INVESTIGATIONAL SUBCUTANEOUS FORMULATION
CLEARS 14% MORE PLAQUE THAN IV, PHARMACOKINETICS (AUC) 11% HIGHER,
AND SIMILAR ARIA RATES TO IV
76% OF PATIENTS SHOWED NO DECLINE AND 60%
SHOWED CLINICAL IMPROVEMENT AT 18 MONTHS IN LOW-TAU SUBPOPULATION
IN ADDITIONAL ANALYSIS OF CLARITY AD
DUAL-ACTING LEQEMBI SUPPORTS BRAIN NEURON
FUNCTION BY REMOVING HIGHLY TOXIC PROTEINS (PROTOFIBRILS) THAT CAN
CONTINUE TO CAUSE NEURONAL INJURY AND DEATH EVEN AFTER PLAQUE
REMOVAL, OFFERING EARLY AD PATIENTS THE OPPORTUNITY FOR CONTINUED
BENEFIT
TOKYO and CAMBRIDGE,
Mass., Oct. 25, 2023 /PRNewswire/ -- Eisai
Co., Ltd. (Headquarters: Tokyo,
CEO: Haruo Naito, "Eisai") and
Biogen Inc. (Nasdaq: BIIB, Corporate headquarters: Cambridge, Massachusetts, CEO: Christopher A. Viehbacher, "Biogen") announced
today that Eisai presented new data for
LEQEMBI® (lecanemab-irmb) 100 mg/mL injection for
intravenous (IV) use, in the Late Breaking Symposium 4 "Lecanemab
for Early Alzheimer's Disease: Long-Term Outcomes, Predictive
Biomarkers and Novel Subcutaneous Administration" at the
16th annual Clinical Trials on Alzheimer's Disease
(CTAD) conference held in Boston,
Massachusetts, United
States and virtually October 24-27,
2023.
U.S. journalists may experience the full interactive
Multichannel News Release here:
https://www.multivu.com/players/English/9211051-eisai-at-ctad2023
1. Subcutaneous Formulation Interim Data; Safety
And Effects On Brain Amyloid
1) Weekly subcutaneous (SC)
administration showed 14% greater amyloid plaque removal than
biweekly IV administration as suggested in a preliminary analysis
using amyloid PET at 6 months of treatment.
- The SC substudy, evaluating the SC formulation in an
open-label extension (OLE) of the Clarity AD study*,
included 72 patients who received LEQEMBI for the first time as the
SC formulation, and 322 patients who received intravenous (IV)
LEQEMBI in the Clarity AD core study followed by SC administration
in this substudy. Reduction from baseline of amyloid in the brain
by amyloid PET at 6 months in the newly treated SC patients by
centiloid reduction was -40.3 ± 2.27 in SC administration
compared to -35.4 ± 1.14 in IV administration.1
2) SC Pharmacokinetics (AUC)
Higher Than IV By 11%
- Weekly SC administration AUC are 11% higher than the
biweekly IV formulation. 90% CI for drug exposure for SC vs. IV is
within the bioequivalence limits of 80 to 125%. These data could
allow Eisai to select a dose that achieves AUC that are
comparable to the IV dose.1
3) Lower Systemic Injection
Reaction Rates With SC As Compared To IV
- Systemic injection/infusion reactions are uncommon and mild
with SC administration, and in particular have not been observed in
patients who received LEQEMBI for the first time as the SC
formulation. There was a low rate of local injection site reactions
(8.1%) in SC treated patients overall. Most were mild and moderate
in severity consisting of redness, irritation, or swelling. No skin
rash or other hypersensitivity reactions were
reported.1
4) ARIA Rates Of IV Formulation
In Clarity AD Core Study Consistent With Rates In First-Time
LEQEMBI Patients Entering The SC Substudy In Clarity AD OLE
- The incidence of ARIA-E with SC was similar to the
IV. The incidences of ARIA-E, ARIA-H (cerebral microhemorrhage
due to ARIA, cerebral hemorrhage, and brain surface hemosiderin
deposition) and ARIA-H alone (ARIA-H without ARIA-E) with IV in the
Clarity AD core study (n=898) were 12.6%, 17.3% and 8.9%,
respectively. In newly treated patients in the SC substudy of the
Clarity AD OLE (n=72), the incidences of ARIA-E, ARIA-H and ARIA-H
alone were 16.7%, 22.2% and 8.3%, respectively. However, due to the
sample size of newly treated patients in the SC substudy, no exact
comparison can be made.1
- Based on Phase II and III clinical studies, Cmax (maximum
exposure) was the strongest predictor of ARIA-E incidence following
IV administration. In the SC substudy, the steady-state exposure
(AUCss) appears to be a better predictor of ARIA-E rates in the SC
due to a relatively stable exposure profile. 1
Eisai aims to submit a LEQEMBI SC formulation Biologics License
Application (BLA) with the U.S. Food and Drug Administration by
March 31, 2024.
