Skye Bioscience, Inc. · NASDAQ:SKYE
Skye Bioscience — Investor Presentation (January 2024)
71 slides from Skye Bioscience's investor presentation, January 2024
Slide 1: Unlocking the Pharmaceutical Potential of the Endocannabinoid System
Unlocking the Pharmaceutical Potential of the Endocannabinoid System January 2024
Slide 2: Disclaimer and Important Information for Investors
Disclaimer and Important Information for Investors This investor presentation (“Presentation”) has been prepared solely for general information purposes by or on behalf of Skye Bioscience, Inc. (together with its subsidiaries and affiliates, “Skye”). This Presentation is for informational purposes o
Slide 3: Skye is Building an Endocannabinoid Pharmaceutical Company
Skye is Building an Endocannabinoid Pharmaceutical Company Our Mission To pioneer and lead the development of new medicines that unlock the pharmaceutical potential of the endocannabinoid system, initially through modulation of the CB1 receptor, to advance the standard of care and treatment alternat
Slide 4: Convergence of Right Space, Technology and Team
Convergence of Right Space, Technology and Team Endocannabinoid system is a renewed area of interest. ENDOCANNABINOIDS Two Phase 2 differentiated, endocannabinoid-system-targeting drugs in development. Supported by 5AM Ventures, Versant, GSK other dedicated life science investors in Bird Rock Bio (a
Slide 5: CB1: High-potential Target for Physiological Regulation
CB1: High-potential Target for Physiological Regulation CB1 is involved in many disease processes • CB1 (cannabinoid receptor 1) is a renewed target of Inflammatory interest for drug discovery. • Modulation of CB1 signaling can impact key biological processes including: • Inflammatory, metabolic, fi
Slide 6: Leadership
Leadership Contributed to commercialization of 47+ drugs/diagnostics, led high-value strategic transactions and co-founded multiple companies Executive Management Board of Directors Punit Dhillon Tu Diep, MSc Andy Schwab Deborah Charych, PhD Keith Ward, PhD CEO & Chair of BOD Chief Development Offic
Slide 7: Endocannabinoids: A Renewed Drug Development Frontier
Endocannabinoids: A Renewed Drug Development Frontier ECS (endocannabinoid system) receptors help modulate and maintain homeostasis of physiological functions. Over- or under-activation of these receptors is involved in an array of diseases Notable ECS Transactions Company Acquirer Deal Value Lead A
Slide 8: Nimacimab
Nimacimab Novel CB1-targeting mAb therapeutic for cardiometabolic conditions: peripheral CB1 inhibitor MOA Disease R&D Phase 1 Phase 2 CB1 Receptor Inhibitor Obesity & Chronic Kidney NIMACIMAB Sub-cutaneous Disease Phase 2-ready molecule with open IND for obesity/weight loss. Best–in-class Monoclona
Slide 9: Key Milestones Position Skye for Near Term Value Generation
Key Milestones Position Skye for Near Term Value Generation Multiple data catalysts across two key programs through end of 2024 2024 2025 Activity Q1 Q2 Q3 Q4 Q1 Q2 Q3 Q4 NIMACIMAB Obesity/CKD Phase 2 Ph. 2 Ph. 2 interim data topline data SBI-100 OE Glaucoma1 Phase 2a (US) Phase 2b (US) Ph. 2a Ph. 2
Slide 10: Broad Metabolic Potential With Clinically Validated Mechanism of Action
Nimacimab Broad Metabolic Potential With Clinically Validated Mechanism of Action 10
Slide 11: Nimacimab: Differentiated Therapeutic in Obesity
Nimacimab: Differentiated Therapeutic in Obesity Upregulation of CB1 signaling is involved in multiple inflammatory, fibrotic and metabolic diseases in various organs with significant prevalence and unmet needs CB1 Nimacimab Key Differentiators 1 Target clinically validated Adipose Tissue Kidneys Li
Slide 12: The Promise of CB1 Inhibition
