENSITIVITY REACTIONS
Hypersensitivity reactions,
including angioedema, bronchospasm, and anaphylaxis, have occurred
with LEQEMBI. Promptly discontinue the infusion upon the first
observation of any signs or symptoms consistent with a
hypersensitivity reaction and initiate appropriate therapy.
INFUSION-RELATED REACTIONS (IRRs)
IRRs were
observed—LEQEMBI: 26% (237/898); placebo: 7% (66/897)—and the
majority of cases with LEQEMBI (75%, 178/237) occurred with the
first infusion. IRRs were mostly mild (69%) or moderate (28%) in
severity. IRRs resulted in discontinuation of LEQEMBI in 1%
(12/898). Symptoms of IRRs included fever and flu-like symptoms
(chills, generalized aches, feeling shaky, and joint pain), nausea,
vomiting, hypotension, hypertension, and oxygen desaturation.
In the event of an IRR, the infusion rate may be reduced or the
infusion may be discontinued and appropriate therapy initiated as
clinically indicated. Consider prophylactic treatment prior to
future infusions with antihistamines, acetaminophen, nonsteroidal
anti-inflammatory drugs, or corticosteroids.
ADVERSE REACTIONS
The most common adverse reaction
leading to discontinuation of LEQEMBI was ARIA-H microhemorrhages
that led to discontinuation in 2% (15/898) with LEQEMBI vs <1%
(1/897) with placebo.
The most common adverse reactions reported in ≥5% with LEQEMBI
(N=898) and ≥2% higher than placebo (N=897) were IRRs (LEQEMBI:
26%; placebo: 7%), ARIA-H (LEQEMBI: 14%; placebo: 8%), ARIA-E
(LEQEMBI: 13%; placebo: 2%), headache (LEQEMBI: 11%; placebo: 8%),
superficial siderosis of central nervous system (LEQEMBI: 6%;
placebo: 3%), rash (LEQEMBI: 6%; placebo: 4%), and nausea/vomiting
(LEQEMBI: 6%; placebo: 4%).
MEDIA
CONTACTS
|
|
Eisai Co.,
Ltd.
Public Relations
Department
TEL: +81
(0)3-3817-5120
Eisai Inc.
(U.S.)
Libby Holman
+
1-201-753-1945
Libby_Holman@eisai.com
Eisai Europe,
Ltd.
(UK, Europe, Australia,
New Zealand and Russia)
EMEA Communications
Department
+44 (0) 786 601
1272
EMEA-comms@eisai.net
|
Biogen
Inc.
Jack Cox
+
1-781-464-3260
public.affairs@biogen.com
|
INVESTOR
CONTACTS
|
|
|
|
Eisai Co.,
Ltd.
Investor Relations
Department
TEL: +81 (0)
3-3817-5122
|
Biogen
Inc.
Chuck Triano
+
1-781-464-2442
IR@biogen.com
|
[Notes to editors]
1. About
LEQEMBI
LEQEMBI (generic name: lecanemab) is the result of a
strategic research alliance between Eisai and BioArctic. It is a
humanized immunoglobulin gamma 1 (IgG1) monoclonal antibody
directed against aggregated soluble (protofibril) and insoluble
forms of amyloid-beta (Aβ).