2. Latest Data From Tau Pet
Longitudinal Substudy, Including A Post-Hoc Analysis Of The Low And
Intermediate + High-Tau Subpopulations In The Clarity AD 18 Month
Core Study
1) 76% of patients showed no
decline and 60% showed clinical improvement at 18 months in low-tau
/ earlier stage early AD population.
- The Clarity AD study included an optional Tau PET substudy
and used the tau PET probe MK6240** to identify patients with a low
accumulation of tau in the brain, which represents the earlier
stage of early AD.
- The low-tau subpopulation, which is in the earlier stages of
early AD, is thought to show slow disease progression. In the
low-tau subpopulation, 76% of the LEQEMBI group showed no
deterioration and 60% showed clinical improvement after 18 months
of treatment in the primary endpoint, Clinical Dementia Rating -
Sum of Boxes (CDR-SB), compared with 55% and 28% of the placebo
group, respectively.1
- Importantly, in this low-tau subgroup, LEQEMBI treatment also
showed consistent clinical response across multiple endpoints.***
In this population, LEQEMBI treatment favored cognition and
function in the earlier stage of early AD.1
- The efficacy results of the Tau PET substudy in the Clarity AD
study, which observed tau pathology in the brain by tau PET, were
consistent with overall results of the Clarity AD
study.1
2) Tau PET Substudy Showed
LEQEMBI Slows Development Of Tau Tangles In Early AD; Tau Spread In
The Brain Is A Hallmark Of Disease Progression.
- In the Clarity AD Tau PET substudy, LEQEMBI treatment
slowed the buildup of tau proteins in the temporal lobe (early
Braak region), where tau accumulation was observed in the earlier
stage of early AD. In the Tau PET substudy, LEQEMBI suppressed the
accumulation of tau in the medial temporal brain region in low-tau
subpopulations, and in a broader range of brain regions in the
intermediate and higher accumulation groups**. This suggests that
LEQEMBI treatment may have different effects on brain regions
indexed by tau depending on the stage of the disease.1
The spread of tau in the brain is a hallmark of AD
progression.2
3. Efficacy Results From LEQEMBI Clarity
AD Open-Label Extension Study
1) LEQEMBI Patients Continued to
Show Benefit at 24 Months of Treatment
- In the 18-month core study of Clarity AD, there was a
statistically significant difference in global cognition and
function as measured by CDR-SB between the LEQEMBI and placebo
groups. The separation in CDR-SB between the group that continued
to receive LEQEMBI (early start group) and the group who switched
from placebo to LEQEMBI (delayed start group) was maintained during
the 6-month OLE following the core study. This indicates that
similar disease trajectory for both early and delayed start groups
occurred with LEQEMBI administration.1
- The blood biomarker results (plasma Aβ42/40 ratio, ptau181,
GFAP and NfL) showed improvement even after delayed initiation of
treatment with LEQEMBI.1 These results suggest that
LEQEMBI treatment may affect clinical outcomes through improvement
of AD pathology.1
4. The Mechanism-Based Rationale Of LEQEMBI
Treatment In Early AD
1) Dual-Acting
LEQEMBI3 Continues To Support Brain Neuron
Function3,4,5 By Removing Highly Toxic Proteins
(Protofibrils****)2,4 That Can Cause
Neuronal Injury And Death Even After Plaque Removal,5-8
Offering Patients The Opportunity For Continued
Benefit.
