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CURRENT REPORT
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Item 7.01 Regulation FD Disclosure.
On September 12, 2022, Acumen Pharmaceuticals, Inc. (the “Company”) posted an updated corporate presentation to its website at https://investors.acumenpharm.com/news-events/presentations, which the Company may use from time to time in communications or conferences. A copy of the corporate presentation is attached as Exhibit 99.1 to this Current Report on Form 8-K (this “Report”).
The information in this Report, including Exhibit 99.1 hereto, is furnished pursuant to Item 7.01 and shall not be deemed “filed” for purposes of Section 18 of the Securities Exchange Act of 1934, as amended (the “Exchange Act”), or otherwise subject to the liabilities of that Section, nor shall it be deemed incorporated by reference in any filing under the Securities Act of 1933, as amended, or the Exchange Act, except as expressly set forth by specific reference in such filing. The Company’s submission of this Report shall not be deemed an admission as to the materiality of any information required to be disclosed solely to satisfy the requirements of Regulation FD.
This Report and Exhibit 99.1 hereto contain forward-looking statements within the meaning of the federal securities laws. These forward-looking statements are based on current expectations and are not guarantees of future performance. Further, the forward-looking statements are subject to limitations listed in Exhibit 99.1 and in the other reports of the Company filed with the Securities and Exchange Commission, including that actual events or results may differ materially from those in the forward-looking statements.
Item 9.01 Financial Statements and Exhibits.
(d) Exhibits
| Exhibit No. |
Description | |
| 99.1 | Corporate Presentation, dated September 2022 | |
| 104 | Cover Page Interactive Data File (the cover page XBRL tags are embedded within the inline XBRL document) | |
SIGNATURES
Pursuant to the requirements of the Securities Exchange Act of 1934, as amended, the Registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.
| Acumen Pharmaceuticals, Inc. | ||||||
| Dated: September 12, 2022 | By: | /s/ Derek Meisner | ||||
| Derek Meisner | ||||||
| Chief Legal Officer and Corporate Secretary | ||||||
Exhibit 99.1 Corporate Overview September 2022 1
Forward-Looking Statements This presentation contains forward-looking statements within the meaning of The Private Securities Litigation Reform Act of 1995. Any statement describing Acumen’s goals, expectations, financial or other projections, intentions or beliefs is a forward-looking statement and should be considered an at-risk statement. Words such as “believes,” “expects,” “anticipates,” “could,” “would,” “seeks,” “aims,” “plans,” “potential,” “will” and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Forward-looking statements include statements concerning Acumen’s business, Acumen’s ability to achieve its strategic and financial goals, including its projected use of cash, cash equivalents and marketable securities and the sufficiency of its cash resources, and the therapeutic potential of Acumen’s product candidate, ACU193, including its potential for improved safety and efficacy as compared to other monoclonal antibodies in development, as well as the expectations concerning the INTERCEPT-AD trial and Acumen’s planned Phase 2/3 clinical trial, including the expected timing of initiation, enrollment and reporting data, and risks and uncertainties relating to the progression and duration of the COVID-19 pandemic and responsive measures thereto and related effects on Acumen. These statements are based upon the current beliefs and expectations of Acumen management, and are subject to certain factors, risks and uncertainties, particularly those inherent in the process of discovering, developing and commercializing safe and effective human therapeutics. Such risks may be amplified by the impacts of the COVID-19 pandemic. These and other risks concerning Acumen’s programs are described in additional detail in Acumen’s filings with the Securities and Exchange Commission (“SEC”), including in Acumen’s10-Q for the quarter ended June 30, 2022, and future filings and reports by Acumen. Copies of these and other documents are available from Acumen. Additional information will be made available in other filings that Acumen makes from time to time with the SEC. These forward-looking statements speak only as of the date hereof, and Acumen expressly disclaims any obligation to update or revise any forward-looking statement, except as otherwise required by law, whether, as a result of new information, future events or otherwise. In this presentation, references to cash also include cash equivalents. 2
