UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

Washington, D.C. 20549

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FORM 8-K

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CURRENT REPORT

Pursuant to Section 13 or 15(d) of the

Securities Exchange Act of 1934

Date of Report (Date of earliest event reported) December 5, 2019

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Cassava Sciences, Inc.

(Exact name of registrant as specified in its charter)

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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.)

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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):

 



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





 

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.

 

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Item 7.01. Regulation FD Disclosure. 

A copy of the Cassava Sciences, Inc. presentation at the 12thInternational Conference on Clinical Trials on Alzheimer’s Disease (CTAD) on December 5, 2019 is furnished as Exhibit 99.1 to this Form 8-K and is incorporated herein by reference.

Item 8.01. Other Events.

On December 5, 2019, 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. 



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.









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CASSAVA SCIENCES One-month Oral Treatment with PTI-125, a New Drug Candidate, Reduces CSF & Plasma Biomarkers of Alzheimer’s Disease Late Breaking Oral Communication 12th Clinical Trials on Alzheimer's Disease (CTAD) December 5, 2019 - San Diego, CA Lindsay H. Burns, PhD; Hoau-Yan Wang, PhD; Zhe Pei, PhD; Kuo-Chieh Lee; Carrie Crowley; Michael Marsman, PharmD; Nadav Friedmann, PhD, MD 1

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Forward-Looking Statements This presentation contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. All statements other than statements of historical fact contained in this presentation including, but not limited to,  statements regarding the status of Phase 2 clinical studies; the interpretation of clinical results, including potential health  benefits, if any, of changes in levels of biomarkers; commentaries made by Cassava Sciences’ employees; and other 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 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 trials on expected timelines, to  demonstrate the specificity, safety, efficacy or potential health benefits of our product candidates 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,  2018 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 presentation 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. The content of this presentation is solely the responsibility of the Company and does not necessarily represent the official views of the National Institutes of Health. The Company does not undertake any obligation to update this presentation or any forward-looking statements included therein, except as required by law. Cassava Sciences 2

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Disclosures and Contributions PTI-125 is a proprietary compound of Cassava Sciences, Inc. Lindsay H. Burns, PhD; Nadav Friedmann, PhD, MD; and Carrie Crowley are employees of Cassava Sciences. Michael Marsman, PharmD and Hoau-Yan Wang, PhD are consultants to Cassava Sciences. Hoau-Yan Wang, PhD; Zhe Pei, PhD; and Kuo-Chieh Lee performed biomarker assays and are affiliated with City University of New York School of Medicine. J Neurosci, Neurobiol Aging and Neuroimmunol Neuroinflammation publications on PTI-125 are online: www.CassavaSciences.com. Research reported in this presentation was supported by the National Institute on Aging of the NIH under award AG060878. The content is solely the responsibility of the authors and does not necessarily represent the official views of NIH. Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 CU NY The City University of New York Cassava Sciences 3

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Phase 2a Clinical Trial of PTI-125 I. Background II. Clinical Results III. Mechanism of Action IV. Conclusions Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 4

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PTI-125 – A Novel Drug for Alzheimer’s disease PTI-125 is our proprietary, small molecule drug candidate to treat Alzheimer’s disease (AD) and other dementias. Our AD program benefits from significant, long-term scientific and financial support from the National Institutes of Health (NIH). By binding a single target, PTI-125 reduces both neurodegeneration and neuroinflammation. Clinical results from a first-in-patient study support PTI-125’s mechanism of action. Clinical biomarker results are consistent with > 10 years of basic science and preclinical data. Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 5

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The Target of PTI-125 is Altered Filamin A (FLNA) FLNA is an intracellular scaffolding protein anchored in the cell membrane. FLNA interacts with > 90 proteins, influencing many signaling pathways. The AD brain carries an ALTERED conformation of FLNA.  Altered FLNA is critical to amyloid beta’s toxicity. Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 6