- LEQEMBI has a unique dual action1,3 that binds more
selectively to highly toxic protein (protofibrils****) in addition
to rapidly clearing plaque,7 and continues to support
neuronal function3,4 by removing protofibrils**** that
can cause neuronal injury and death after plaque has been
cleared.5-8
Eisai is hosting a live webcast of the scientific session
featuring the LEQEMBI presentations, which can be viewed on the
investors section of the Eisai Co., Ltd. website. The content will
be available on demand afterward.
Eisai serves as the lead of LEQEMBI development and regulatory
submissions globally with both Eisai and Biogen co-commercializing
and co-promoting the product and Eisai having final decision-making
authority.
This release discusses investigational uses of agents in
development and is not intended to convey conclusions about
efficacy or safety. There is no guarantee that such investigational
agents will successfully complete clinical development or gain
health authority approval.
*Phase III Clarity AD study is a placebo-controlled,
double-blind, parallel-group, randomized study to evaluate the
efficacy and safety of LEQEMBI 10 mg/kg bi-weekly for 18 months in
1,795 people living with early AD (core study). An OLE is being
conducted after the core study. SC dosing is currently being
evaluated in the Clarity AD OLE.
**Using the MK6240 tau PET probe, tau accumulation in the brain
was defined as low tau accumulation group (MK6240 cutoff value
<1.06, 141 subjects), intermediate accumulation group (MK6240
cutoff value between 1.06 and 2.91, 191 subjects), and high
accumulation group (MK6240 cutoff value >2.91, 10 subjects).
***Multiple endpoints: CDR-SB, a numeric scale used to quantify
the severity of symptoms of dementia; ADAS-Cog14, common cognitive
assessment instrument used in AD clinical trials all over the
world; and ADCS MCI-ADL, a scale to assess the parties' activities
of daily living.
****Protofibrils:
- One of the AD pathological features is the accumulation of
clusters (plaques) of amyloid beta (Aβ) in the brain. The formation
of these plaques is the result of a continuous process by which
individual Aβ proteins join together, latching onto each other, one
at a time, like adding links to a chain.9 In the early
part of this process these small chains of Aβ are soluble and are
toxic to the nerves within the brain.10,11
- The most toxic of the soluble chains is called a protofibril.
Protofibrils are believed to contribute to the brain injury that
occurs with AD and are considered to be the most toxic form of Aβ,
having a primary role in the cognitive decline associated with this
progressive, debilitating condition.4,11
- Protofibrils cause injury to neurons in the brain, which in
turn, can negatively impact cognitive function via multiple
mechanisms, not only increasing the development of insoluble Aβ
plaques but also increasing direct damage to brain cell membranes
and the connections that transmit signals between nerve cells or
nerve cells and other cells. It is believed the reduction of
protofibrils may prevent the progression of AD by reducing damage
to neurons in the brain and cognitive
dysfunction.12
INDICATION
LEQEMBI is indicated for the treatment of Alzheimer's disease.
Treatment with LEQEMBI should be initiated in patients with mild
cognitive impairment or mild dementia stage of disease, the
population in which treatment was initiated in clinical trials.
WARNING: AMYLOID
RELATED IMAGING ABNORMALITIES (ARIA)
- Monoclonal antibodies directed against
aggregated forms of amyloid beta, including LEQEMBI, can cause
amyloid related imaging abnormalities (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 usually asymptomatic,
although serious and life-threatening events rarely can occur.
Serious intracerebral hemorrhages >1 cm, some of which have been
fatal, have been observed in patients treated with this class of
medications.
- Apolipoprotein E ε4 (ApoE ε4)
Homozygotes: Patients who are ApoE ε4 homozygotes
(approximately 15% of Alzheimer's disease patients) treated with
this class of medications, including LEQEMBI, 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. Prior to
testing, 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 Alzheimer's disease and potential risk of serious
adverse events associated with ARIA 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. ARIA-E can be observed on
MRI as brain edema or sulcal effusions, and ARIA-H as
microhemorrhage and superficial siderosis. ARIA can occur
spontaneously in patients with Alzheimer's disease. ARIA-H
associated with monoclonal antibodies directed against aggregated
forms of beta amyloid generally occurs in association with an
occurrence of ARIA-E. ARIA-H and ARIA-E can occur together. ARIA
usually occurs early in treatment and is usually asymptomatic,
although serious and life-threatening events, including seizure and
status epilepticus, rarely can occur. Reported symptoms associated
with ARIA may include headache, confusion, visual changes,
dizziness, nausea, and gait difficulty. Focal neurologic deficits
may also occur. Symptoms associated with ARIA usually resolve over
time.
