8-K

UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

Washington, D.C. 20549

___________________

FORM 8-K

___________________

CURRENT REPORT

Pursuant to Section 13 or 15(d) of the

Securities Exchange Act of 1934

Date of Report (Date of earliest event reported) September14, 2020

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Cassava Sciences, Inc.

(Exact name of registrant as specified in its charter)

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Delaware	000-29959	91-1911336
(State or other jurisdiction of incorporation)	(Commission File Number)	(I.R.S. Employer Identification Number)

7801 N Capital of Texas Highway, Suite 260

Austin, Texas 78731

(Address of principal executive offices, including zip code)

(512) 501-2444

(Registrant’s telephone number, including area code)

Not Applicable

(Former name or former address, if changed since last report.)

___________________

Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions (see General Instruction A.2 below):

☐	Written communication pursuant to Rule 425 under the Securities Act (17 CFR 230.425)
☐	Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)
☐	Pre-commencement communication pursuant to Rule 14d-2(b) under the Exchange Act (17CFR 240.14d-2(b))
☐	Pre-commencement communication pursuant to Rule 13e-4(c) under the Exchange Act (17CFR 240.13e-4(c))

Securities registered pursuant to Section 12(b) of the Act:

0
Title of each class	Trading Symbol(s)	Name of each exchange on which registered
Common Stock, $0.001 par value	SAVA	NASDAQ Capital Market

Indicate by check mark whether the registrant is an emerging growth company as defined in as defined in Rule 405 of the Securities Act of 1933 (§230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§240.12b-2 of this chapter).

Emerging growth company   ☐

If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act.☐☐

Item 7.01. Regulation FD Disclosure.

A copy of the Cassava Sciences, Inc. Final Results of a Phase 2b Study of Sumifilam in Alzheimer’s Diseasepresentation, dated September 14, 2020, is furnished as Exhibit 99.1 to this Form 8-K and is incorporated herein by reference.

Item 8.01. Other Events.

On September14, 2020, Cassava Sciences, Inc. issued a press release, a copy of which is attached hereto as Exhibit 99.2 and is incorporated herein by reference.

Item 9.01 Financial Statements and Exhibits.

(d)    Exhibit No.    Description
99.1	Cassava Sciences, Inc. Final Results of a Phase 2b Study of Sumifilam in Alzheimer’s Disease presentation, dated September 14, 2020
99.2	Cassava Sciences, Inc. press release dated September14, 2020

SIGNATURE

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 thereunto duly authorized.

	CASSAVA SCIENCES, INC.
	a Delaware corporation
Date:   September14, 2020
	By:	/s/ ERIC J. SCHOEN
		Eric J. Schoen
		Chief Financial Officer

EX-99.1

Exhibit 99.1

CASSAVA sciences Final Results of a Phase 2b Study of Sumifilam in Alzheimer’s Disease September 14, 2020 1

Forward-Looking Statements & Safe Harbor This presentation contains “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995. To identify such forward-looking statements, in some cases we use terms such as “predicts, “believes,” “potential,” “estimates,” “anticipates,” “expects,” “plans,” “intends,” “may,” “could,” “might,” “should” or other words that will convey risk or uncertainty of future events or outcomes. All statements other than statements of historical fact contained in this presentation including, but not limited to, statements regarding plans or timing for future Phase 3 clinical studies with sumifilam; the interpretation of prior or current results of our Phase 2 clinical studies, including the measured effects of sumifilam on cognition; plans to publish results in a peer-reviewed journal; potential health benefits, if any, of changes in levels of biomarkers; verbal commentaries made by Cassava Sciences’ employees; and potential benefits, if any, of the Company’s product candidates for Alzheimer’s disease are forward-looking statements. Such statements are based largely on our current expectations and projections about future events. Such statements speak only as of the date of this presentation and are subject to a number of risks, uncertainties and assumptions, including, but not limited to, those risks relating to the ability to conduct or complete clinical studies on expected timelines, to demonstrate the specificity, safety, efficacy or potential health benefits of our product candidates, the severity and duration of health care precautions given the international outbreak of an infectious disease and including those described in the section entitled “Risk Factors” in our Annual Report on Form 10-K for the year ended December 31, 2019 and future reports to be filed with the SEC. In light of these risks, uncertainties and assumptions, forward-looking statements and events discussed in this presentation are inherently uncertain and may not occur.Actual results could differ quickly, materially and adversely from those anticipated or implied in the forward-looking statements. Accordingly, you should never rely upon forward-looking statements as predictions of future events. This presentation may also contain statistical data based on independent industry publications or other publicly available information. We have not independently verified the accuracy or completeness of the data contained in these industry publications and other publicly available information. Accordingly, we make no representations as to the accuracy or completeness of that data. You are cautioned not to give undue weight to such data. We do not undertake any obligation to update this corporate presentation or any forward-looking statements included therein, except as required by law. The content of this presentation is solely our responsibility and does not necessarily represent the official views of the National Institutes of Health (NIH).CASSAVA sciences 2