The Promise of CB1 Inhibition Clinically validated MOA Rimonabant RIO-lipids Phase 3 study placebo (n=342); 5 mg rimonabant (n=345); \20 mg rimonabant (n=346) Rimonabant (Accomplia) developed by Sanofi and approved for weight loss in 2006 in EU Demonstrated up to 10% weight loss over 1 year Improvem
Slide 13: Rimonabant in the Periphery: Metabolic Benefits Beyond Caloric Restriction
Rimonabant in the Periphery: Metabolic Benefits Beyond Caloric Restriction Study highlights impact of peripheral CB1 inhibition Central Inhibition Only Global Inhibition 6/7 6/7 Using a DIO model with a specific vehicle arm to control for the anorexigenic effect (hashed bars = vehicle-pf) by matchin
Slide 14: 2nd Generation Peripherally Restricted CB1 Inhibitors Remain Efficacious
2nd Generation Peripherally Restricted CB1 Inhibitors Remain Efficacious Peripherally restricted CB1 inhibitors reduce food intake and body weight (DIO model) comparable to non-restricted CB1 inhibitors Peripheral CB1 inhibitors mediate reduction in fat mass but not lean mass Insulin Sensitivity Lep
Slide 15: Peripheral CB1 Receptors and Fat Metabolism
Peripheral CB1 Receptors and Fat Metabolism Blocking CB1 potentially triggers metabolic reprogramming in adipose tissues, mediating conversion of white adipose tissue to beige adipose tissue CB1R WAT • The ECS is deeply involved in controlling energy metabolism. x • CB1 is highly expressed in adipos
Slide 16: Targeting Obesity Comes in Different Flavors
Targeting Obesity Comes in Different Flavors CB1 impacts key metabolic pathways that complement existing products & strategies KEY TARGETS / MECHANISMS Key Targets Characteristics GLP-1 GIP Glucagon CB1 Decreases Appetite / Increases Satiety ✓ ? (limited) x ✓ Opportunities for Nimacimab Delays Gastr
Slide 17: Preclinical Rationale for Combination of CB1 and GLP-1
Preclinical Rationale for Combination of CB1 and GLP-1 Complementary pathways may provide additive therapeutic effects for GLP-1 agonists CB1 and GLP-1-dependent caloric restriction Increased insulin sensitivity with Significant weight loss with combination +/- Rimonabant CB1 inhibition CB1 KO mice
Slide 18: Preclinical Strategy to Evaluate Key Opportunities
Preclinical Strategy to Evaluate Key Opportunities Skye’s human CB1 transgenic mouse: critical tool to model obesity and nephropathy Human CB1 knockin mice (C57BL/6) Obese Mice HFD: 8-10 weeks STZ: 8-10 weeks Diabetic Mice Q: Can peripheral CB1 blockade mediate weight loss comparable Q: Can peripher
Slide 19: Phase 1 Clinical Data and Phase 2 Update
Nimacimab: Development Plan for Obesity and Chronic Kidney Disease Phase 1 Clinical Data and Phase 2 Update
Slide 20: Nimacimab Biodistribution
Nimacimab Biodistribution Little to no accumulation in the brain Day 1 Day 8 Day 15 Cyno (post 1st dose) (post 2nd dose) (post 3rd dose) Little to no nimacimab found in CSF/Serum 3 mg/kg IV q1w BLQ <0.02% <0.02% the brain High levels of nimacimab found Level in CSF determined Cyno 9 hours using quan
Slide 21: Nimacimab Toxicology – NOAEL > 75 mg/kg
Nimacimab Toxicology – NOAEL > 75 mg/kg Safe with significant safety window established • IND-enabling toxicology study completed with up to 75 mg/kg nimacimab administered weekly IV for 4 weeks. • No nimacimab-related observations in toxicology assessments performed including neurological observati
Slide 22: Nimacimab Phase 1 Data
Nimacimab Phase 1 Data Demonstrated encouraging tolerability, pharmacokinetics and encouraging evidence of efficacy Phase 1 SAD in Healthy Volunteers and MAD in NAFLD (diabetic/pre-diabetic) • SAD • 24 patients enrolled (18 patients used as PK population) • 0.6 mg/kg, 1.2 mg/kg and 2.5 mg/kg adminis
Slide 23: Nimacimab Bioavailability Study
Nimacimab Bioavailability Study Intravenous versus subcutaneous dosing Study Design • Single 100 mg SC dose vs. single 100 mg IV dose of nimacimab • 10 subjects dosed SC vs. 10 subjects with IV Conclusions • Absolute bioavailability approximately 60% after a single dose • No new trends in safety par