ARIA Monitoring and Dose Management Guidelines
- Obtain recent baseline brain magnetic resonance imaging (MRI)
prior to initiating treatment with LEQEMBI. Obtain an MRI prior to
the 5th, 7th and 14th infusions.
- Recommendations for dosing in patients with ARIA-E and ARIA-H
depend on clinical symptoms and radiographic severity. Depending on
ARIA severity, use clinical judgment in considering whether to
continue dosing, temporarily discontinue treatment, or permanently
discontinue LEQEMBI.
- Enhanced clinical vigilance for ARIA is recommended during the
first 14 weeks of treatment with LEQEMBI. If a patient experiences
symptoms suggestive of ARIA, 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.
- There is no experience in patients who continued dosing through
symptomatic ARIA-E or through asymptomatic, but radiographically
severe, ARIA-E. There is limited experience in patients who
continued dosing through asymptomatic but radiographically mild to
moderate ARIA-E. There are limited data in dosing patients who
experienced recurrent ARIA-E.
Incidence of ARIA
- In Study 2, symptomatic ARIA occurred in 3% (29/898) of
LEQEMBI-treated patients. Serious symptoms associated with ARIA
were reported in 0.7% (6/898) of patients treated with LEQEMBI.
Clinical symptoms associated with ARIA resolved in 79% (23/29) of
patients during the period of observation.
- Including asymptomatic radiographic events, ARIA was observed
in LEQEMBI: 21% (191/898); placebo: 9% (84/897). ARIA-E was
observed in LEQEMBI: 13% (113/898); placebo: 2% (15/897). ARIA-H
was observed in LEQEMBI: 17% (152/898); placebo: 9% (80/897). There
was no increase in isolated ARIA-H for LEQEMBI vs placebo.
ApoE ε4 Carrier Status and Risk of ARIA
- In Study 2, 16% (141/898) of patients in the LEQEMBI arm were
ApoE ε4 homozygotes, 53% (479/898) were heterozygotes, and 31%
(278/898) were noncarriers.
- 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%). Among
patients treated with LEQEMBI, symptomatic ARIA-E occurred in 9% of
ApoE ε4 homozygotes compared with 2% of heterozygotes and 1%
noncarriers. Serious events of ARIA occurred in 3% of ApoE ε4
homozygotes, and approximately 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 early
in treatment (within the first 7 doses), although ARIA can occur at
any time and patients can have more than 1 episode. The maximum
radiographic severity of ARIA-E in patients treated with LEQEMBI
was mild in 4% (37/898), moderate in 7% (66/898), and severe in 1%
(9/898). Resolution on MRI occurred in 52% of ARIA-E patients by 12
weeks, 81% by 17 weeks, and 100% overall after detection. The
maximum radiographic severity of ARIA-H microhemorrhage in
LEQEMBI-treated patients 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). Among LEQEMBI-treated patients, the rate of
severe radiographic ARIA-E was highest in ApoE ε4 homozygotes 5%
(7/141), compared to heterozygotes 0.4% (2/479) or noncarriers 0%
(0/278). Among LEQEMBI-treated patients, the rate of severe
radiographic ARIA-H was highest in ApoE ε4 homozygotes 13.5%
(19/141), compared to 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) of patients in Study 2 after treatment with LEQEMBI
compared to 0.1% (1/897) on placebo. Fatal events of intracerebral
hemorrhage in patients taking LEQEMBI have been reported.
Concomitant Antithrombotic Medication:
- In Study 2, 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 patients) in patients
taking LEQEMBI with a concomitant antithrombotic medication at the
time of the event compared to 0.6% (3/545 patients) 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
patients) compared to none in patients who received placebo.
- Because intracerebral hemorrhages >1 cm in diameter have
been observed in patients taking LEQEMBI, additional 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 Study 2 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) that
could potentially increase the risk of intracerebral hemorrhage.