LEQEMBI's FDA approval was based on Phase 3 data from Eisai's,
global Clarity AD clinical trial, in which it met its primary
endpoint and all key secondary endpoints with statistically
significant results.9,10 The primary endpoint was the
global cognitive and functional scale, Clinical Dementia Rating Sum
of Boxes (CDR-SB). In the Clarity AD clinical trial, treatment with
LEQEMBI reduced clinical decline on CDR-SB by 27% at 18 months
compared to placebo. The mean CDR-SB score at baseline was
approximately 3.2 in both groups. The adjusted least-squares mean
change from baseline at 18 months was 1.21 with LEQEMBI and 1.66
with placebo (difference, −0.45; 95% confidence interval [CI],
−0.67 to −0.23; P<0.001). In addition, the secondary endpoint
from the AD Cooperative Study-Activities of Daily Living Scale for
Mild Cognitive Impairment (ADCS-MCI-ADL), which measures
information provided by people caring for patients with AD, noted a
statistically significant benefit of 37% compared to placebo. The
adjusted mean change from baseline at 18 months in the ADCS-MCI-ADL
score was −3.5 in the LEQEMBI group and −5.5 in the placebo group
(difference, 2.0; 95% CI, 1.2 to 2.8; P<0.001). The ADCS MCI-ADL
assesses the ability of patients to function independently,
including being able to dress, feed themselves and participate in
community activities. The most common adverse events (>10%) in
the LEQEMBI group were infusion reactions, ARIA-H (combined
cerebral microhemorrhages, cerebral macrohemorrhages, and
superficial siderosis), ARIA-E (edema/effusion), headache, and
fall.
LEQEMBI is approved in the U.S., Japan, China,
South Korea, Hong Kong and Israel for the treatment of MCI due to AD and
mild AD dementia. Eisai has also submitted applications for
approval of LEQEMBI in 12 countries and regions. A supplemental
Biologics License Application (sBLA) for intravenous maintenance
dosing was submitted to the U.S. Food and Drug Administration (FDA)
in March 2024, which was accepted in
June 2024. The rolling submission of
a Biologics License Application (BLA) for maintenance dosing of a
subcutaneous injection formulation, which is being developed to
enhance convenience for patients, was initiated in the U.S. under
Fast Track status in May 2024.
Since July 2020, the Phase 3
clinical study (AHEAD 3-45) for individuals with preclinical AD,
meaning they are clinically normal and have intermediate or
elevated levels of amyloid in their brains, is ongoing. AHEAD 3-45
is conducted as a public-private partnership between the
Alzheimer's Clinical Trial Consortium that provides the
infrastructure for academic clinical trials in AD and related
dementias in the U.S, funded by the National Institute on Aging,
part of the National Institutes of Health, Eisai, and Biogen. Since
January 2022, the Tau NexGen clinical
study for Dominantly Inherited AD (DIAD), that is conducted by
Dominantly Inherited Alzheimer Network Trials Unit (DIAN-TU), led
by Washington University School of
Medicine in St. Louis, is ongoing
and includes lecanemab as the backbone anti-amyloid therapy.
2. About the Collaboration between Eisai and
Biogen for Alzheimer's Disease
Eisai and Biogen have been
collaborating on the joint development and commercialization of AD
treatments since 2014. Eisai serves as the lead of lecanemab
development and regulatory submissions globally with both Eisai and
Biogen co-commercializing and co-promoting the product and Eisai
having final decision-making authority.
3. About the Collaboration between Eisai and
BioArctic for Alzheimer's Disease
Since 2005, Eisai and
BioArctic have had a long-term collaboration regarding the
development and commercialization of AD treatments. Eisai obtained
the global rights to study, develop, manufacture and market
lecanemab for the treatment of AD pursuant to an agreement with
BioArctic in December 2007. The
development and commercialization agreement on the antibody
lecanemab back-up was signed in May
2015.
4. About Eisai Co., Ltd.
Eisai's
Corporate Concept is "to give first thought to patients and people
in the daily living domain, and to increase the benefits that
health care provides." Under this Concept (also known as human
health care (hhc) Concept), we aim to effectively
achieve social good in the form of relieving anxiety over health
and reducing health disparities. With a global network of R&D
facilities, manufacturing sites and marketing subsidiaries, we
strive to create and deliver innovative products to target diseases
with high unmet medical needs, with a particular focus in our
strategic areas of Neurology and Oncology.
In addition, we demonstrate our commitment to the elimination of
neglected tropical diseases (NTDs), which is a target (3.3) of the
United Nations Sustainable Development Goals (SDGs), by working on
various activities together with global partners.
