Skip To Main Content
Lilly
Menu closed
Lilly
  • Account Login / Register
  • Medical Home
    • Medical Information
  • Medical Education
  • Science
Ask Lilly

We're here to help.

Chat
Chat with us
Question Contact Us
Expand contact lilly
Lilly

You are now leaving the Lilly Medical website

The link you clicked on will take you to a site maintained by a third party, which is solely responsible for its content. Lilly USA, LLC does not control, influence, or endorse this site, and the opinions, claims, or comments expressed on this site should not be attributed to Lilly USA, LLC. Lilly USA, LLC is not responsible for the privacy policy of any third-party websites. We encourage you to read the privacy policy of every website you visit.
Click "Continue" to proceed or "Return" to return to Lilly Medical

  1. Medical Information Right
  2. Neuroscience Right
  3. Kisunla (donanemab-azbt) injection, for intravenous infusion Right
  4. What is the efficacy of Kisunla® (donanemab-azbt) in the treatment of early symptomatic Alzheimer’s disease?
Search Kisunla™ (type in keywords)
Search Medical Information

If you wish to report an adverse event or product complaint, please call 1-800-LILLYRX (1-800-545-5979)

Loading icon

Kisunla ™ (donanemab-azbt) injection, for intravenous infusion

350 mg/20 mL (17.5 mg/mL)

Full Prescribing Information

This information is provided in response to your request. Resources may contain information about doses, uses, formulations and populations different from product labeling. See Prescribing Information above, if applicable.

What is the efficacy of Kisunla® (donanemab-azbt) in the treatment of early symptomatic Alzheimer’s disease?

At week 76 of TRAILBLAZER-ALZ 2, donanemab slowed clinical progression by 22.3% (iADRS) and reduced amyloid in 76% of participants (<24.1 CL). In the LTE, early start group had 27% reduction in risk of progression at 3 years versus delayed start group.

US_cFAQ_DON001A_EFFICACY_ESAD_OFF
US_cFAQ_DON001A_EFFICACY_ESAD_OFFen-US

See important safety information, including boxed warning, in the attached prescribing information.

Content Overview

TRAIBLAZER-ALZ 2 Trial: Efficacy Results at 76 weeks

  • Study Design and Participants
  • Primary and Secondary Clinical Outcomes
  • Key Biomarker Outcomes
  • Exploratory Outcomes: Time prolonged in current disease state

TRAILBLAZER_ALZ 2 Long Term Extension: Efficacy Results up to 3 Years

References

Appendix

TRAIBLAZER-ALZ 2 Trial: Efficacy Results at 76 weeks

The Appendix provides a description of the donanemab phase 3 clinical studies.

Study Design and Participants

The safety and efficacy of donanemab were evaluated in TRAILBLAZER-ALZ 2, a phase 3, placebo-controlled 76-week study. This study enrolled adults aged 60 to 85 years with early symptomatic Alzheimer's disease (AD), defined as

  • prodromal AD, the symptomatic phase of AD in which mild cognitive impairment is apparent, or
  • AD with mild dementia, in which symptoms are sufficiently severe to meet diagnostic criteria for dementia.1

Eligible participants had

  • a Mini-Mental State Examination (MMSE) score of 20 to 28 (scores range from 0 to 30, with higher scores indicating better mental performance), and 
  • presence of amyloid pathology assessed by amyloid positron emission tomography (PET) imaging (≥37 centiloids [CL]) with either florbetapir F 18 or florbetaben F 18, and tau pathology assessed by flortaucipir F 18 PET imaging.1

Tau PET scans were interpreted by visual and quantitative reads and categorized as

  • low/medium or
  • high tau.1

The Appendix provides a description of the study populations by tau PET level at baseline.