Advancing a Potential Best-/First-In-Class Antibody Product for Early Alzheimer’s disease (Early AD) $ ACU193: First, Alzheimer’s Experienced Phase 1 Clinical Scientific Strong Clinical-Stage Represents an Consensus Leadership Trial in Early AD Balance Sheet: Monoclonal Enormous Market Supports Comprised of Patients Ongoing ~$210M in cash Antibody (mAb) to Proof of Driven by High Amyloid-Beta Industry Leaders at 30-Jun-22 Selectively Target with AD Drug Mechanism Unmet Need and Oligomers (AβOs) July 2021 IPO AβOs and has Discovery, Target Engagement Recent Scientific as the Most toxic ~$184M Gross Promising Pre- and Regulatory form of Aβ and a Development, and Safety Data RA Capital Clinical Evidence Momentum Novel Target for Regulatory Topline Results Deep Track Supporting its Expected Effective AD Expertise from Eli Sands Capital Differentiation Lilly & Co. 1H 2023 Treatment PBM Capital We believe that Acumen has the organizational expertise and fiscal resources to advance ACU193 through 2025. 3
Acumen Business Strategy – 2022-2025 → Rapidly advance ACU193 through clinical development in patients with early AD; → Evaluate combination approaches to complement our core ACU193 monotherapy strategy; → Selectively explore potential of ACU193 for other diseases; → Expand our product portfolio by in-licensing and/or developing additional candidates and/or alternative formulations for or derivatives of ACU193; and → Optimize value of ACU193 and future drug candidates in major markets. 4
INTERCEPT-AD Trial Update – 3Q 2022 • INTERCEPT-AD: Phase 1 clinical trial of ACU193 in patients with early AD (RCT) → Topline results (Proof of Mechanism) following full database lock expected in 1H 2023 § Safety / ARIA-E § PK § Target engagement → Trial enrollment on-going at 15 active sites, 2 additional sites selected for potential activation → Strong cash position has provided us the ability to expand study footprint to support recruitment and complete follow-up period (Cohort 7 Day 168) prior to read out → Complete trial results anticipated for presentation at major Alzheimer’s meeting in 1H 2023 • Phase 2/3 ‘Ready’ Activities → Chronic GLP toxicity testing ongoing → New drug substance production process and drug product formulation being finalized → Developing Phase 2/3 study for ACU193; design and planning for FDA End of Phase 2 meeting 5
AD, Amyloid & Abeta Oligomers
Alzheimer’s Pathophysiology Build-up of amyloid-beta (Aβ) is believed to lead to neurodegeneration and dementia Previous and current anti-amyloid and related drug targets have attempted to intervene γ secretase Amyloid β (Aβ) Inhibitors Anti-monomer Aβ mAb Amyloid plaque Aβ monomers Anti-amyloid plaque mAb Aβ fibrils BACE inhibitors Aβ oligomers Anti-Aβ Symptomatic and oligomer mAb neuroprotective treatments Tau destabilization Tau directed treatments Data indicate that soluble amyloid β oligomers (AβOs) are the most toxic species and should be preferentially targeted for removal. 7
What is an Aβ Oligomer? AβOs may consist of 2 to >200 Aβ peptides. Figure 1. AβOs composed of 3 (a) and 18 (b) Aβ peptides are depicted below. (b) (a) ____________________ Sources: Kelley et al. J Chem Physics 2008. Quaternary structures of Aβ oligomers, protofibrils and fibrils Figure 2. Atomic force microscopy images of representative steps of amyloid aggregation: (A) oligomers; (B) protofibrils; (C) mature fibrils. Scan size 1.0 µm. Z range (A) 8.0 nm; (B) 15 nm; (C) 20 nm. ____________________ Source: Relini et al. Biomolecules 2014 . 8
Scientific Evidence Supports Anti-AβO Hypothesis Predominant forms of Aβ in AD: Aβ monomers (non-toxic), AβOs, Aβ fibrils, and amyloid plaques Aβ Oligomers Aβ monomers AβOs bind to neurons, impair synaptic function, contribute to Amyloid plaque impairment of memory and cognition, and plaques serve induce tau hyper phos- as a reservoir phosphorylation of Abeta and may induce toxicity due to Inflammatory Aβ fibrils responses microglial and astrocytic Growing understanding of disease mechanisms indicate that AβOs are the activation most toxic Aβ species and have the potential to be an ideal target for effective AD therapy ____________________ Sources: Adopted From: Selkoe, Hardy EMBO Molecular Medicine, 2016 Cline, Journal of Alzheimer’s Disease, 2018 The only approved antibody product for AD and three late stage products all preferentially target amyloid plaques with only limited effects on AβOs. Acumen’s drug candidate ACU193 targets AβOs. 9