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PTI-125 Mechanism of Action Altered FLNA enables A42 signaling via two different receptors: i. α7-nicotinic acetylcholine receptor (α7nAChR) hyperphosphorylates tau ii. Toll-like receptor 4 (TLR4) releases inflammatory cytokines PTI-125 preferentially binds altered FLNA, restores its proper shape/function, potently suppressing A42 signaling via α7nAChR and TLR4. Through a single target, PTI-125 reduces both neurodegeneration and neuroinflammation. Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 7

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Phase 2a Clinical Trial of PTI-125 I. Background II. Clinical Results III. Mechanism of Action IV. Conclusions Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 8

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Phase 2a Study Design Objective: Safety, PK and biomarkers under an IND filed by Cassava Sciences Study Design: First-in-patient, open-label treatment at 5 sites in the US Patients: Mild-to-moderate AD, MMSE ≥ 16 ≤ 24, age 50-85 Key Inclusion: CSF Total tau/Aβ42 ≥ 0.30 Enrollment: Thirteen (13) patients PTI-125 Dose: 100 mg oral tablets, b.i.d. for 28 days Biomarkers: CSF samples collected at screening and Day 28 Blood samples for plasma/lymphocyte markers at Days 1, 14 and 28 Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 9

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Phase 2a Safety and Pharmacokinetics Drug was well-tolerated, no drug-related adverse events observed PK parameters of PTI-125 100 mg b.i.d. in AD patients: Day Cmax (ng/mL) Tmax (h) Clast (ng/mL) Tlast (h) λz (1/h) AUClast (h*ng/mL) T1/2 (h) CSF/Plasma Day 1 1,020 2.00 176 12 0.176 5,320 4.51 – Day 28 1,100 2.06 238 12 0.174 6,700 4.35 0.61 Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 10

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CSF Biomarker Methods CSF biomarkers were measured by CUNY using commercial ELISA kits (LifeSpan BioSciences, Inc.)  according to manufacturer’s instructions. Samples were pre-treated with protease and phosphatase inhibitors. Screening and Day 28 samples were run in the same ELISA plate, in triplicate, for each biomarker. Assays used 50 µl CSF per well (YLK40 used 100 µl), subtracting background for chromogen and the no-CSF control. Values were fit to standard curves; standard curves had R2 values of 0.85-0.99. CSF samples were tested blind to Baseline/Day 28. Statistical analyses were conducted by an independent biostatistician. Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 11

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Phase 2a Summary Results - CSF Biomarkers Change from Baseline to Day 28 Neurogranin Nfl T-tau P-tau181 YKL40 IL-6 IL- 1β TNFa -32% -22% -20% -34% -9% -14% -11% -5% * p < 0.0001; + p < 0.001 by paired t-test Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 12

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Slight Increase in CSF Amyloid-beta (Aβ42) Levels of CSF Aβ42 (pg/mL) CSF concentration (pg/mL) Screening Day 28 Note: Low CSF levels of Aβ42 indicates Alzheimer's disease. Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 13

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Phase 2a Biomarkers – CSF vs. Plasma Change from Baseline to Day 28 T-tau 4% 8% NfL Neurogranin YKL40 -20% -16% Aβ42 -22% -11% -32% -41% -9% -4% CSF Plasma * p < 0.0001; + p < 0.001 Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 14

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CSF Biomarkers – Individual Patient Responses CSF (pg/mL) Neurofilament Light Chain Phospho-tau(T181) CSF (pg/mL) Total tau Aβ42 YKL40 Screening Day 28 Screening Day 28 Screening Day 28 0 200 400 600 800 1000 1200 0 100 200 300 400 500 600 700 800 0 2 4 6 8 10 12 0 100 200 300 400 500 0 50 100 150 200 250 300 350 400 450 0 10 20 30 40 50 60 70 80 90 Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 15