Company Presenters Guest Presenter Remi Barbier Remi Barbier - Chairman, President & CEO Nadav Friedmann, PhD, MD - CMO, Board member Eight FDA drug approvals prior to Cassava Sciences. Lindsay H. Burns, PhD - SVP Neuroscience Eric Schoen - Chief Financial Officer Dr. Gonzalez-Rojas, MDDr. Gonzalez-Rojas is Principal Investigator (PI) on the Phase 2b study of sumifilam, and PI on an ongoing, one-year open-label study of sumifilam in patients with Alzheimer’s disease. Dr. Gonzalez-Rojas will be available for commentary during the Q&A session.Background - Yaneicy Gonzalez-Rojas MD, Internal Medicine, is an ACRP-certified Principal Investigator working in Coral Gables, FL. Besides being an established medical practitioner treating hundreds of Alzheimer’s patients annually, she has a keen interest in conducting quality clinical trials. Dr. Gonzalez-Rojas has participated in 13 clinical trials of various investigational drug agents for Alzheimer’s disease.EXELIXIS XOMA ARQULE Johnson Johnson Daiichi-Sankyo Abbott Abgenix elan UNIVERSITY OF CAMBRIDGE VERMILLION PriceWaterHouseCoopers CASSAVA sciences 3

Our Mission Cassava Sciences is dedicated to the development of novel approaches to detect and to treat Alzheimer’s disease. CASSAVA sciences 4

Our Company Cassava Sciences is dedicated to the development of novel approaches to detect & treat Alzheimer’s disease.Our initial focus is on developing sumifilam, a proprietary, investigational drug to treat Alzheimer's disease.Sumifilam is the first of a new class of drugs that target filamin proteins. Filamin-binding molecules are new to Alzheimer’s research and may represent an important advance towards the goal of disease-modifying drugs.Sumifilam reduces neurodegeneration and neuroinflammation in Alzheimer's disease by binding a single target. The underlying science is published in peer-reviewed journals and benefits from long-term scientific and financial support from the National Institutes of Health (NIH).In 2019, we announced positive results of an open-label, Phase 2a study of sumifilam in Alzheimer’s disease. In 2020, we completed a randomized, placebo-controlled Phase 2b study of sumifilam in Alzheimer’s disease, funded by a research grant from the NIH (NIA grant #AG060878). The purpose of this presentation is to inform our stakeholders of the final clinical results of our Phase 2b study with sumifilam in Alzheimer’s disease.Our future goal is to conduct a Phase III efficacy program with sumifilam in Alzheimer’s disease. CASSAVA sciences 5

Alzheimer’s Disease – Significant Unmet Needs Alzheimer’s disease (AD) is a progressive brain disorder that destroys memory and thinking skills.AD is the largest potential drug market in the world, where diagnostic methods are currently limited, treatment options are inadequate and the ability to slow disease progression is non-existent.About 5-6 million people live with AD in the U.S. today; incidence is expected to grow dramatically.There are no disease-modifying therapies for AD patients. Normal Brain Alzheimer’s DiseaseCASSAVA sciences 6

First Bioanalysis – Invalid Data As previously reported (May 2020), an outside lab conducted an initial bioanalysis of the Phase 2b study.Biomarker data received from that lab made no sense. A post-hoc analysis showed significant data anomalies in patients who took placebo for 28 days. Expected Observations for Patients Who Took Placebo Small changes in levels of biomarkers over 28 days.Biomarkers generally move in the same direction.Biomarkers that move in tandem show robuststatistical correlations. Lab’s Observations for Patients Who Took Placebo Placebo patients showed large, dramatic swings (>100%) in levels of biomarkers over 28 days.Biomarkers appeared to follow a random walk; some moved in opposite directions from each other in the same patient.Changes in levels of biomarkers are uncorrelated (R2 = 0.06, on average) in placebo patients. See Appendix for more statistical data on placebo patients. CASSAVA sciences 7

Second Bioanalysis – Valid Data An academic lab conducted a second, final bioanalysis of the Phase 2b study.The academic lab shows proper biomarker data in patients who took placebo for 28 days.Data from the academic lab shows modest (4-6%, on average) changes in levels of biomarkers over 28 days; biomarkers that generally move in the same direction; robust statistical correlations (R2 = 0.96, on average) among changes in levels of biomarkers; and negative correlation with Aβ42.Aβ42Total TauP-tau181NfLNgYKL40IL-6Aβ421-0.82-0.89-0.83-0.86-0.82-0.85Total Tau-0.8210.960.960.970.940.96P-tau181-0.890.9610.960.970.940.95NfL-0.830.960.9610.970.940.97Ng-0.860.970.970.9710.920.96YKL40-0.820.940.940.940.9210.96IL-6-0.850.960.950.970.960.961CASSAVA sciences 8

Science Lindsay Burns, PhD, SVP, Neuroscience CASSAVA sciences 9

Sumifilam - A Novel Drug for Alzheimer’s Disease Sumifilam is our proprietary, small molecule drug candidate to treat Alzheimer’s disease (AD) and other dementias and neurodegenerative diseases.Program benefits from long-term scientific & financial support from the National Institutes of Health (NIH).Sumifilam reduces neurodegeneration and neuroinflammation by binding a single target.In 2020, we concluded a comprehensive Phase 2 clinical testing program of sumifilam in AD, in collaboration with clinical/scientific advisors and NIH. CASSAVA sciences 10