Participants were randomized at the beginning of double-blind treatment in a 1:1 ratio to receive intravenous infusions every 4 weeks of either

  • donanemab 700 mg for the first 3 doses and 1400 mg thereafter (n=860), or
  • placebo (n=876; administered as saline).1,2

Completion of active treatment in the clinical trial was guided by amyloid PET levels measured at week 24 and week 52. Participants were eligible to be switched to placebo if the amyloid plaque level was 

  • <11 CL on a single PET scan, or
  • 11 to <25 CL on 2 consecutive PET scans.1

Primary and Secondary Clinical Outcomes

Donanemab-treated participants had amyloid plaque clearance as early as week 24 in both the combined and low/medium tau populations (Percentage of Donanemab-Treated Participants With Amyloid Plaque Reduction in TRAILBLAZER-ALZ 2).1,3

Worsening scores on the iADRS have been significantly associated with decreased patient quality of life, as well as increased burden on caregivers and society.4 The iADRS is an integrated score ranging from 0 to 144, and includes the

  • Alzheimer’s Disease Assessment Scale-Cognitive Subscale 13-item version (ADAS-Cog13), range 0-85, with higher scores correlating to greater global cognition deficit, and
  • Alzheimer’s Disease Cooperative Study-Instrumental Activities of Daily Living (ADCS-iADL), range 0 to 59, with lower scores correlating to greater deficit in daily function.5

To align the scales, the ADAS-Cog13 score is multiplied by -1, so that lower iADRS overall score correlates to greater impairment.5

The baseline iADRS score was similar between donanemab and placebo (approximately 104 in the combined population and approximately 106 in the low/medium tau population, on scale of 0 to 144). TRAILBLAZER-ALZ 2 Clinical Outcomes at Week 76  shows that compared with placebo, the donanemab cohort had a slowing of clinical progression at week 76 as evidenced by iADRS scores in the

  • combined population (22.3%, p<.001), and
  • low/medium tau population (35.1%, p<.001).1

Secondary clinical outcome measures included change from baseline through week 76 in either the combined or low/medium tau population as measured by the

  • Clinical Dementia Rating scale sum of boxes (CDR-SB)
  • ADAS-Cog13 score
  • ADCS-iADL score, and
  • MMSE score.1

Participants in the donanemab cohort experienced statistically significantly less decline on these measures at week 76 compared with placebo, in both the combined and low/medium tau populations (TRAILBLAZER-ALZ 2 Clinical Outcomes at Week 76 ).1

TRAILBLAZER-ALZ 2 Clinical Outcomes at Week 761,3 

Clinical Endpointsa

Combined Population

Low/Medium Tau

Donanemab
(N=860)

Placebo
(N=876)

Donanemab
(N=588)

Placebo
(N=594)

iADRSb,c

Mean baseline

104.55

103.82

105.92

105.95

Change from baseline

-10.19

-13.11

-6.02

-9.27

Difference from placebo (%)

2.92 (22)d

NA

3.25 (35)d

NA

CDR-SBe,c

Mean baseline

3.92

3.89

3.72

3.64

Change from baseline

1.72

2.42

1.20

1.88

Difference from placebo (%)

-0.70 (29)d

NA

-0.67 (36)d

NA

ADAS-Cog13b,c

Mean baseline

28.53

29.16

27.41

27.60

Change from baseline

5.46

6.79

3.17

4.69

Difference from placebo (%)

-1.33 (20)d

NA

-1.52 (32)d

NA

ADCS-iADLb,c

Mean baseline

47.96

47.98

48.20

48.56

Change from baseline

-4.42

-6.13

-2.76

-4.59

Difference from placebo (%)

1.70 (28)d

NA

1.83 (40)d

NA

MMSEb

Mean baseline

22.52

22.20

23.11

22.88

Change from baseline

-2.47

-2.94

-1.61

-2.09

Difference from placebo (%)

0.47 (16)f

NA

0.48 (23)g

NA

Abbreviations: ADAS-Cog13 = Alzheimer’s Disease Assessment Scale – 13-item Cognitive Subscale; ADCS-iADL = Alzheimer’s Disease Cooperative Study – instrumental Activities of Daily Living subscale; CDR-SB = Clinical Dementia Rating Scale – Sum of Boxes; iADRS = integrated Alzheimer’s Disease Rating Scale; NCS2 = natural cubic spline with 2 degrees of freedom; MMRM = mixed model for repeated measures; MMSE = Mini-Mental State Examination; NA = not applicable.