For more information about Eisai, please visit
www.eisai.com (for global headquarters: Eisai. Co., Ltd.),
us.eisai.com (for U.S. headquarters: Eisai, Inc.) or
www.eisai.eu (for Europe,
Middle East, Africa, Russia, Australia and New
Zealand headquarters: Eisai Europe Ltd.), and connect with
us on X (global and U.S), LinkedIn (for global, U.S. and
EMEA) and Facebook (global).
5. About Biogen
Founded in 1978, Biogen
is a leading biotechnology company that pioneers innovative science
to deliver new medicines to transform patients' lives and to create
value for shareholders and our communities. We apply deep
understanding of human biology and leverage different modalities to
advance first-in-class treatments or therapies that deliver
superior outcomes. Our approach is to take bold risks, balanced
with return on investment to deliver long-term growth.
The company routinely posts information that may be important to
investors on its website at www.biogen.com. Follow Biogen on social
media – Facebook, LinkedIn, X, YouTube. The website and social
media channels are intended for audiences outside of the UK and
Europe.
Biogen Safe Harbor
This news release contains
forward-looking statements, about the potential clinical effects of
lecanemab; the potential benefits, safety and efficacy of
lecanemab; potential regulatory discussions, submissions and
approvals and the timing thereof; the treatment of Alzheimer's
disease; the anticipated benefits and potential of Biogen's
collaboration arrangements with Eisai; the potential of Biogen's
commercial business and pipeline programs, including
lecanemab; and risks and uncertainties associated with drug
development and commercialization. These statements may be
identified by words such as "aim," "anticipate," "believe,"
"could," "estimate," "expect," "forecast," "intend," "may," "plan,"
"possible," "potential," "will," "would" and other words and terms
of similar meaning. Drug development and commercialization involve
a high degree of risk, and only a small number of research and
development programs result in commercialization of a product.
Results in early-stage clinical studies may not be indicative of
full results or results from later stage or larger scale clinical
studies and do not ensure regulatory approval. You should not place
undue reliance on these statements.
These statements involve risks and uncertainties that could
cause actual results to differ materially from those reflected in
such statements, including without limitation unexpected concerns
that may arise from additional data, analysis or results obtained
during clinical studies; the occurrence of adverse safety events;
risks of unexpected costs or delays; the risk of other unexpected
hurdles; regulatory submissions may take longer or be more
difficult to complete than expected; regulatory authorities may
require additional information or further studies, or may fail or
refuse to approve or may delay approval of Biogen's drug
candidates, including lecanemab; actual timing and content of
submissions to and decisions made by the regulatory authorities
regarding lecanemab; uncertainty of success in the development and
potential commercialization of lecanemab; failure to protect and
enforce Biogen's data, intellectual property and other proprietary
rights and uncertainties relating to intellectual property claims
and challenges; product liability claims; and third party
collaboration risks, results of operations and financial condition.
The foregoing sets forth many, but not all, of the factors that
could cause actual results to differ from Biogen's expectations in
any forward-looking statement. Investors should consider this
cautionary statement as well as the risk factors identified in
Biogen's most recent annual or quarterly report and in other
reports Biogen has filed with the U.S. Securities and Exchange
Commission. These statements speak only as of the date of this news
release. Biogen does not undertake any obligation to publicly
update any forward-looking statements.
References
- Sperling, R., Selkoe, D., Reyderman, L., Youfang, C.,
Van Dyck, C. (2024, July 28 - August 1). Does the Current Evidence
Base Support Lecanemab Continued Dosing for Early Alzheimer's
Disease? [Perspectives Session] Alzheimer's Association
International Conference, Philadelphia,
PA, United States.
- Cohen S., et al. J Prev Alzheimers
Dis.2022;9(3):507-522.
- Morris JC. Neurology. 1993;43(11):2412-4.
- LEQEMBI® (lecanemab-irmb) [package insert].
Nutley, NJ. Eisai Inc.; 2023.
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