The Target of Sumifilam is Altered Filamin A (FLNA) Filamin A (FLNA) is a scaffolding proteinhighly expressed in the brain. FLNA cross-links actin to provide structure and motility, but also interacts with>90 proteins, influencing many signaling pathways.The Alzheimer's brain carries an altered form of FLNA.Altered FLNA is critical to amyloid beta toxicity. CASSAVA sciences 11

Sumifilam Mechanism of Action The altered conformation of FLNA is a proteopathy in the AD brain.Altered FLNA enables A42 signaling via two different receptors:α7-nicotinic acetylcholine receptor (α7nAChR) hyperphosphorylates tauToll-like receptor 4 (TLR4) releases inflammatory cytokinesSumifilam preferentially binds altered FLNA, restores its proper shape/function, potently suppressing A42 signaling via α7nAChR and TLR4.Through a single target, sumifilam reduces both neurodegeneration & neuroinflammation.CASSAVA sciences 12

10+ Year Discovery/Development Program 1 <2008Basic research around neurobiology of Filamin A (FLNA). 2 2009Discovery that altered FLNA associates with ��7nAChR when A signals. 3 2010Screening/testing of compounds that bind altered FLNA and block ��7nAChR/A interaction. 4 2011Sumifilam (formerly, PTI-125) binds altered FLNA with high affinity, blocks ��7nAChR/A interactions. Preclinical testing of sumifilam. 5 2017 - presentClinical testing ofsumifilam. Positive results reported in Alzheimer’s patients. CASSAVA sciences 13

Peer-reviewed Science The underlying science for sumifilam has been subject to the scrutiny of many experts in the field………. including NIH, which has awarded our science programs >$10 million in research grant awards.NIH National Institutes of Health CASSAVA sciences 14

Hypothesis and Objective Clinical Hypothesis AD patients desperately need disease-modifying drug therapies.Published pre-clinical data support sumifilam’s potential as a disease-modifying drug for AD.Can sumifilam provide early clinical evidence of disease-modifying effects in a well-controlled study? Phase 2b Study Objective Evaluate safety, biomarkers and cognition following 28-day treatment with sumifilam, a new, first-in-class therapy. CASSAVA sciences 15

Bring on the Biomarkers Biological markers (‘biomarkers’) refers to objective measures of Alzheimer’s disease at the level of biology.Biomarkers present hard evidence for the presence and progression of Alzheimer’s disease.Alzheimer’s disease can take a decade or more to present. Over that time certain biomarkers rise dramatically, while cognition and health decline. One drug, one biomarker is the traditional paradigm in AD research.Sumifilam’s goal is to improve an entire panel of biomarkers of AD pathology, neuroinflammation and neurodegeneration. CASSAVA sciences 16

Clinical ResultsNadav Friedmann, PhD/MD, Chief Medical OfficerLindsay Burns, PhD, SVP, Neuroscience CASSAVA sciences 17

Phase 2b - Study Design Randomized, Double-blind, Placebo-controlled, Multicenter Clinical StudyPatient Enrollment Mild-to-moderate AD, MMSE ≥16 to 26, age 50-85 Sixty (64) patients recruited across 9 study sites in the U.S. Key Inclusion Criteria:CSF Total tau/Aβ42 ≥ 0.28 at screening CSF (1st lumbar puncture) and blood collected at screening/Day 11:1:1 Randomization First Cognition TestDay 1 Second Cognition TestDay 28Sumifilam 50 mg, twice-daily, 28 days Sumifilam 100 mg, twice-daily, 28 days Matching placebo, twice daily, 28 days Primary Endpoint:biomarkers of diseaseSecondary Endpoint:cognitionCSF (2nd lumbar puncture) and blood collected at Day 28 CASSAVA sciences 18

Phase 2b – Safety Sumifilam was safe and well-toleratedNo serious adverse eventsNo drug-related adverse eventsCommon, non-persistent side-effects observed in placebo & drug groupsNo drug-related patient discontinuation CASSAVA sciences 19

Phase 2b - AD Pathology Decreased Significantly Levels of CSF Tau Proteins Decreased Significantly in Both Drug Groups % Change - Baseline to Day 28 -25% -20% -15% -10% -5% 0% Total Tau -2% -15% p <0.01 -18% p<0.01 P-Tau181 -2% -8% p<0.01 -11% p<0.01 Placebo 50 mg 100 mg All p-values vs placebo CASSAVA sciences 20

Phase 2b - Aβ42, Low in AD, Increased Significantly Change in Levels of CSF Amyloid-β42 Day 0 to Day 28 % Change - Baseline to Day 28 -5% 0% 5% 10% 15% 20% Placebo 0% 50 mg p < 0.01 17% 100 mg p < 0.01 14% Note: CSF amyloid-β42 levels are low in early stages of dementia in patients with Alzheimer’s disease. All p-values vs placebo CASSAVA sciences 21

