Biovie Inc. · NASDAQ:BIVI

Biovie — 2023 Clinical Trials on Alzheimer's Disease (CTAD) Conference

15 slides from Biovie's conference presentation, Oct 24, 2023

  1. Slide 1: Clinical Outcomes From a Phase 3 Trial of NE3107 in Alzheimer's Disease

    Clinical Outcomes From a Phase 3, Randomized, Placebo-Controlled Trial of NE3107 in Subjects With Mild to Moderate Probable Alzheimer's Disease Christopher L. Reading1, Clarence Ahlem1, Joseph M. Palumbo1, Nily Osman1, Marcia A. Testa2, Donald C. Simonson3 1BioVie Inc., Carson City, Nevada, USA; 2De

  2. Slide 2: Disclosures

    Disclosures This study was funded by BioVie Inc. MAT has received grant support from BioVie Inc. CLR, CA, JMP and NO are employees of BioVie Inc. DCS has nothing to disclose. 1

  3. Slide 3: NE3107: an oral, BBB-permeable small molecule and insulin sensitizer

    NE3107: an oral, BBB-permeable, small molecule that inhibits ERK, NF-κB, and TNF-α signaling and acts as an insulin sensitizer1  In a placebo-controlled phase 2a PD study5: NE3107 was associated with: • Improved levodopa activity • Sleep ADAS-Cog11, 11-item cognitive subscale of the Alzheimer’s Dis

  4. Slide 4: NM101 trial (NCT04669028): NE3107 in mild to moderate AD

    NM101 trial (NCT04669028): NE3107 in patients with mild to moderate AD Phase 3 Placebo-controlled 40 weeks Safety, tolerability, and efficacy Double-blind Multicenter Probable AD NE3107 dosing key NE3107 (BID; 12 hours apart) 5 mg 1:1 Active Treatment, 30 weeks Safety follow-up 10 mg 20 mg N=400 Pla

  5. Slide 5: Study endpoints

    Study endpoints Efficacy assessments: Co-primary endpoints – change from baseline to treatment completion (week 30) • Cognitive impairment and global change: ADAS-Cog12 and ADCS-CGIC Secondary endpoints – change from baseline to treatment completion (week 30) • Neurocognitive functioning: MMSE, ADCO

  6. Slide 6: Disclosures regarding current data analyses

    Disclosures regarding current data analyses  Data presented in the following slides are based on evaluable blinded data as of October 18, 2023  Data for Adiponectin, Leptin, p-Tau 217, NfL, GFAP and DNAm are pending  The blinded analyses presented in these slides do not necessarily imply a treatm

  7. Slide 7: Consistent population changes from baseline

    Consistent population changes from baseline (cfb) Blinded data ADAS-Cog12 change Mini-Mental State Exam Clinical Dementia Rating CDR Sum of Boxes AD Composite Score Activities of Daily Living ADCS-clinician global (CDR) change (ADL) change (MMSE) change (CDR SB) change (ADCOMS) change 30 impression

  8. Slide 8: Reduced Amyloid Burden

    ADAS ADL Total Subject # Total CFB CFB Subject # V2 WHOLECFB CINGULATTEMPORA PARIETAL_FRONTAL_LOBE_SUPERIOR_R Subject # V2 WHOLECFB CINGULAT TEMPORA PARIETAL_FRONTAL_ 101-0001 5.33 -9 103-0001 -6 103-0002 4.67 -22 103-0003 2 107-0002 0.67 10 107-0002 1.15 0.02 0.07 -0.09 0.25 0.26 107-0008 -6.34 4 1

  9. Slide 9: Potential evidence of target engagement

    Blinded data Potential evidence of target engagement • Many of the genes associated with Late Onset AD are related to cholesterol metabolism, which is decreased in AD neuron membranes • Insulin and glycemic control are known to be involved in neurodegeneration. Increased Insulin and HOMA2-% β cell f

  10. Slide 10: Imaging sub-study: FDG-PET

    Imaging sub-study: FDG-PET Blinded data • FDG PET was analyzed in 21 evaluable subjects with baseline and week 30 data • Sum of ROIs in regional cortical FDG-PET standard uptake value ratios (SUVR) INCREASED in 10/21 subjects o If unblinded data concur with this, it would also be evidence of target

  11. Slide 11: Imaging sub-study: vMRI

    Blinded data Imaging sub-study: vMRI • vMRI was analyzed in 23 evaluable subjects with baseline and V10 data o Median volumes INCREASED in hippocampus and amygdala vMRI Hippocampus volume vMRI Amygdala volume 400 200 Hippocampus cfb μL Amygdala cfb μL 200 100 0 0 -200 -100 -400 -200 Hippocampus CFB

  12. Slide 12: Neuropsychiatric inventory

    Blinded data Neuropsychiatric inventory Depression Anxiety Irritability Sleep Disorders Appetite Disorders 10 10 10 10 10 Appetite Disorders FxS cfb Sleep Disorders FxS cfb Depression FxS cfb 5 5 5 Irritability FxS cfb 5 5 Anxiety FxS cfb 0 0 0 0 0 -5 -5 -5 -5 -5 -10 -10 -10 -15 -10 -15 -10 Depressi

  13. Slide 13: Decreased TNF-α correlated with improved sleep

    Blinded data Decreased TNF-α correlated with improved sleep Sleep Disorders TNFα 10 2 5 Subjects with improved Sleep disorders Subjects with worsened Sleep disorders vs TNFα vs TNFα 0 1 0.5 Sleep Disorders FxS cfb TNFα CFB pg/mL TNFα cfb pg/mL 0 0 TNFa cfb pg/mL 0.0 -2 -1 -0.5 -5 -2 -3 -1.0 -12 -10

  14. Slide 14: Conclusions

    Conclusions • The study overall had a very low rate of AEs reported and only 10 subjects discontinued due to a reported AE (2.3%, blinded) • There were observed blinded changes between baseline and week 30 for Aβ42/40, and APS • There were observed correlations in the blinded analysis for the cognit

  15. Slide 15: References

    References 1. Reading CL, Ahlem CN, Murphy MF. NM101 phase III study of NE3107 in Alzheimer's disease: rationale, design and therapeutic modulation of neuroinflammation and insulin resistance. Neurodegener Dis Manag. 2021;11(4):289-298. 2. Haroon J, Mahdavi K, Jordan K, et al. Biomarker assessments

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