aClinical outcomes were scored as follows: iADRS range from 0 to 144, with lower scores indicating greater impairment; CDR-SB scores range from 0 to 18, with higher scores indicating greater impairment; ADAS-Cog13 scores range from 0 to 85, with higher scores indicating a greater deficit; ADCS-iADL scores range from 0 to 59, with lower scores indicating greater impairment; MMSE scores range from 0 to 30, with lower scores indicating greater impairment.

bAssessed using NCS2 analysis.

cGated outcome.

dp<.001 vs placebo.

eAssessed using MMRM analysis.

fp=.01 vs placebo.

gp=.02 vs placebo.

Key Biomarker Outcomes

Secondary biomarker outcome measures included

  • percentage of participants with amyloid reduction to minimal levels (ie, <24.1 CL on amyloid PET) at 24 and 76 weeks, and
  • change from baseline in amyloid plaque levels at 76 weeks.1

Donanemab-treated participants met eligibility to switch to placebo1,6 and had amyloid reduction to minimal levels1 as early as week 24 in both the combined and low/medium tau populations (Percentage of Donanemab-Treated Participants With Amyloid Plaque Reduction in TRAILBLAZER-ALZ 2). In contrast, ≤0.3% of participants receiving placebo had amyloid reduction to minimal levels at all time points assessed (p<.0001 vs donanemab).1

Percentage of Donanemab-Treated Participants With Amyloid Plaque Reduction in TRAILBLAZER-ALZ 21,6

 

Combined Population, % (n/N)

Low/Medium Tau Population, % (n/N)

Week 24

Week 52

Week 76

Week 24

Week 52

Week 76

Eligible for switch to placeboa,b

17
(130/761)

47
(313/672)

69
(429/620)

20
(106/521) 

52
(241/464) 

 74
(321/437)

Amyloid plaque reduction to minimal levelsc

30
(226/761)

66
(443/670)

76
(469/614)

34
(178/521)

71
(330/463)

80
(347/433)

Abbreviations: CL = centiloids; PET = positron emission tomography.

aEligibility criteria: amyloid plaque level of <11 CL on any single amyloid PET scan or 11 to <25 CL on 2 consecutive scans.

bIncluded participants from unscheduled visits at each time point.

cDefined as <24.1 CL on amyloid PET scan, consistent with a negative visual read.

As shown in Change From Baseline in Amyloid Plaque Levels at Week 76 in TRAILBLAZER-ALZ 2, donanemab-treated participants had statistically significantly greater amyloid plaque reduction from baseline compared with placebo-treated participants as assessed by amyloid PET measurement in the

  • combined population (-87 CL), and
  • low/medium tau population (-88 CL).1

Placebo-treated participants had a change of -0.7 CL in the combined population and 0.2 CL in the low/medium tau population at week 76.1

Change From Baselinea in Amyloid Plaque Levels at Week 76 in TRAILBLAZER-ALZ 21,3,6

 

Combined Population

Low/Medium Tau

Donanemab
(N=765)

Placebo
(N=812)

Donanemab
(N=525)

Placebo
(N=556)

Amyloid beta PET centiloid

Mean baseline

104.0

101.8

103.0

100.9

Change from baseline (%)

-87.0 (-83.7)

-0.7

-88.0 (-85.5)

0.2

Difference from placebo

-86.4b

NA

-88.2b

NA

Abbreviations: MMRM = mixed model for repeated measures; NA = not applicable; PET = positron emission tomography.

aChange from baseline derived using MMRM methodology with fixed factors for treatment, visit, treatment-by-visit interaction, and covariates for baseline score, baseline score-by-visit interaction, baseline tau category, and age at baseline.

bp<.0001 vs placebo.