Phase 2b - Total tau/Aβ42 Dropped Significantly A Key Diagnostic Criteria for AD Decreased Significantly in Both Drug GroupsChange in Ratio of CSF T-tau/Aβ42 Day 0 to Day 28 CSF T-tau/Aβ42 0.00 0.20 0.40 0.60 0.80 1.00 1.20 1.40 Placebo, no change 1.2 Day 0 1.2 Day 28 Placebo 50 mg25% Decrease (p < 0.01) 1.2 Day 0 0.9 Day 28 50 mg 100 mg30% Decrease (p < 0.01) 1.0 Day 0 0.7 Day 28 100 mg CASSAVA sciences 22

Phase 2b - P-tau/Aβ42 Dropped Significantly A Key Diagnostic Criteria for AD Decreased Significantly in Both Drug GroupsChange in Ratio of CSF P-tau/Aβ42 Day 0 to Day 28 CSF P-tau/Aβ42 0.00 0.05 0.10 0.15 0.20 0.25 0.30 0.35 0.40 Placebo, no change 0.34 Day 0 0.34 Day 28 Placebo 50 mg 20% Decrease (p < 0.01) 0.35 Day 0 0.28 Day 28 50 mg 100 mg 21% Decrease (p < 0.01) 0. 28 Day 0 0.22 Day 28 100 mg CASSAVA sciences 23

Phase 2b - Neurodegeneration Decreased Biomarkers of Neurodegeneration Decreased Significantly in Both Drug GroupsChange in Levels of CSF Ng and NfL Day 0 to Day 28% Change - Baseline to Day 28 -50% -40% -30% -20% -10% 0% Neurogranin -2% -36% p < 0.01 -43% p < 0.01 Neurofilament Light Chain -4% -28% p < 0.05 -34% p < 0.01 Placebo 50 mg 100 mg All p-values vs. placebo 24

Phase 2b - Neuroinflammation Decreased Biomarkers of Neuroinflammation Decreased Significantly in Both Drug GroupsChange in Levels of CSF YKL-40, IL-6 and soluble TREM2, Day 0 to Day 28% Change - Baseline to Day 28 -60% -50% -40% -30% -20% -10% 0% YKL-40 0% -10% -12% Both, p < 0.01 IL-6 -3% -10% -11% Both, p < 0.01 sTREM2 3% -43% -46% Both, p < 0.01 Placebo 50 mg 100 mg All p-values vs placebo CASSAVA sciences 25

Phase 2b - Summary of CSF Results Sumifilam Significantly Improved An Entire Panel of AD-related Biomarkers % Change - Baseline to Day 28 -50% -40% -30% -20% -10% 0% 10% 20% Aβ42 0% 17% 14% Total Tau -2% -15% -18% P-Tau181 -2% -8% -11% Neurogranin -2% -36% -43% NfL -4% -28% -34% YKL40 0% -10% -12% IL-6 -3% -10% -11% sTREM2 3% -43% -46% CASSAVA sciences Placebo 50 mg 100 mg CASSAVA sciences 26

Phase 2b – Cognition CANTAB (Cambridge Neuropsychological Test Automated Battery) is a widely used, computer-based battery of memory tests sensitive to subtle changes in cognition.Tests are independent of language skills, speed, gender or education.Cognitive assessments were made on Day 1 (pre-dose) and again on Day 28.Patients were tested on ‘episodic memory’ and ‘spatial working memory’.Patients advance through progressively more difficult levels.Outcome measure = total errors, with errors imputed for more difficult levels not reached, so…….Lower score is better! CASSAVA sciences 27

Phase 2b - CognitionDrug Groups Show Directional Improvements in Episodic Memory Change – Baseline to Day 28 -6 -5 -4 -3 -2 -1 0 Placebo -1.5 50 mg -5.7 100 mg -4.5 37% Effect Size 23% Effect Size Episodic Memory Endpoint:Lower score is better on change from baseline in Total Errors on Paired Associates Learning (PAL).Effect sizes vs. placebo were calculated by Hedge’s g after removing the most and least impaired subjects across all groups by baseline score.Effect size measures the magnitude of effect; in contrast, statistical significance measures the probability of effect occurring by chance.CASSAVA sciences 28

Phase 2b – Cognition Drug Groups Show Directional Improvements in Spatial Working MemoryChange – Baseline to Day 28 -3.5 -3 -2.5 -2 1.5 -1 -0.5 0 Placebo -0.41 50 mg -1.65 100 mg -3.33 17% Effect Size 46% Effect Size Spatial Working Memory Endpoint:Lower score is better on change from baseline in Total Errors on Spatial Working Memory task.Effect sizes vs. placebo were calculated by Hedge’s g.Patients who did not take drug (no blood levels) were removed.CASSAVA sciences 29

Phase 2b - Cognition/Biomarker Correlation Cognitive Improvement Correlates Most (R2 = 0.5) With Decreases in CSF P-tau181 YKL 0.30 NfL 0.36 T-tau 0.37 Albumin 0.37 IL-6 0.41 P-tau181 0.48 CASSAVA sciences 30