Slide 24: Chronic Kidney Disease in Obesity
Chronic Kidney Disease in Obesity ~30% of obese patients have CKD; >80% of CKD patients are overweight/obese Chronic Kidney Disease (CKD) in Obesity More than 1 in 7 US adults have CKD; obesity is one of leading Obesity Population causes • Patients who develop CKD are at risk of build-up of toxic wa
Slide 25: Proposed Phase 2 Clinical Trial Design: Obesity and Diabetic Kidney Disease
Proposed Phase 2 Clinical Trial Design: Obesity and Diabetic Kidney Disease Key Inclusion Criteria Primary Endpoint Secondary Endpoint • Obese: BMI ≥ 30 kg/m2 • Change in weight from baseline • Change in UACR, UPCR and eGFR • Overweight: BMI ≥ 27 and < 30 kg/m2 from baseline • UACR ≥ 200 mg/g • Expl
Slide 26: Multiple Shots on Goal: Metabolic Data Points from Phase 2 Design
“Multiple Shots on Goal”: Multiple Metabolic-Related Data Points from Phase 2 Design Obesity Chronic Kidney Disease Other Biomarkers of Metabolic Disorder • Changes in weight loss • Changes in eGFR • Markers of inflammation • Changes in muscle wasting • Changes in UACR and UPCR • Markers of fibrosis
Slide 27: Metabolic Diseases Indications and Usage By Drug Class
Metabolic Diseases Indications and Usage By Drug Class Potential for targeting obesity and diabetic kidney disease as an indication ACEi ARB SGLT2 MRA GLP-1 CB1 Ozempic / Lotensin Avapro Jardiance Farxiga Invokana Kerendia Mounjaro INV-202 Wegovy CKD * * * / Phase 3 Phase 3 Phase 3 Phase 2*
Slide 28: Challenges Associated with Long-Term Use of GLP-1 RA Treatment
Challenges Associated with Long-Term Use of GLP-1 RA Treatment Plateau and rebound effect Considerations of Long-term Treatment with GLP-1 Receptor Agonists STEP 5: Durability of Weight-loss Over 2 Years STEP 1 Trial Extension: Withdrawal of Semaglutide Garvey et al., Nat Med. 2022 Wilding et al., D
Slide 29: GLP-1 RA Effects on Muscle Wasting
GLP-1 RA Effects on Muscle Wasting Opportunities for improvement Clinical Data Ongoing Collaborations • As the FDA has not required body composition as a primary endpoint in weight loss • Lilly and Bioage Labs announced a collaboration (Oct 2023) studies, data surrounding GLP-1’s effect on lean body
Slide 30: Nimacimab Clinical Development Summary
Nimacimab Clinical Development Summary Broad metabolic potential • Nimacimab has significantly improved peripheral restriction than INV-202. • Potentially better safety. • Nimacimab has potential to treatment multiple metabolic indications • Rimonabant has demonstrated clinical efficacy in obesity.
Slide 31: Significant Unmet Needs in Glaucoma with Opportunity for New Class of Medicine
SBI-100 OE Significant Unmet Needs in Glaucoma with Opportunity for New Class of Medicine
Slide 32: SBI-100 Ophthalmic Emulsion
SBI-100 Ophthalmic Emulsion Improving CB1-targeting drug design for glaucoma MOA Disease R&D Phase 1 Phase 2 CB1 Receptor Agonist SBI-100 OE Glaucoma Topical Best–in-class Molecule First/only prodrug of THC developed and currently in the clinic for glaucoma. Clear Clinical Endpoint Lowering intraocu
Slide 33: Targeting Glaucoma (POAG & OH): Large Market, Unmet Needs
Targeting Glaucoma (POAG & OH): Large Market, Unmet Needs World’s leading cause of irreversible blindness $7B drug market worldwide MARKET LACKS INNOVATION Predominantly using legacy classes of drugs and generic compounds. ~60M patients worldwide 1% ROCK Inhibitor 7% ~110M patients by 2026 Carbonic
Slide 34: CB1 Agonism as New Therapeutic Class to Treat Glaucoma
CB1 Agonism as New Therapeutic Class to Treat Glaucoma Reduced IOP and associated mechanisms suggest potential for a novel therapeutic • Research with THC and other CB1 agonists have highlighted relevant mechanisms CB1 is expressed in key ocular tissues and its engagement1: to support the use of can