The treatment effect of donanemab on changes in plasma phosphorylated-tau 217 (P-tau217) at week 76 was also evaluated as an exploratory outcome.1

A reduction in plasma P-tau217 was observed with donanemab compared to placebo in the combined and low/medium tau populations (Change From Baseline in Plasma P-tau217 at Week 76 in TRAILBLAZER-ALZ 2).1,3

Change From Baselinea in Plasma P-tau217 at Week 76 in TRAILBLAZER-ALZ 21,3,6

 

Combined Population

Low/Medium Tau

Donanemab
(N=758)

Placebo
(N=786)

Donanemab
(N=522)

Placebo
(N=537)

Mean baseline

0.67

0.66

0.62

0.59

Change from baseline (% of original value)

-0.19 (-35.0)

0.03

-0.22 (-39.0)

0.04

Difference from placebo

-0.22b

NA

-0.25b

NA

Abbreviations: MMRM = mixed model for repeated measures; NA = not applicable; P-tau217 = tau phosphorylated at threonine 217.

aChange from baseline and p-value are derived using MMRM methodology with fixed factors for treatment, visit, treatment-by-visit interaction, and covariates for baseline score, baseline score-by-visit interaction, and age at baseline.

bp<.0001 vs placebo.

Back to ⇒ Content Overview

Exploratory Outcomes: Time prolonged in current disease state

The TRAILBLAZER-ALZ 2 study evaluated the efficacy of donanemab to prolong time in the current disease state for participants as exploratory outcomes by assessing the

  • delay in clinical progression on the iADRS and CDR-SB (ie, months saved with treatment)
  • risk of progression to a later stage using CDR-Global (CDR-G), and
  • probability of remaining stable at 1 year on the CDR-SB (ie, nonprogressing).1

Donanemab-treated participants experienced statistically significantly less disease progression compared with placebo in all the time-based efficacy analyses.1

Assessing Delay in Clinical Progression

The delay in clinical progression due to donanemab treatment as assessed by the iADRS and CDR-SB was estimated using a time-progression model for repeated measures (PMRM).1,6

As summarized in Delayed Disease Progression at 76 Weeks in TRAILBLAZER-ALZ 2, donanemab treatment statistically significantly delayed disease progression at week 76 compared with placebo as measured by the iADRS and CDR-SB in the

  • combined population, and
  • low/medium tau population.1
Delayed Disease Progression at 76 Weeks in TRAILBLAZER-ALZ 21,6

 

iADRSab

CDR-SBac

Combined populationd

Months saved vs placebo

2.5

5.4

Percent time savings

14.1

31

P value vs placebo

<.001

<.001

Low/medium tau population

Months saved vs placebo

4.4b

7.5

Percent time savings

24.9

42.9

P value vs placebo

<.001

<.001

Abbreviations: CDR-SB = Clinical Dementia Scale - Sum of Boxes; iADRS = Integrated Alzheimer's Disease Rating Scale. 

aiADRS scores range from 0 to 144, with lower scores indicating greater impairment, and CDR-SB scores range from 0 to 18, with higher sores indicating greater clinical impairment.

bThe model did not assume proportional time slowing. Results from the prespecified test of proportional time slowing assumption at 76 weeks was 2.6 months saved, p=.002, but the proportional time slowing assumption was not met for the iADRS (p=.001 from a likelihood ratio test).

cThe model assumed proportional time slowing.

dNot prespecified as gated in the statistical analysis plan.

Risk of Disease Progression

A clinical worsening event was defined as meeting a CDR-G score increase from baseline at 2 consecutive visits. A Cox proportional hazard model was fit to estimate the hazard ratio of progressing to clinical worsening between treatment groups.6

Donanemab-treated participants had a lower risk of disease progression to the next stage through week 76 compared with placebo as measured by the CDR-G scale in the

  • combined population (-37%, p<.0001 vs placebo), and
  • low/medium tau population (-39%, p<.001 vs placebo).1,3

Probability of Remaining Stable at 1 Year (Nonprogressing)

To evaluate the probability of remaining stable, participants' status was classified as "nonprogressing" if their CDR-SB change from baseline was ≤0 at each of the scheduled visits.6

At Week 52, a statistically significantly greater proportion of donanemab-treated participants were non-progressing compared with placebo, in the 