Summary of Drug Effects 98% of patients treated with sumifilam 50 mg or 100 mg b.i.d. for 28 days showed improvements in validated biomarkers of AD pathology; neuroinflammation; and neurodegeneration; with no safety issues.Sumifilam appears to stabilize or improve memory.37% and 23% effect sizes in episodic memory vs placebo17% and 46% effect sizes in spatial working memory vs placeboImproved cognition correlated most strongly with reduction in levels of P-tau181 (R2 = 0.5)Target engagement and mechanism of action were demonstrated in prior clinical and non-clinical studies and was demonstrated again in this Phase 2b. These data validate FLNA as a promising new therapeutic target for AD. CASSAVA sciences 31

Conclusions & Next StepsRemi Barbier, President & CEOEric Schoen, Chief Financial Officer CASSAVA sciences 32

Conclusions A well-controlled Phase 2b study of sumifilam showed promising treatment effects in mild-to-moderate AD patients.No other clinical-stage drug candidate has improved an entire panel of biomarkers of disease pathology, neurodegeneration and neuroinflammation, and appears to benefit cognition.Phase 2b drug effects are consistent with Phase 2a clinical results, preclinical data, mechanism of action and basic research.The dataset highlight sumifilam’s potential as a disease-modifying drug candidate for Alzheimer’s disease. Clinical data will need to be replicated in large, Phase 3 efficacy studies. CASSAVA sciences 33

Next Steps - Replicate Drug Effects in Phase 3 Phase 2b publication, peer-reviewed journal.End-of-phase 2 (EOP2) meeting with FDA.Complete patient enrollment in on-going, open-label study of sumifilam.Develop study plan for Phase 3 efficacy program in Alzheimer’s disease.Manufacture Phase 3 clinical trial supplies (drug substance + oral tablets).Initiate Phase 3 efficacy program, estimated 2021+ CASSAVA sciences 34

Intellectual Property Sumifilam was discovered in-house. Cassava Sciences owns exclusive, worldwide rights to this and other drug asset and related technologies, without milestone or royalty obligations to any third party.Sumifilam is a novel molecule. Cassava Sciences owns composition of matter claims on sumifilam and other novel, filamin-binding molecules.Cassava Sciences’ patent protection in this area currently runs beyond 2037, plus extensions, and includes seven issued patents and related patent filings and applications. CASSAVA sciences 35

Key Financials Nasdaq ticker: SAVA Shares Outstanding 24.9 million Warrants Outstanding 1.4 million Total Shares outstanding – 26.3 million Unaudited FinancialsCash Balance at June 30, 2020≈ $25.3 millionExpected Net Cash Use Full-year 2020≈ $5.0 millionNo DebtCASSAVA sciences 36

Clinical Discussion withDr. Gonzalez-Rojas, MD, Principal InvestigatorYaneicy Gonzalez-Rojas MD, Internal Medicine, is an ACRP-certified Principal Investigator working in Coral Gables, FL. Besides being an established medical practitioner treating hundreds of Alzheimer’s patients annually, she has a keen interest in conducting quality clinical trials. Dr. Gonzalez-Rojas has participated in 13 clinical trials of various investigational drug agents for Alzheimer’s disease, including sumifilam.Q & A SessionCASSAVA sciences 37

Thank you! CASSAVA sciences 38

Appendix: Key Publications Journal of Prevention of Alzheimer’s Disease2020; DOI: 10.14283PTI-125 Reduces Biomarkers of Alzheimer’s Disease In Patients:http://link.springer.com/article/10.14283/jpad.2020.6Neuroimmunology and Neuroinflammation2017;4:263-71:Altered filamin A enables amyloid beta induced tau hyperphosphorylation and neuroinflammation in Alzheimer’s disease:http://nnjournal.net/article/view/2313Neurobiology of Aging(Volume 55) July 2017, Pages 99—114)PTI-125 binds and reverses an altered conformation of filamin A to reduce Alzheimer's disease pathogenesis:http://www.neurobiologyofaging.org/article/S0197-4580(17)30087-8/Alzheimer's & DementiaVolume 8, Issue 4, Supplement, 1 July 2012, Pages p259-p260PTI-125 reduces amyloid-related Alzheimer's pathogenesis by targeting filamin A:https://www.sciencedirect.com/science/article/pii/S1552526012008242Journal of Neuroscience18 July 2012, 32 (29) 9773-9784Reducing amyloid-related Alzheimer's disease pathogenesis by a small molecule targeting filamin Ahttp://www.jneurosci.org/content/32/29/9773.shortCASSAVA sciences 39

Appendix - Biomarkers Generally Correlate! AD biomarkers generally move in tandem as disease progresses. Therefore, a valid and sound bioanalysis should show data from placebo patients with robust statistical correlations among changes in biomarkers.The first bioanalysis showed no correlation in the placebo samples (R2=0.06, on average). Correlation Values (R2) Between Changes in CSF Biomarkers.Placebo patients only – Baseline vs. Day 28.Total TauP-tau181NfLNgYKL40IL-6Total Tau1.000.410.070.390.25-0.05P-tau1810.411.00-0.130.00-0.040.26NfL0.07-0.131.00-0.05-0.16-0.07Ng0.390.00-0.051.000.43-0.21YKL400.25-0.04-0.160.431.00-0.15IL-6-0.050.26-0.07-0.21-0.151.00CASSAVA sciences CONFIDENTIAL, NON-PUBLIC INFORMATION 40