ACU193 Positioning Relative to Late-stage and Approved Anti-Aβ/plaque mAbs crenezumab bapineuzumab* solanezumab IgG4, Ph3 stop, API 1H22 IgG1, Ph3, stop IgG1, Ph3 stop, A4, DIAN Aβ oligomers Aβ protofibrils ACU193 lecanemab donanemab* gantenerumab* aducanumab* IgG2m4, Ph1 IgG1 IgG1 IgG1 IgG1 AAP filed 2Q22 Ph2 positive Ph3 4Q22 Approved (AAP), Filing AAP 2Q22 CMS CED Ph3 3Q22 Ph3 1H23 commercial stop ACU193’s high selectivity for AβOs combined with an expected lack of ARIA-related safety concerns is anticipated to provide superior cognitive efficacy compared to anti-plaque mAbs • IgG1 monoclonal antibodies that bind amyloid plaque are associated with high rates of ARIA-E. See e.g., Plotkin, Neurobiology of Disease, 2020. • There have been no head-to-head clinical trials between any of the product candidates listed above. Study designs and protocols for each product candidate were different, and results may not be comparable between product candidates. 10
Positive Signals and Proof of Concept from Recent Phase 2-3 Anti-Amyloid mAb AD Studies Percent Slowing of Cognitive/Functional Decline* solanezumab aducanumab aducanumab lecanemab EXPEDITION 3 EMERGE ENGAGE BAN2401 donanemab Measured Outcome** (Phase 3) (Phase 3) (Phase 3) (Phase 2) (Phase 2) ADAS-cog -11% -27% -12% -47% -39% -15% -40% -18% N.A. -23% ADCS-ADL -15% -23% 2% -26% -23% CDR-SB MMSE -13% -15% 3% N.A. -21% -11% N.A. N.A. N.A. -32% iADRS * Percent Slowing = P[1- [(endpoint score-baseline score)active/(endpoint score-baseline score)placebo]]*100%*(-1) ** ADAS-cog: Alzheimer's Disease Assessment Scale – Cognitive Subscale ADCS-ADL: Alzheimer's Disease Cooperative Study – Activities of Daily Living CDR-SB: Clinical Dementia Rating – Sum of Boxes MMSE: Mini-Mental State Examination iADRS: Integrated Alzheimer's Disease Rating Scale Note: ENGAGE Post-Protocol Version 4 – at least 14 doses of 10 mg/kg, High Dose cohort achieved 27% improvement on CDR-SB compared to placebo We're looking for a biological foothold against Alzheimer's that we can build on. And so, these effects are small, but I think + they are meaningful, and I hope they're the beginning of a process that we can add to.” - Stephen Salloway, MD of Brown University ____________________ +Source: Wall Street Journal, Biogen Details Case for Controversial Alzheimer's Drug, published December 5, 2019. See e.g., Plotkin, Neurobiology of Disease, 2020. There have been no head-to-head clinical trials between any of the product candidates listed above. Study designs and protocols for each product candidate were different, and results may not be comparable between product candidates. 11
Anti-plaque mAbs demonstrate dose-related ARIAs that will likely limit their use Percent of ARIA Events for Anti-Aβ/plaque mAbs* TARGETING TARGETING AB MONOMERS AMYLOID PLAQUES solanezumab aducanumab aducanumab lecanemab donanemab EXPEDITION 3 EMERGE ENGAGE BAN2401 (Phase 2) (Phase 3) (Phase 3) (Phase 3) (Phase 2) PC Treated PC Low High PC Low High PC High PC Treated 0.2% 0.1% 2.2% 26.1% 34.4% 3.0% 25.6% 35.7% 0.8% 9.9% 0.8% 27.5% ARIA-E ApoE ε4 carriers 1.9% 29.8% 42.5% 2.4% 28.7% 41.8% 1.2% 14.6% 3.6% 44.0% ApoE ε4 non- 2.9% 18.1% 17.9% 4.3% 17.5% 27.7% 0.0% 8.0% carriers 10.3% 32.8% 41.2% 9.8% 30.7% 40.3% N.A. 8.0% 38.9% Any ARIA E or H * PC = Placebo, Low = Low Dose; High = High Dose Shows the absence of ARIA after treatment with antibodies targeting Aβ monomers (solanezumab) in comparison to the increasing presence of ARIA after treatment at increasing dose levels with antibodies targeting amyloid plaques (aducanumab, BAN2401, and donanemab), indicate that ARIA results from the removal of amyloid plaques around blood vessels and likely does not result from treatment with antibodies that target other species of Aβ, i.e. Aβ monomers and AβOs. ARIA-E represents a dose limiting adverse effect for mAbs with amyloid plaque binding. We believe antibodies that avoid ARIAs should be safer and more feasible to administer, possibly at higher doses. There have been no head-to-head clinical trials between any of the product candidates listed above. Study designs and protocols for each product candidate were different, and results may not be comparable between 12 product candidates.