  • combined population, and
  • low/medium tau population (No Progression at 52 Weeks as Measured by CDR-SB in TRAILBLAZER-ALZ 2 ).1
No Progressiona at 52 Weeks as Measured by CDR-SBb in TRAILBLAZER-ALZ 21 

 

Donanemab

Placebo

Combined populationc

Estimated percent with no progression

36%

23%

P value vs placebo

<.001

NA

Low/medium tau population

Estimated percent with no progression

47%

29%

P value vs placebo

<.00001

NA

Abbreviations: CDR-SB = Clinical Dementia Rating Scale - Sum of Boxes; NA = not applicable.

aNo progression was defined as a CDR-SB score change from baseline of ≤0.

bCDR-SB scores range from 0 to 18, with higher scores indicating greater clinical impairment.

cNot specified as gated in the statistical analysis plan.

Back to ⇒ Content Overview

TRAILBLAZER_ALZ 2 Long Term Extension: Efficacy Results up to 3 Years

Participants who completed the placebo-controlled period of the TRAILBLAZER-ALZ 2 study were eligible to enter a 78-week double-blind long-term extension. Early start participants were those initially randomized to donanemab in the placebo-controlled period. Delayed start participants were those initially randomized to placebo in the placebo-controlled period and started donanemab in the long-term extension. Participants from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) were selected as external control.7

Clinical Efficacy

In the long-term extension, early start treatment

  • slowed disease progression with a difference in the CDR-SB of -1.2 (95% CI: -1.7, -0.7), and
  • saved approximately 6.9 months as measured by the CDR-SB versus the weighted ADNI control group at 3 years.7

Early start participants who met treatment course completion by 52 weeks of the placebo-controlled period showed a difference on the CDR-SB of -1.3 (95% CI: -1.9, -0.7) versus the ADNI group at 3 years.7

Delayed start participants had more advanced disease and also benefited from donanemab treatment with a difference on the CDR-SB of -0.8 (95% CI: -1.3, -0.3) vs the weighted ADNI group at 1.5 years of treatment.7

On the CDR-G score, treatment with donanemab

  • showed a 27% reduction in risk of progression to the next stage of disease in the early start donanemab group compared with the delayed start donanemab group, and
  • demonstrated disease modification by continued treatment differences between the early and delayed start groups.7

Biomarkers

In the long-term extension, after 1.5 years from initiation of treatment (154 weeks) delayed start participants experienced similar amyloid reduction (approximately 86 CL) compared to early start participants at 76 weeks.7

A subset of participants who achieved amyloid clearance (<24.1 CL) in the long-term extension period also met the study treatment course completion criteria, defined as an amyloid plaque level of <11 CL on any single PET scan or <25 CL on two consecutive PET scans.7

For delayed-start participants with amyloid PET scans who were randomized to placebo during the 76-week placebo-controlled period and received donanemab in the long-term extension

  • 17.6 % (105/595) met treatment course completion criteria at 102 weeks (24 weeks after starting donanemab),
  • 51.3 % (267/520) at 130 weeks (52 weeks after starting donanemab), and
  • 70.7 % (319/451) at 154 weeks (76 weeks after starting donanemab).7

In participants who met the treatment course completion criteria by week 52 of the placebo-controlled period, the mean amyloid levels remained below 24.1 CL at 3 years.7

Among the subset of patients who met treatment course completion at week 52 of the placebo-controlled period (n=126), 82% had amyloid levels below 24.1 CL at 3 years.6  

Of participants initially randomized to donanemab in the placebo-controlled period, 85% met criteria to complete the course of donanemab therapy based on amyloid PET criteria within 3 years.6

Enclosed Prescribing Information

KISUNLA® (donanemab-azbt) injection, for intravenous use, Lilly

References

The published references below are available by contacting 1-800-LillyRx (1-800-545-5979).

1Sims JR, Zimmer JA, Evans CD, et al; TRAILBLAZER-ALZ 2 Investigators. Donanemab in early symptomatic Alzheimer disease: the TRAILBLAZER-ALZ 2 randomized clinical trial. JAMA. 2023;330(6):512-527. https://doi.org/10.1001/jama.2023.13239

2Solomon PR. TRAILBLAZER-ALZ 2: clinical background and study design. Abstract presented at: Alzheimer's Association International Conference (AAIC); July 16-20, 2023; Amsterdam, Netherlands.