EX-99.2

Exhibit 99.2

Cassava Sciences AnnouncesFinal Results of a Phase 2b Clinical Study of Sumifilam in

Patients with Alzheimer’s Disease

Alzheimer’s Patients in Drug Groups ShowedStatistically Significant Improvements in Biomarkers of Disease Compared toPlacebo Group (P<0.05)

Alzheimer’s Patients in Drug Groups Showed Improved CognitionCompared toPlacebo Group(Effect Size 46-17%)

Sumifilam Was Safe and Well-Tolerated

COMPANY TO HOST CONFERENCE CALL TODAY AT 8:30 AM ET.  

Conference Call Will Include Dr.  Gonzalez-Rojas, MD,Principal Investigator on Both the Phase 2b Study of Sumifilam and an Ongoing, One-Year Open-Label Study of Sumifilam In Patients withAlzheimer’s Disease

AUSTIN, TX – September14, 2020 – Cassava Sciences, Inc. (Nasdaq: SAVA)  today announced final results of a Phase 2b study with its lead drug candidate, sumifilam, in Alzheimer’s disease.In a  clinical study funded by the National Institutes of Health (NIH),  sumifilam significantly improved an entirepanel of validated biomarkers of disease in patients with Alzheimer’s disease. The ability to improve multiplebiomarkers from distinct biological pathways with one drug has never been shown before in patients with Alzheimer’s disease.  Study results are expected to be published in a peer-reviewed publication.Sumifilam is the first of a new class of drug compounds that bind to a protein called Filamin A.

“Filamin-binding molecules are new to Alzheimer’s research and may represent an  important advance if these data can be replicated in larger studies,” said Jeffrey Cummings,  M.D., Sc.D., Founding Director of the Cleveland Clinic Lou Ruvo Center for Brain Health, and Chambers Professor of Brain Science at the University of Nevada, Las Vegas. “I am pleased to see early evidence of disease-modifying effects in patients with this investigational drug. The data appear to represent a step forward toward urgently needed treatments for Alzheimer’s disease.”

In addition,  Alzheimer’s patients treated with sumifilam showed directional improvements in tests of remembering new information, versus patients on placebo. Improvements in cognition correlated most strongly with decreases in P-tau181, a biomarker that, when elevated, leads to tangles in the brain. Sumifilam decreased brain levels of Ptau-181 by 8-11%, versus placebo.

In this study, Alzheimer’s patients treated with 50 mg or 100 mg of sumifilam twice-daily for 28 days showed statistically significant (p<0.05) improvements in biomarkers of disease pathology,

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neurodegeneration and neuroinflammation, versus Alzheimer’s patients who took placebo.In addition, Alzheimer’s patientstreated with sumifilam showed directional improvements in validated tests of episodic memory and spatialworking memory, versus patients on placebo (Effect Sizes 46-17%). Cognitive improvements correlated most strongly (R2=0.5) with decreases in P-tau181. The study achieved a 98% response rate, defined as the proportion of study participants taking sumifilam who showed improvements in biomarkers.

“The clinical data suggest sumifilam may be slowing disease progression in Alzheimer’s patients,” said Nadav Friedmann, PhD/MD, Chief Medical Officer, Cassava Sciences.“This exciting possibility will need to be evaluated in future collaborations with patients, physicians, advisors and others.”

“Other than a few drugs to help ease the decline, there’s really nothing out there to treat people with Alzheimer’s,” said Remi Barbier, Chairman, President & CEO, Cassava Sciences. “Theimprovement on multiple biomarkers in this clinical studyisa first and offers hope that sumifilam has potential to become a transformative treatment for people with Alzheimer’s disease.”

Phase 2b Study Design

Phase 2b was a randomized, placebo-controlled, double-blind, multi-centerclinical study of sumifilam (formerly, PTI-125).Sixty-four patients with mild-to-moderate Alzheimer’s disease, age 50-85, were randomized (1:1:1) to 100 mg or 50 mg oral sumifilam or matching placebo. Treatment was administered twice daily for 28 days. Nine U.S. study sites enrolled patients. A  clinical diagnosis of Alzheimer’s disease was confirmed with the Mini-Mental State Examination (MMSE) ≥16 to ≤26 and a CSF T-tau/Aβ₄₂ ratio ≥0.28. Safety was assessed by ECGs, clinical labs, adverse event monitoring and physical examinations.

Phase 2b Study Results

In this study, drug was safe and well-tolerated, with no drug-related patient discontinuations.  The study used biomarkers to measure drug effects. Biomarkersare objective biological endpoints used to trackthe progression of Alzheimer’s disease. Molecular aberrations in the brain are reflected in biomarkers found in cerebrospinal fluid (CSF), a fluid that surrounds the brain.A key objective of this study was to measurechanges in levels of CSF biomarkers in study participantsbefore and after 28 days of treatment (i.e., percent change from baseline).