Slide 35: SBI-100 Ophthalmic Emulsion: Synthetic THC-based Prodrug
SBI-100 Ophthalmic Emulsion: Synthetic THC-based Prodrug Prodrug technology and novel formulation addresses hurdles with THC therapeutics DESIGN FACTOR RATIONALE SBI-100 STRUCTURE Therapeutic backbone is not water soluble Tetrahydrocannabinol (THC) and has poor bioavailability. Improves solubility,
Slide 36: Clinical Trial Design– SAD/MAD Randomized Placebo-Controlled
Clinical Trial Design– SAD/MAD Randomized Placebo-Controlled • Randomized, placebo-controlled study in up to 48 healthy volunteers across 6 treatment cohorts. • Primary objective: establish safety and tolerability of single ascending and multiple ascending doses of SBI-100 Ophthalmic Emulsion relati
Slide 37: Pharmacokinetics – Little to no Exposure of THC in Plasma
Pharmacokinetics – Little to no Exposure of THC in Plasma MAD PK population 0.5% SBI-100 1.0% SBI-100 2.0% SBI-100 N=6 N=6 N=6 Day 1 PK Parameters, Mean (SD) AUC (h*ng/mL) SBI-100 0.9184 (0.4252) 0.8252 (0.2533) 2.131 (1.139) Cmax (ng/mL) SBI-100 0.2742 (0.07336) 0.2973 (0.1103) 0.7202 (0.3403) Day
Slide 38: SBI-100 OE Demonstrates Significantly Less Hyperaemia Compared to Other Therapies
SBI-100 OE Demonstrates Significantly Less Hyperaemia Compared to Other Therapies Hyperaemia has notable impact on patient adherence to drug regimen Incidence of hyperaemia in currently approved drugs vs. SBI-100 OE Latanoprost 16.5% Travoprost 33% Rhopressa SBI-100 OE Bimatoprost 53% <10% 40% 10% 2
Slide 39: MAD Day 5 – Discomfort is Transient and Quickly Resolves
MAD Day 1 & 5 – Discomfort is Transient and Quickly Resolves Day 1 (am) Day 1 (pm) 100 100 Level of Discomfort Level of Discomfort None Discomfort Score None Discomfort Score Mild Mild Moderate 50 Moderate 50 Severe Severe 0 0 Post-Dose 15 min Post-Dose 15 min Post-Dose 15 min Post-Dose 15 min Post-
Slide 40: Intraocular Pressure Analysis – Full Population
Intraocular Pressure Analysis – Full Population Low baseline IOP across all subjects • Historically, glaucoma drugs do not significantly reduce IOP in healthy volunteers • Participants receiving placebo and active had similar reductions in IOP. • This is potentially due to the lower baseline IOP mea
Slide 41: Subgroup Analysis 1 – High IOP
Subgroup Analysis1 – “High IOP” • Because of the relatively low mean baseline IOP in this healthy volunteer population, we did not see any significant reductions in IOP when evaluating active against placebo. • A subgroup analysis of participants with “high” baseline IOP was evaluated. • We evaluate
Slide 42: SBI-100 OE Phase 1 Safety Profile/Data Summary
SBI-100 OE Phase 1 Safety Profile/Data Summary Good Safety Profile: Generally safe and well-tolerated. No participants dropped out due to SBI-100 OE. Transient Discomfort: Main side effect is discomfort/pain upon drop instillation, but average duration of discomfort was less than 15 minutes. Lack of
Slide 43: SBI-100 OE Phase 2 Glaucoma Proof-of-Concept Study
SBI-100 OE Phase 2 Glaucoma Proof-of-Concept Study Primary open-angle glaucoma and ocular hypertension Key Inclusion Criteria 4 Weeks 14 Days 21mmHg ≥ IOP < 34mmHg Screening Dosing Safety Follow-up No prior surgical interventions for Double-masked, POAG or OHT placebo-controlled Cohort 1 0.5 % BID P
Slide 44: Summary
Summary
Slide 45: Skye Next Steps
Skye Next Steps • Advance nimacimab clinical trials with longer-term view toward franchise expansion • Achieve SBI-100 Ophthalmic Emulsion/glaucoma proof-of-concept milestone • Maintain focused operational and clinical development strategy • Selectively evaluate business development opportunities to
Slide 46: Capitalization