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CSF Cytokines – Individual Patient Responses CSF concentration (pg/mL) IL-6 IL-1β TNFa CSF concentration (pg/mL) 0 5 10 15 20 25 0 10 20 30 40 50 60 0 5 10 15 20 25 30 35 40 45 Screening Day 28 Screening Day 28 Screening Day 28 Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 16

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Plasma Biomarkers – Individual Patient Responses Plasma (pg/mL) Plasma (pg/mL) Plasma Neurogranin Plasma Neurofilament Light Chain Plasma P-tau(T181) by immunoblot Plasma Total Tau Plasma Aβ42 Plasma YKL40 0 20 40 60 80 100 0 10 20 30 40 50 60 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0 10 20 30 40 50 60 70 80 26 27 28 29 30 31 32 33 34 35 36 50 55 60 65 70 75 Screening Day 28 Screening Day 28 Screening Day 28 Screening Day 28 Screening Day 28 Screening Day 28 Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 17

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P-Tau and Nitrated Tau Reduced in Plasma Reductions in Tau, P-tau and N-tau: Baseline to Day 14 & Day 28 IP: Anti-Tau Dosing days: 0 14 28 0 14 28 28 14 0 70- 100- 70- 100 70- 100- 70- 100- 70- 100 IB nY29Tau pT21Tau pT181Tau pS202Tau Tau Relative to Day 0 Tau level 0 0.4 0.8 1.2 Dosing days 0 14 28 Tau pS202Tau pT181Tau pT231Tau nY29Tau * p < 0.001 Baseline vs. Day 28 Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 18

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Phase 2a Clinical Trial of PTI-125 I. Background II. Clinical Results III. Mechanism of Action IV. Conclusions Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 19

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Altered FLNA links to α7-nicotinic acetylcholine receptor Aβ42 binds α7nAChR with femtomolar affinity. Altered FLNA linkage to α7nAChR enables Aβ42 signaling through α7nAChR to hyperphosphorylated tau. Altered FLNA Aβ42 a7nAChR ERK/JNK1 Hyperphosphorylated tau and destabilized microtubule Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 20

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Altered FLNA links to α7-nicotinic acetylcholine receptor Aβ42 binds α7nAChR with femtomolar affinity. Altered FLNA linkage to α7nAChR enables Aβ42 signaling through α7nAChR to hyperphosphorylated tau. PTI-125 binds altered FLNA, restores its normal shape, stops Aβ42 signaling and tau hyperphosphorylation. Aβ42 α7nAChR PTI-125 Stable microtubule FLNA, shape restored Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 21

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Altered FLNA links to Toll-like Receptor 4 (TLR4) Altered FLNA linkage to TLR4 enables Aβ42 to activate TLR4. Persistent TLR4 activation results in chronic neuroinflammation. Aβ42 MD2 MD2 CD14 Co-receptor TLR4 Altered FLNA Inflammatory cytokine release Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 22

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Altered FLNA links to Toll-like Receptor 4 (TLR4) Altered FLNA linkage to TLR4 enables Aβ42 to activate TLR4. Persistent TLR4 activation results in chronic neuroinflammation. PTI-125 binds altered FLNA, restores its normal shape, stops Aβ42 signaling and neuroinflammation. Aβ42 MD2 MD2 CD14 Co-receptor TLR4 FLNA PTI-125 Inflammatory cytokine release Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 23

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Target Engagement & Mechanism of Action Evidence in patient lymphocytes from Day 0 to 14 to 28 by three methods: i. Reversal of altered conformation of FLNA Assessed by isoelectric focusing point ii. Reduced FLNA linkages to α7nAChR and TLR4 Assessed by co-immunoprecipitation iii. Reduced Aβ42 complexed with α7nAChR and CD14 Assessed by co-immunoprecipitation Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 24

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FLNA’s Native Shape Restored in Patient Lymphocytes pl 3.5- 4.2- 4.5- 5.3- 6.0- 6.9- 8.0- 9.5- Dosing days: 0 14 28 0 14 28 0 14 28 Percentage of Total 0% 25% 50% 75% 100% 0 14 28 pl:5.9 pl:5.3 * p < 0.0001 vs. pI 5.9; # p < 0.0001 vs. Day 0;+ p < 0.0001 vs. Day 14 Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 25