Key biomarker results includethe following (all p-values versus placebo):

· Core markers of Alzheimer’s pathology aretotal tau (T-tau), phosphorylated tau (P-tau181),  and amyloid beta42 (Aβ₄₂). In Alzheimer’s, tau and P-tau levels are elevated and Aβ₄₂ is low.

o T-tau decreased 15% (p<0.01)for patients in the 50 mg drug group.

o T-tau decreased 18% (p<0.01) for patients in the 100 mg drug group.

o P-tau decreased 8% (p<0.01) for patients in the 50 mg drug group.

o P-tau decreased 11% (p<0.01) for patients in the 100 mg drug group.

o Aβ₄₂ increased 17% (p<0.01) for patients in the 50 mg drug group.

o Aβ₄₂increased 14%  (p<0.01)  for patients in the 100 mg drug group.  

· Elevated CSF levels of two proteins, Neurogranin (Ng) and Neurofilament Light Chain (NfL) indicate neurodegeneration.

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o Ng decreased 36% (p<0.01) for patients in the 50 mg drug group.  

o Ng decreased 43% (p<0.01) for patients in the 100 mg drug group.

o NfL decreased 28% (p<0.05) for patients in the 50 mg drug group.

o NfL decreased 34% (p<0.01) for patients in the 100 mg drug group.

· Proinflammatory IL-6 (Interleukin 6) is produced in response to tissue stress and injury.

o IL-6 decreased 10% (p<0.01) for patients in the 50 mg drug group.

o IL-6 decreased 11% (p<0.01) for patients in the 100 mg drug group.

· Elevated levels of neuroinflammatory marker YKL-40 indicate microglial activation.  

o YKL-40 decreased 10% (p<0.01) for patients in the 50 mg drug group.

o YKL-40 decreased 12% (p<0.01) for patients in the 100 mg drug group.

· sTREM2 is a neuroinflammation biomarkerthat has commanded substantial recent attention from researchers for its role in Alzheimer’s disease and frontotemporal dementia.

o sTREM2 decreased 43% (p<0.01) for patients in the 50 mg drug group.

o sTREM2 decreased 46% (P<0.01) for patients in the 100 mg drug group.

A  further objective of this study was to measure drug effects on cognition. Patientswere tested at baseline and again on Day 28. Changes in episodic memory and spatial working memory were assessed on CANTAB,  avalidated,computer-based battery of tests. CANTAB is designed to measure cognitive skills regardless of the subject’slanguage skills, speed, gender or education. Only directional trends are observed, due to limitations around study size (N=64).

Key cognition results include:

· Alzheimer’s patients in both drug groups showed directional improvementson tests of episodic memory and spatial memory after 28 days of treatment,  versus patients on placebo.  Effect Sizes were 46-17% versus placebo.

· Episodic memory improved by -5.7 (lowerscore is better) for Alzheimer’s patients in the 50 mg drug group,versus-1.5 for patients on placebo.  

· Episodic memory improved by -4.3 (lowerscore is better) for Alzheimer’s patients in the 100 mg drug group,versus -1.5 for patients on placebo.  

· Spatial memory improved by -1.6 (lower score is better) for Alzheimer’s patients in the 50 mg drug group,versus -0.4 for patients on placebo.  

· Spatial memory improved by -3.3 (lower score is better) for Alzheimer’s patients in the 100 mg drug group, versus -0.4 for patients on placebo.  

· Improvements in cognition correlated most strongly (statistical R2=0.5) with decreases in CSF P-tau181,  a biomarker that, when elevated, leads to tangles in the brain. Sumifilam decreased brain levels of Ptau-181 by 8-11%, versus placebo.

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September 14, 2020

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Study Methods for Cerebrospinal Fluid (CSF) Bioanalysis

CSF was drawn from all study participants by lumbar puncture, an outpatient procedure used to remove a small sample of CSF from the lower spine. Study participants underwent two CSF draws: before treatment started and again after 28 continuous days of treatment. All CSF samples were sent to outside labs for bioanalysis. Bioanalysis refers to a set of laboratory tests that detect and measure very small amounts (pg/mL) of biomarkers in CSF.  Bioanalyses were conducted under blinded conditions to eliminate any possibility of bias. An academic lab generated final results.  The validity of final results is evidenced byrobust correlations (R2=0.96, on average) between biomarker movements over 28 days in the dataset for  placebo samples,  and only small changes in biomarkers in the placebo group, as expected.  

As previously disclosed, an initial bioanalysis by a different lab showed highly anomalous data, e.g., huge swings (in both directions) in levels of biomarkers, as well as biomarkers moving in opposite directions in the same patients, all in the groupwho took placebo for 28 days.With its validityin question, the initial bioanalysis serves no useful purpose.