Capitalization Cap Table1 Top Holders4 Common shares o/s 12.3 M 5 AM Ventures 37% Options and RSUs 0.5 M Versant Ventures 16% Warrants 3.3 M GSK 6% Convertible note (as-converted basis) 1.0 M Apposite Healthcare Fund LP 6% Common shares f/d 17.1 M Other Inst./Corp. 9% Float2 3.2 M Total 74% Cash & C
Slide 47: Thank you
Thank you Learn more, please contact: ir@skyebioscience.com, +1 (858) 410-0266
Slide 48: Appendix – Nimacimab Supplemental Slides
Appendix – Nimacimab Supplemental Slides
Slide 49: Some CNS Exposure with Small Molecule 2nd Generation CB1 Inhibitors
Some CNS Exposure with Small Molecule 2nd Generation CB1 Inhibitors Since the demise of rimonabant, multiple groups have tried to develop new CB1 inhibitors that are peripherally restricted Most are small molecules and also inverse agonists similar to rimonabant However, even current lead 2nd genera
Slide 50: CB1 Up-regulation is Associated with Human Kidney Disease
CB1 Up-regulation is Associated with Human Kidney Disease Patient biopsies in IgAN, nephritis and diabetic nephropathy demonstrate increased CB1 • Elevated CB1 expression was found in tubules, interstitial cells and podocytes in diabetic patients • Elevated CB1 expression was found in mesangial cell
Slide 51: CB1 Contributes to Obesity-induced Kidney Disease
CB1 Contributes to Obesity-induced Kidney Disease CB1 knockout mice protected from renal dysfunction, fibrosis and inflammation • Obesity-related structural and functional changes in the kidney develop early in the course of obesity and occur independently of hypertension, diabetes, and dyslipidemia
Slide 52: Nimacimab: Powerful Negative Allosteric Modulating Antibody for CB1
Nimacimab: Powerful Negative Allosteric Modulating Antibody for CB1 Nimacimab is effective at inhibiting CB1 signaling; similar antagonist activity to rimonabant • Cisbio’s competitive cAMP assay was used to quantify nimacimab’s antagonist activity • RYI-018 (nimacimab) compares favorably to neutral
Slide 53: Peripheral CB1 Receptors and Appetite Hormones
Peripheral CB1 Receptors and Appetite Hormones CB1modulates the activity of key appetite-regulating hormones leptin, ghrelin, and CCK Increases release of cholecystokinin (CCK) Increases sensitivity of leptin in the brain Reduces ghrelin secretion from the stomach • CCK release inhibited by CB1 acti
Slide 54: Comparison of Key Mechanism with CB1 and GLP-1 Therapeutics
Comparison of Key Mechanism with CB1 and GLP-1 Therapeutics Overlapping as well as unique mechanisms provide a rationale for differentiation GLP-1R Agonist CB1 Inhibitor • Incretin released by L cells in the small intestine following food ingestion and is rapidly degraded by DPP-4; ~15% of secreted
Slide 55: Peripheral CB1 Antagonism Reverses Fully Developed Diabetic Nephropathy
Peripheral CB1 Antagonism Reverses Fully Developed Diabetic Nephropathy • Zucker diabetic fatty (ZDF) rats were treated daily with 3 mg/kg JD5037 (CB1 inhibitor) or vehicle P.O. for 4 weeks • Polyuria, albuminuria, uricosuria, increased plasma and urinary creatinine, and increased plasma levels of a
Slide 56: Preclinical and Clinical Data Demonstrate CB1 Affects Metabolic, Inflammatory and Fibrotic Pathways
Preclinical and Clinical Data Demonstrate CB1 Affects Metabolic, Inflammatory and Fibrotic Pathways Important in the Development of Diabetic Nephropathy Compelling evidence for CB1 blockade in diabetic nephropathy Parameter CB1 Effect Expression in human disease Increased in diabetic nephropathy pat
Slide 57: Competitive Landscape – 2nd Gen CB1 Inhibitors
Competitive Landscape – 2nd Gen CB1 Inhibitors Nimacimab sets itself apart from other CB1 peripherally-targeted agents GOLDFINCH CORBUS INVERSAGO SKYE GFB-024 CRB-913 INV-202 NIMACIMAB Molecule Type Antibody Small Molecule Small Molecule Antibody Allosteric Modulator N/A N/A N/A Inverse Agonist N/A
Slide 58: Appendix – SBI-100 Supplemental Slides