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FLNA Linkages to α7 and TLR4 Reduced in Lymphocytes IP: Anti-FLNA 250- 55- 70- 100- 130- 250- 55-70- 100- 130- 250- IB TLR4 a7nAChr FLNA Aβ42 Dosing days: 0 14 28 0 14 28 Relative to FLNA 0 0.25 0.5 0.75 Aβ42 (0.1) Dosing days: 0 14 28 0 14 28 TLR4 a7nAChr * p < 0.001 vs. Day 0; + p < 0.01, ++ p < 0.05 vs. Day 14 Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 26

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Aβ42 Bound to α7nAChR or CD14 Reduced in Lymphocytes IP: Anti- Aβ42/-Actin 55- 35- 55- 70- 100- 130- 35- 55- 70- 100- 130- Aβ42 Dosing Days 0 14 28 0 14 28 IB CD14 a7nAChR β-Actin Relative to β-Actin 0 0.25 0.5 0.75 Aβ42 (0.1) Dosing days: 0 14 28 0 14 28 a7AChr CD14 * p < 0.001 vs. Day 0; + p < 0.01, ++ p < 0.05 vs. Day 14 Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 27

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Phase 2a Clinical Trial of PTI-125 I. Background II. Clinical Results III. Mechanism of Action IV. Conclusions Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 28

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Summary of PTI-125 Effects Validated CSF biomarkers of AD pathology improved in all patients treated with PTI-125: Reduced post-synaptic damage: Reduced tau: Reduced axonal degeneration: Reduced neuroinflammation: Neurogranin -32% Total tau -20%, P-tau -34% Neurofilament light chain -22% YKL40, IL-6, IL-1β, TNFα reduced 5-14% Consistent improvements in biomarkers across CSF, plasma and lymphocytes. PTI-125 at 100 mg b.i.d. for 28 days appeared to slow the rate of neurodegeneration and suppress neuroinflammation,  consistent with the drug’s mechanism of action and preclinical data. Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 29

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Phase 2a data are….. Promising because: PTI-125 improved all biomarkers of AD pathology,  neurodegeneration and neuroinflammation. Consistent effects across CSF, plasma, lymphocytes All patients responded to PTI-125 Drug was safe and well-tolerated Clinical results are consistent with PTI-125’s mechanism of action and > 10 years of basic science. Biomarker data imply disease-modifying effects. Viewed conservatively because: Treatment was open-label. The number of patients is small. Dose-response remains undefined. Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 30

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Conclusions This first-in-patient study of PTI-125, a new drug candidate, demonstrated: Evidence of target engagement and mechanism of action in AD patients Significant improvements in biomarkers of AD Clinical validation for FLNA as a target for AD drug development These data highlight PTI-125’s potential as a disease-modifying drug therapy for Alzheimer’s disease. Clinical results are being confirmed in an ongoing 60-patient, blinded, randomized, placebo-controlled clinical trial. Cassava Sciences COPYRIGHT © Cassava Sciences, Inc. 2019 31

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Cassava Sciences Announces Additional Positive

Phase 2a Clinical Data in Alzheimer’s Disease

at CTAD 2019



- New Data Shows Clinical Evidence of Target Engagement and Target Validation –



- Company Expects Data Publication in a Peer-reviewed Medical Journal –







AUSTIN, Texas – December 5, 2019 – Cassava Sciences, Inc. (Nasdaq: SAVA), a clinical-stage biopharmaceutical company focused on Alzheimer’s disease, today announced additional clinical data from a Phase 2a study of PTI-125, its investigational drug candidate for Alzheimer’s disease.  Company scientists presented the new data during a late-breaking oral presentation today at the 12th International Conference on Clinical Trials on Alzheimer’s Disease (CTAD),  in San Diego, Ca.    