Phase 2b Study Conclusions

A small, well-controlled study of sumifilam showed promising treatment effects in patients with mild-to-moderate Alzheimer’s disease. In this study, sumifilam treatment over 28 days improved an entire panel of validated biomarkers of Alzheimer’s disease, decreased measurements of neuroinflammation, showed a 98% responder rate, appears safe and well-tolerated, and appears to benefit cognition. Importantly, the data are consistent with prior clinical and preclinical results, the drug’s mechanism of action and over 10 years of basic research.

Ongoing Open Label Study

Cassava Sciences is conducting an ongoing, long-term, open-label, multi-center, extension study of sumifilam 100 mg twice-daily for 12 months. The study’s target enrollment is approximately 100 patients with mild-to-moderate Alzheimer’s disease, including patients from prior studies of sumifilam.  The open-label study is currently over 50% enrolled. 

About Alzheimer's Disease

Alzheimer’s disease is a progressive brain disorder that destroys memory and thinking skills. Currently, there are no drug therapies to halt Alzheimer’s disease, much less reverse its course. In the U.S. alone, approximately 5.8 million people are currently living with Alzheimer’s disease, and approximately 487,000 people age 65 or older developed Alzheimer’s in 2019.1 The number of people living with Alzheimer’s disease is expected to grow dramatically in the years ahead, resulting in a growing social and economic burden.2

1,2  Source: Alzheimer’s Association. 2019 Alzheimer’s Disease Facts and Figures. Available online at: https://www.alz.org/media/documents/alzheimers-facts-and-figures-2019-r.pdf

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About Sumifilam

Sumifilam is a proprietary, small molecule (oral) drug that restores the normal shape and function of altered filamin A (FLNA), a scaffolding protein, in the brain. Altered FLNA in the brain disrupts the normal function of neurons, leading to Alzheimer’s pathology, neurodegeneration and neuroinflammation.The underlying science for sumifilam is published in  peer-reviewed journals, including Journal of Neuroscience,  Neurobiology of Aging,  Journal of Biological Chemistry, Neuroimmunology and Neuroinflammation and Journal of Prevention of Alzheimer’s Disease.The Company is also developing an investigational diagnostic, called SavaDx, to detect Alzheimer’s disease with a simple blood test.

Sumifilam and SavaDx were both developed in-house. Both product candidates are substantially funded by peer-review research grant awards from the National Institutes of Health. Cassava Sciences owns worldwide development and commercial rights to its research programs in Alzheimer’s disease, and related technologies, without royalty obligations to any thirdparty. Patent protection in this area currently runs beyond 2037, plus extensions, and includes seven issued patents and related patent filings and applications.

About Cassava Sciences, Inc.

Cassava Sciences’ mission is to discover and develop innovations for chronic, neurodegenerative conditions. Over the past 10 years, Cassava Sciences has combined state-of-the-art technology with new insights in neurobiology to develop novel solutions for Alzheimer’s disease. For more information, please visit: https://www.CassavaSciences.com

For More Information Contact:

Eric Schoen, Chief Financial Officer

Cassava Sciences, Inc.

eschoen@CassavaSciences.com

(512) 501-2450

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September 14, 2020

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Cassava Sciences’ Phase 2b study of sumifilam in Alzheimer’s disease was funded by clinical research grant #AG060878 from the National Institutes of Health (NIH/NIA).  

The content of this press release is solely the responsibility of Cassava Sciences and does not necessarily represent the official views of the NIH/NIA.

Cautionary Note Regarding Forward-Looking Statements: This press release contains “forward-looking statements” for purposes of the Private Securities Litigation Reform Act of 1995 (the Act). Cassava Sciences claims the protection of the Safe Harbor for forward-looking statements contained in the Act. All statements other than statements of historical fact contained in this press release including, but not limited to,statements regarding the status of current and future clinical studies with sumifilam; the interpretation of results of our Phase 2 clinical studies including cognition data and plans to publish results in a peer-reviewed journal; potential health benefits, if any, of changes in levels of biomarkers; verbal commentaries made by Cassava Sciences’ employees and scientific advisors; and potential benefits, if any, of the Company’s product candidates for Alzheimer’s disease are forward-looking statements.Such statements are based largely on the Company’s current expectations and projections about future events. Such statements speak only as of the date of this press release and are subject to a number of risks, uncertainties and assumptions, including, but not limited to, those risks relating to the ability to conduct or complete clinical studies on expected timelines, to demonstrate the specificity, safety, efficacy or potential health benefits of our product candidates, the severity and duration of health care precautions given the COVID-19 pandemic, any unanticipated impacts of the pandemic on our business operations, and including those described in the section entitled “Risk Factors” in Cassava Sciences’ Annual Report on Form 10-K for the year ended December 31, 2019 and future reports to be filed with the SEC. In light of these risks, uncertainties and assumptions, the forward-looking statements and events discussed in this press release are inherently uncertain and may not occur, and actual results could differ materially and adversely from those anticipated or implied in the forward-looking statements. Accordingly, you should not rely upon forward-looking statements as predictions of future events. Except as required by law, the Company disclaims any intention or responsibility for updating or revising anyforward-looking statements contained in this press release.For further information regarding these and other risks related to our business, investors should consult our filings with the SEC, which are available on the SEC's website atwww.sec.gov.

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