ACU193’s High Selectivity for toxic AβOs, Combined with its Expected Lack of ARIA- related Safety Concerns, Is Anticipated to Provide Superior Efficacy Compared to Peers + TARGET SELECTIVITY SAFETY PROFILE Lack of ARIA-related Company Asset Amyloid plaque Aβ fibrils Aβ monomers Aβ oligomers safety concerns ACU193 û untested û ü ü TM Aduhelm Biogen üûü üû lecanemab Eisai / Biogen û üûü ü gantenerumab Roche üüûüû Lilly donanemab untested ûûû ü solanezumab* Lilly ûûû ü ü crenezumab* Roche / Genentech üü üü ü bapineuzumab* Pfizer / Janssenüû üüü ____________________ *Phase 3 discontinued for primary AD indication. + There have been no head-to-head trials between any of the product candidates listed above. Study designs and protocols for each product candidate were different, and results may not be comparable between product candidates.. 13
ACU193: Our differentiated approach
Target Product Profile: ACU193 Best-in-Class, 1st line, anti-AβO, Disease-modifying Immunotherapy for Early AD DRUG: ACU193 is a humanized, affinity-matured, mAb with high selectivity for toxic AβOs vs. Aβ monomers (>500x) and amyloid plaques. ACU193 is an IgG2m4 subclass mAb which lacks inflammatory effector functions of other IgG subclasses. POPULATION: Early AD - Mild Cognitive Impairment and Mild Dementia due to AD (amyloid positive by PET) DOSING: IV infusion every 4 weeks DURATION: Chronic therapy for duration of Early AD VALUE Selectivity for toxic AβOs is expected to provide superior cognitive efficacy and improved PROPOSITION: safety and tolerability relative to non-selective anti-Aβ/plaque mAbs, including: • Slowing the decline of memory and cognition in Early AD • Decreasing AβO induced synaptic and neuronal network toxicity • Slowing disease progression and downstream effects on tau, neurodegeneration, and neuro- inflammation • With expected low rate of ARIA • Effective as stand-alone therapy or potentially in combination with other symptomatic, anti-inflammatory, and/or tau directed therapies 15
ACU193: Extensive Data Package Supporting Development — Nanomolar affinity for AβOs, >500-fold greater selectivity for AβOs over Aβ monomer, with limited or no discernable binding to vascular amyloid or dense core amyloid plaques SELECTIVITY — Binds broad range of endogenous AβOs present in transgenic mice and human AD samples (binds dimers to mid-sized molecular weight AβOs) — Dose-dependent effects in multiple in vitro neuroprotection assays PHARMACOLOGY — Positive memory and behavioral effects in multiple in vivo transgenic mouse models for AD — Brain penetration and biodistribution demonstrated in multiple species PK/PD — Performs like other peripherally administered CNS mAbs — IgG2m4 subclass lacks inflammatory effector function signaling (C1q, FcγR1, FcγRIII) — Microhemorrhage studies show no increased risk of SAFETY microhemeorrhage — GLP studies demonstrated acceptable safety margin for clinical dosing plans ACU193 is a promising immunotherapy for Early AD expected to provide meaningful cognitive and functional benefits, slow disease progression, and offer an attractive safety profile. 16
SELECTIVITY ACU193 is the First mAb Developed to Selectively Target AβOs Highly selective for Aβ oligomers versus Aβ monomers ACU193 Selectivity in presence of ACU193 Selectivity 5μM monomeric Aβ Log [Competing Antigen] μM ACU193 Log μM Even in the presence of a large excess of Aβ monomer, Binding of ACU193 to AβOs >500x binding of ACU193 to AβOs is unchanged binding to Aβ monomer ACU193 selective binding to AβOs is preserved even in the presence of a large excess of Aβ monomer which is present in brain – limited target distraction. 17 % Percent Control AβOs binding (RLUs)
SELECTIVITY ACU193 has a greater preference for AβOs than other mAbs Comparison of Aβ species-mAb complex signals across SEC fractions Synthetic AβOs SEC ACU193 binds to a wide range of oligomeric species of Aβ that are differentiated from those bound by hu266 (solanezumab) or hu3D6 (bapineuzumab). 18