Consistent with over 10 years of basic research and pre-clinical data, the new data show clinical evidence of PTI-125’s mechanism of action and drug-target engagement, including:





Cassava Sciences expects to publish a manuscript of these new clinical data in a peer-reviewed medical journal.





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“Today’s data milestone is exciting because it provides additional support for the clinical benefits of slowing down both neurodegeneration and neuroinflammation in patients with Alzheimer’s,” said Remi Barbier, President & CEO of Cassava Sciences. “We’re eager to gain more insight on the effects of PTI-125 in Alzheimer’s after we conclude, in 2020, an on-going Phase 2b study.”



Details of CTAD Presentation:

Title: “One-Month Oral Treatment With PTI-125, A New Drug Candidate, Reduces CSF and Plasma Biomarkers of Alzheimer’s Disease.”





The CTAD presentation is available on-line at CassavaSciences.com under the ‘Investors’ page.    



PTI-125 targets both neurodegeneration and inflammatory components of Alzheimer’s disease. As previously reported, in a Phase 2a study funded by the National Institutes of Health (NIH), open-label treatment with PTI-125 for 28 days significantly improved key CSF biomarkers of Alzheimer’s pathology, neuroinflammation and neurodegeneration (p<0.001).



Cassava Sciences is now evaluating PTI-125 in a confirmatory Phase 2b study.  This blinded, randomized, placebo-controlled, multi-dose study is enrolling approximately 60 patients with mild-to-moderate Alzheimer’s disease.  The primary endpoint is improvement in biomarkers of Alzheimer’s disease from baseline to Day 28. Top-line study results are expected in 2020.   



About PTI-125

The target of PTI-125 is an altered form of filamin A (FLNA), a scaffolding protein. Published studies have shown that altered FLNA in the brain disrupts the normal function of neurons, leading to Alzheimer’s pathology, neurodegeneration and neuroinflammation. Cassava Sciences’ lead drug candidate, PTI-125, is a small molecule that restores the normal shape and function of FLNA in the brain. This action improves the function of certain receptors in the brain, which slows neurodegeneration and exerts powerful anti-neuroinflammatory effects.

 

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Cassava Sciences is also developing an investigational diagnostic to detect Alzheimer’s disease with a simple blood test. This program, called PTI-125Dx, also receives significant scientific and financial support from NIH.



The underlying science for Cassava Sciences’ programs in neurodegeneration is published in prestigious peer-reviewed technical journals, including Journal of Neuroscience,  Neurobiology of Aging, and Journal of Biological Chemistry. As previously announced, NIH has awarded Cassava Sciences two research grants following an in-depth, confidential review of its science and technology. These two grant awards represent up to $6.7 million of non-dilutive financing.



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 will develop Alzheimer’s in 2019.  1  The number of people living with Alzheimer’s disease is expected to grow dramatically in the years ahead, which may also result in a growing social and economic burden.  2



About Cassava Sciences, Inc.

The mission of Cassava Sciences is to detect and treat neurodegenerative diseases, such as Alzheimer’s disease.  Over the past ten years, Cassava Sciences has combined state-of-the-art

technology with new insights in neurobiology to develop novel solutions for Alzheimer’s disease. Cassava Sciences owns worldwide development and commercial rights to its research programs in Alzheimer’s disease, and related technology, without royalty obligations to any third-party.









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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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Acknowledgment and Disclaimer: Research reported in this press release was supported by the National Institute of Aging of the NIH under award AG060878. The content is solely the responsibility of Cassava Sciences and does not necessarily represent the official views of NIH.





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 Phase 2 clinical studies; the interpretation of clinical results, including potential health benefits, if any, of changes in levels of biomarkers; commentaries made by Cassava Sciences’ employees; and other 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 trials on expected timelines, to demonstrate the specificity, safety, efficacy or potential health benefits of our product candidates 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, 2018 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 any forward-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 at www.sec.gov.





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