The presence of an ApoE ε4 allele is also associated with cerebral
amyloid angiopathy, which has an increased risk for intracerebral
hemorrhage. Caution should be exercised when considering the use of
LEQEMBI in patients with factors that indicate an increased risk
for intracerebral hemorrhage and in particular for patients who
need to be on anticoagulant therapy.
Hypersensitivity Reactions
Hypersensitivity reactions, including angioedema, bronchospasm,
and anaphylaxis, have occurred in LEQEMBI-treated patients.
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
- In Study 2, infusion-related reactions were observed
in LEQEMBI: 26% (237/898); placebo: 7% (66/897), and the
majority of cases in LEQEMBI-treated patients (75%, 178/237)
occurred with the first infusion. Infusion-related reactions were
mostly mild (69%) or moderate (28%) in severity. Infusion-related
reactions resulted in discontinuations in 1% (12/898) of
LEQEMBI-treated patients. Symptoms of infusion-related reactions
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 infusion-related reaction, the infusion rate
may be reduced, or the infusion may be discontinued, and
appropriate therapy initiated as clinically indicated. Prophylactic
treatment with antihistamines, acetaminophen, nonsteroidal
anti-inflammatory drugs, or corticosteroids prior to future
infusions may be considered.
ADVERSE REACTIONS
- In Study 2, the most common adverse reactions leading to
discontinuation of LEQEMBI was ARIA-H microhemorrhages that
led to discontinuation in 2% (15/898) of patients treated with
LEQEMBI compared to <1% (1/897) of patients on placebo.
- In Study 2, the most common adverse reactions reported in ≥5%
of patients treated with LEQEMBI (N=898) and ≥2% higher than
placebo (N=897) were infusion-related reactions (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%).
Please see full Prescribing Information for
LEQEMBI, including Boxed WARNING.
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 Lecanemab (generic name, U.S. brand
name: LEQEMBI®),
Lecanemab is the result of a strategic research alliance between
Eisai and BioArctic. Lecanemab is a humanized immunoglobulin gamma
1 (IgG1) monoclonal antibody directed against aggregated soluble
(protofibril) and insoluble forms of amyloid-beta (Aβ). In the
U.S., LEQEMBI was granted traditional approval by the U.S. Food and
Drug Administration (FDA) on July 6,
2023. LEQEMBI is an amyloid beta-directed antibody indicated
as a disease-modifying treatment for Alzheimer's disease (AD) in
the U.S. 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. There are no safety or effectiveness data on
initiating treatment at earlier or later stages of the disease than
were studied. In Japan, Eisai
received approval from the Ministry of Health, Labour and Welfare
(MHLW) on September 25, 2023 to
manufacture and market of lecanemab as a treatment for slowing
progression of MCI and mild dementia due to AD.
Please see full U.S. Prescribing Information for LEQEMBI,
including Boxed WARNING.
Eisai has also submitted applications for approval of lecanemab
in EU, China, Canada, Great
Britain, Australia,
Switzerland, South Korea and Israel. In China and Israel, the applications have been designated
for priority review, and in Great
Britain, lecanemab has been designated for the Innovative
Licensing and Access Pathway (ILAP), which aims to reduce the time
to market for innovative medicines.
Eisai has completed a lecanemab subcutaneous bioavailability
study, and subcutaneous dosing is still being evaluated in the
Clarity AD (Study 301) open-label extension (OLE). A maintenance
dosing regimen has been evaluated as part of Study 201.
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 AD
Eisai and Biogen have been collaborating on the joint
development and commercialization of AD treatments since 2014.
Eisai serves as the lead of LEQEMBI development and regulatory
submissions globally with both companies co-commercializing and
co-promoting the product and Eisai having final decision-making
authority.
3. About the Collaboration between Eisai and
BioArctic for AD
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 LEQEMBI for the treatment of AD pursuant to
an agreement with BioArctic in December
2007. The development and commercialization agreement on the
antibody LEQEMBI 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.), and connect with us on
X, LinkedIn and Facebook.
5. About Biogen
Founded in 1978, Biogen is a leading global biotechnology
company that has pioneered multiple breakthrough innovations
including a broad portfolio of medicines to treat multiple
sclerosis, the first approved treatment for spinal muscular
atrophy, and two co-developed treatments to address a defining
pathology of Alzheimer's disease. Biogen is advancing a pipeline of
potential novel therapies across neurology, neuropsychiatry,
specialized immunology and rare diseases and remains acutely
focused on its purpose of serving humanity through science while
advancing a healthier, more sustainable and equitable world.