SELECTIVITY ACU193 is highly selective for AβOs versus Aβ plaques ACU193 staining in human AD brain slices ACU193 (red) binds non-Thioflavin S positive Aβ (green) AD Hippocampus AD Hippocampus ACU193/AβOs species ThioS/amyloid plaque ACU193 has little or no binding to thioflavin S positive fibrillar Aβ plaque in human AD brain tissue. ____________________ Sources: E. Cline et al. CTAD 2019. 19
SELECTIVITY PHARMACOLOGY AβOs Bind to Neurons and are Toxic; mouse analogue of ACU193 prevents toxicity After binding to neurons, AβOs disrupt Long Term Potentiation (LTP) and cause pathologic increases in intracellular calcium that is destructive to cells. ACU3B3 prevents AβO inhibition of ACU3B3 prevents AβO mediated Ca2+ hippocampal LTP ex vivo elevation in cell cultures Control Aβ (50 nM) 42 Aβ (50 nM) + 42 ACU3B3 (100 pM) Note: (1) ACU3B3 is the mouse monoclonal antibody precursor to and equivalent of humanized ACU193 ACU3B3 prevents changes in aberrant neuronal activity underlying memory loss in AD and prevents AβO mediated disruption of calcium homeostasis in neuronal cultures. 20
SELECTIVITY PHARMACOLOGY Treatment of a Transgenic Mouse Model of AD results in Behavioral Improvements Murine parent version of ACU193 (ACU3B3) was used to treat younger mice with depositing plaque or older mice with abundant plaque Morris Water Maze Open Field MWM swim speed Open field total abnormality distance measurement, (**p<0.02). APP-Veh vs. APP-3B3, *p=0.029. Deficits in younger (5-7 months) transgenic mice are Deficits in older (9-10 months) transgenic mice are markedly reduced with treatment markedly reduced with treatment 21
SELECTIVITY PHARMACOLOGY PK/PD ACU193 Enters the CNS and Binds to AβOs in Transgenic Mice in Dose Dependent Manner ACU193 engages target AβOs in transgenic mouse brain (tg2576) in dose dependent manner. Ability to push doses higher in patient clinical trials may provide increased target coverage. 22
Clinical Development Plans
(ACU-001) INTERCEPT-AD trial: Phase 1 Overview TRIAL Randomized Placebo Controlled Phase 1 DESIGN: • Part A : Single-Ascending Doses • Part B : Multiple-Ascending Doses ENROLLMENT Early AD CRITERIA: • Mild Cognitive Impairment and Mild Dementia due to AD (amyloid positive by PET) TRIAL Proof of Mechanism (PoM) OBJECTIVES: — Safety and tolerability — Pharmacokinetics — Target Engagement — Biomarkers; cognition For more information on the INTERCEPT-AD trial, see https://clinicaltrials.gov/ct2/show/NCT04931459. 24
INTERCEPT-AD a Randomized Placebo Controlled Phase 1 in Early AD patients 60mg COHORT 4: ≥ 1wk 60 mg/kg ACU193 PART A: or Placebo SINGLE- COHORT 3: ASCENDING DOSE 25mg ≥ 1wk 25 mg/kg ACU193 n = 8 per cohort (32 total) or Placebo COHORT 2: ≥ 1wk 10 mg/kg ACU193 10mg or Placebo ≥ 1wk COHORT 1: 2 mg/kg ACU193 60mg COHORT 7: 2mg or Placebo ≥ 4wk 60 mg/kg ACU193 or Placebo (Q2W) ≥ 1wk 60mg COHORT 6: PART B: 60 mg/kg ACU193 or Placebo (Q4W) MULTIPLE- ASCENDING DOSE COHORT 5: 10 mg/kg ACU193 n = 10 per cohort (30 total) 10mg or Placebo (Q4W) 25
Phase 1 Objectives: Proof of Mechanism –Ability to move to Phase 2/3 1. SAFETY AND TOLERABILITY • Assessment of ARIA-E • Absence of problematic immunogenicity PROOF OF MECHANISM 2. PHARMACOKINETICS Requirements for Phase 2/3 • Peripheral and Central ✓ Acceptable safety and 3. EVIDENCE OF TARGET ENGAGEMENT tolerability • CSF level of ACU193:AβO complexes (bound) ✓ Show ACU193 gets into central compartment 4. FLUID BIOMARKER EFFECTS • Phospho-tau, Neurofilament light, et. al. ✓ Target engagement 5. CLINICAL MEASURES ✓ Other indicators of target • Assessment of clinical cognitive measures, mechanism of action computerized tests (Cogstate Ltd.) 6. MRI EFFECTS • Potential improvements in cerebral blood flow shown with MRI ASL pulse sequence Topline Results anticipated in 1H 2023: primary outcomes Safety / ARIA-E, PK and Target Engagement. Detailed study results anticipated to be presented at major Alzheimer’s meeting. 26