3Kisunla [package insert]. Indianapolis, IN: Eli Lilly and Company; 2025.

4Wessels AM, Belger M, Johnston JA, et al. Demonstration of clinical meaningfulness of the Integrated Alzheimer’s Disease Rating Scale (iADRS): association between change in iADRS scores and patient and caregiver health outcomes. Alzheimers Dis. 2022;88(2):577-588. https://doi.org/10.3233/JAD-220303

5Wessels AM, Rentz DM, Case M, et al. Integrated Alzheimer's Disease Rating Scale: clinically meaningful change estimates. Alzheimer's Dement. 2022;8(1):e12312. https://doi.org/10.1002/trc2.12312

6Data on file, Eli Lilly and Company and/or one of its subsidiaries.

7Zimmer JA, Sims JR, Evans CD, et al; Alzheimer’s Disease Neuroimaging Initiative. Donanemab in early symptomatic Alzheimer's disease: results from the TRAILBLAZER-ALZ 2 long-term extension. J Prev Alzheimers Dis. 2026;13(2):100446. https://doi.org/10.1016/j.tjpad.2025.100446

8Wang H, Nery ESM, Ardayfio P, et al. The effect of modified donanemab titration on amyloid-related imaging abnormalities with edema/effusions and amyloid reduction: 18-month results from TRAILBLAZER-ALZ 6. J Prev Alzheimers Dis. 2025;21(8):100266. https://doi.org/10.1016/j.tjpad.2025.100266

Appendix

Donanemab Phase 3 Clinical Studies

The effectiveness of donanemab for the treatment of Alzheimer’s disease was established by TRAILBLAZER-ALZ 2,1 which assessed a dosing regimen of 700 mg every 4 weeks for the first 3 doses, and then 1,400 mg every 4 weeks (referred to as standard dosing in TRAILBLAZER-ALZ 6). The TRAILBLAZER-ALZ 6 study8 was conducted to assess different titration regimens, including the modified dosing regimen (ie, currently approved dosing of every 4 weeks with 350 mg the first infusion, 700 mg the second infusion, 1,050 mg the third infusion, and then 1,400 mg thereafter). The currently approved dose demonstrated

  • comparable pharmacodynamic effects on amyloid plaque reduction, and 
  • a reduced incidence of amyloid-related imaging abnormalities compared to the standard dosing regimen.3,8

Definitions of Populations by Baseline Tau PET Levels

Populations by Baseline Flortaucipir F 18 Tau PET Levels1

Population Analyzed

Description

Low/medium tau

Population including participants with baseline

  • SUVr ≤1.46 and a topographic deposition pattern consistent with advanced AD neuropathology, or
  • 1.10 ≤ SUVr ≤1.46 and a topographic deposition pattern consistent with moderate AD neuropathology.

High tau

Population including participants with baseline SUVr >1.46 and a topographic deposition pattern consistent with either moderate or advanced AD neuropathology.

Overall population

Population including participants with both low/medium tau and high tau levels.

Abbreviations: AD = Alzheimer's disease; PET = positron emission tomography; SUVr = standard uptake value ratio. 

Back to ⇒ Content Overview

Date of Last Review: January 16, 2026

Are you satisfied with this content?

Can't find what you're looking for? Contact us for answers to your medical questions.

  • Copyright
  • Terms of Use
  • Privacy Statement
  • Consumer Health Privacy Notice
  • Accessibility Statement
  • Sitemap

    This site is intended for US Healthcare Professionals only.

    4.0.53 05/2026 | GLOOTH00001 04/2015 | © Lilly USA, LLC 2026. All rights reserved.

    Product names listed above are trademarks or registered trademarks owned by or licensed to Eli Lilly and Company, its subsidiaries, or affiliates

    California Consumer Privacy Act (CCPA) Opt-Out Icon Your Privacy Choices
    Cookie Settings
    facebook twitter linkedin
    visit www.phactmi.org
    Lilly