The company routinely posts information that may be important to
investors on its website at www.biogen.com. Follow Biogen on
social media – X, LinkedIn, Facebook, YouTube.
Biogen Safe Harbor
This news release contains forward-looking statements about the
potential clinical effects of LEQEMBI; the potential benefits,
safety and efficacy of LEQEMBI; 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
LEQEMBI; 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, including the Clarity AD clinical trial,
AHEAD 3-45 study and SC substudy; 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 LEQEMBI; actual timing and content of
submissions to and decisions made by the regulatory authorities
regarding LEQEMBI; uncertainty of success in the development and
potential commercialization of LEQEMBI; 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; third party collaboration
risks; and the direct and indirect impacts of the ongoing COVID-19
pandemic on Biogen's business, 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
- van Dyck, C., Irizarry, M., Johnson, K., & Sperling,
R. (2023, October 24-27). Lecanemab
for Early Alzheimer's Disease: Long-Term Outcomes, Predictive
Biomarkers and Novel Subcutaneous Administration [Conference
Presentation]. Clinical Trials on Alzheimer's Disease Conference,
Boston, MA, United States.
- Hampel, H., Hardy, J., Blennow, K. et al. The Amyloid-β Pathway
in Alzheimer's Disease. Mol Psychiatry. 2021;26:5481–5503.
https://doi.org/10.1038/s41380-021-01249-0.
- LEQEMBI US Prescribing Information.
- van Dyck CH, Swanson CJ, Aisen P, et al. Lecanemab in
early Alzheimer's disease. N Engl J Med.
2023;388(1):9-21.
- Brendza RP, et al. Anti-Aβ antibody treatment promotes the
rapid recovery of amyloid-associated neuritic dystrophy in PDAPP
transgenic mice J Clin Invest. 2005;115(2):428-433.
https://doi.org/10.1172/JCI23269.
- Ono K, Tsuji M. Protofibrils of Amyloid-β are Important
Targets of a Disease-Modifying Approach for Alzheimer's Disease.
Int J Mol Sci. 2020;21(3):952. Doi: 10.3390/ijms21030952.
PMID: 32023927; PMCID: PMC7037706.
- Söderberg L, et al. Lecanemab, Aducanumab, and Gantenerumab —
Binding Profiles to Different Forms of Amyloid–Beta Might Explain
Efficacy and Side Effects in Clinical Trials for Alzheimer's
Disease. Neurotherapeutics (2023) 20:195–206
https://doi.org/10.1007/s13311-022-01308-6 Accessed October 12, 2023.
- Hartley DM, Walsh DM, Ye CP, Diehl T, Vasquez S, Vassilev PM,
Teplow DB, Selkoe DJ. Protofibrillar intermediates of amyloid
beta-protein induce acute electrophysiological changes and
progressive neurotoxicity in cortical neurons. J Neurosci.
1999;19(20):8876-84. doi: 10.1523/JNEUROSCI.19-20-08876.1999. PMID:
10516307; PMCID: PMC6782787.
- Alzheimer's Association. (2022). Brain Tour Part 2 -
Alzheimer's Effect. Retrieved September 27,
2023, from
https://www.alz.org/alzheimers-dementia/what-is-alzheimers/brain_tour_part_2.
- Chen, Gf., Xu, Th., Yan, Y. et al. Amyloid beta:
structure, biology and structure-based therapeutic development.
Acta Pharmacol. 2017;38:1205.
https://doi.org/10.1038/aps.2017.28.
- Habashi M., Vulta S., Tripathi K., et al. Early diagnosis and
treatment of Alzheimer's disease by targeting toxic soluble Aβ
oligomers. Biophysics and Computational Biology.
2022;10.1073.
https://www.pnas.org/doi/epdf/10.1073/pnas.2210766119.
- Amin L, Harris DA. Aβ receptors specifically recognize
molecular features displayed by fibril ends and neurotoxic
oligomers. Nat Commun.
2021;12:3451. doi:10.1038/s41467-021-23507-z.
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