Cogstate computerized test battery Test Domains tested Time (minutes) International shopping list test Immediate recall 5 (immediate) Cogstate brief battery Attention, working memory, 15 learning International shopping list test (delayed) Delayed recall 1 Groton maze learning test Executive function 7 International digit-symbol substitution test Processing speed 3 Total = 31 Frequency of administration sensitivity of battery offers improved possibility to observe effects. 27
Arterial Spin Labelling (ASL) as an MRI measure of cerebral blood flow Literature supports use of ASL to assess hypoperfusion in AD • Mild cognitive impairment patients show hypoperfusion in parietal cortex, precuneus, posterior cingulate cortex and medial temporal lobe • AD patients show global hypoperfusion, but especially cingulate, precuneus, parietal lobes and inferior frontal regions • Perfusion correlates with several neuropsychological tests • Hypoperfusion can be improved in middle and posterior cingulate cortex with cholinesterase inhibitors and was associated with improvement in ADAS-cog scores 28
ACU193 Development Summary ⇒ Non-clinical data consistent with toxicity of Aβ oligomers and selective binding of ACU193 to Aβ oligomers – differentiated profile ⇒ Enrollment in a Phase 1study assessing safety, PK and target engagement is ongoing ⇒ Although unlikely with this small sample size, the possibility of improvement in cognitive scales, computerized cognitive testing and cerebral blood flow will also be assessed as exploratory outcomes in the Phase 1 study ⇒ Anticipate next clinical study, with success in Phase 1, to be Phase 2/3 starting as Proof-of-Concept trial with potential to expand to a Phase 3 registration study based on an expansion analysis 29
Business Considerations
Experienced in AD/neuro drug development ACUMEN LEADERSHIP TEAM ERIC SIEMERS, MD JANICE HITCHCOCK, PHD DANIEL O'CONNELL Chief Medical Officer VP Regulatory Affairs President & CEO ROBERT DEAN, MD, PHD RUSSELL BARTON MATT ZUGA Sr. Development Advisor Chief Operating Officer Chief Financial Officer & Chief Business Officer SIEW TIN GAN LIEAN SCHENK JASNA JERECIC, PHD VP, Head of CMC Head of Clinical Analytical Methods Operations Leader, Research Scientist Acumen team has decades of experience in Alzheimer’s drug discovery and development. 31
ACU193 IP & Market Exclusivity • Exclusive, perpetual, worldwide, royalty-free license from Merck to all Merck Amyloid Derived Diffusible Ligand (ADDL) IP including, issued ACU193 patents • ACU193 Global IP estate: ü Issued patents in 19 countries ü Composition of matter patents and methods of use run into July 2031 ü Patent term extensions available, 3-5 years depending on jurisdiction • Biologics market exclusivity is expected for ACU193 as a novel biologic drug ü US provides 12 years market exclusivity for novel biologics ü Europe provides 10 years of market exclusivity for novel biologics 32
Acumen is Well Capitalized, with Expected Cash Runway through 2025 STATUS/ MILESTONES EXPECTED TIMING ~$210M Initiated Ph1 clinical trial INTERCEPT-AD ü Cash, cash equivalents and marketable securities as of June 30, 2022 INTERCEPT-AD Trial updates 2022 Proof of Mechanism Topline Results 1H 2023 We believe that Acumen has the organizational expertise and cash and marketable securities on hand to advance ACU193 through 2025. 33
ABOS: Key Takeaways Massive unmet need in AD, recent favorable trends and cumulative learnings position field for future successes Upcoming sector catalysts 2H22 - 1H23 Differentiated Product Candidate targeting toxic AβOs Experienced AD drug development team Blue chip investors, very strong balance sheet and cash $ runway with multiple milestones through 2025 Value-inflection clinical data 1H2023 34
Thank you! 35