Appendix – SBI-100 Supplemental Slides
Slide 59: Prodrug Strategy Enhances Ocular Biodistribution of THC
Prodrug Strategy Enhances Ocular Biodistribution of THC THC amino dicarboxylic acid prodrugs further enhance bioavailability • Different prodrug strategies were functionally evaluated in vitro and in vivo • Solubility, stability and bioavailability were associated with control of IOP Increased perme
Slide 60: SBI-100 OE Demonstrates Superior IOP Lowering
SBI-100 OE Demonstrates Superior IOP Lowering Nonclinical head-to-head studies highlight favorable comparison with standard-of-care drugs 20 Timolol 25 Latanoprost SBI-100 18 IOP (mmHg) IOP (mmHg) 20 16 Latanoprost SBI-100 Rhopressa 14 SBI-100 + Rhopressa 15 0 3 6 9 0 3 6 9 12 15 18 21 24 Hours Hour
Slide 61: Human Trabecular Meshwork Model Highlights Key Mechanism of Action
Human Trabecular Meshwork Model Highlights Key Mechanism of Action Measuring outflow facility via trabecular meshwork Reduced markers of inflammation & fibrosis • Both human 3D models demonstrated a significant increase • Significant reduction in fibrotic and inflammatory of outflow with SBI-100’s a
Slide 62: Potential Neuroprotective Benefits with SBI-100 OE
Potential Neuroprotective Benefits with SBI-100 OE Additional complementary therapeutic mechanism to potentially address associated neuropathy Biodistribution studies demonstrated the Glaucoma: Without Introduction of THC presence of SBI-100 OE in the back of the eye SBI-100 OE’s active ingredient,
Slide 63: Clinical Biomarker Program to Support SBI-100 OE
Clinical Biomarker Program to Support SBI-100 OE Analyses of immunological and neuroprotective markers in tear and blood components Serum/Tear Analyses • Multiplex proteomics Unlike a typical biomarker program, our • Olink - target 96 inflammation/neurology panels rationale is not to develop patient
Slide 64: Near-term R&D Efforts Support Pipeline Development
Near-term R&D Efforts Support Pipeline Development Glaucoma • Biomarker program: analysis of bio-samples from Ph2 glaucoma clinical trial • Preclinical studies to further SBI-100 development • Combination studies with 1L/2L glaucoma drugs in normotensive and glaucomatous models • Mechanistic studies
Slide 65: Challenges & Unmet Needs in Treating Patients with Glaucoma
Challenges & Unmet Needs in Treating Patients with Glaucoma Achieving and maintaining effective IOP lowering (20-30%) from baseline with existing medications: • Magnitude of IOP reduction is often titrated by disease severity and benefit/risk of desired treatment. • The more severe the disease the m
Slide 66: Key Opportunities for SBI-100 OE
Key Opportunities for SBI-100 OE • Targets the tissue of disease PGA Market Non-PGA Market • Current medications either: – Inhibit aqueous production from the ciliary body: beta- blockers and carbonic anhydrase inhibitors – Increase uveoscleral outflow (secondary physiological outflow): prostaglandi
Slide 67: Current Treatment Paradigm
Current Treatment Paradigm Treatment Paradigm Prostaglandin Depending on data SBI-100 OE could potentially be 1L Selective Laser Analogue (PGA) 1L Trabeculoplasty (SLT) therapy (e.g. latanoprost) PGA + Added Agent Strong safety data and competitive efficacy could secure 2L (Added agents: beta blocke
Slide 68: Current Annual Price of Pharmacologic Products
Current Annual Price of Pharmacologic Products Marketed branded agents for the treatment of glaucoma are priced at <$3 K annually in the U.S. SBI-100 OE: competitive product profile with significant market opportunity Travatan Z (travoprost) Lumigan (bimatoprost) Rocklatan Current Pricing Landscape
Slide 69: 2L+ Pharmacologic Treatment in POAG and OH
2L+ Pharmacologic Treatment in POAG and OH In 2L+, KOLs report adding a pharmacologic treatment (e.g., beta blocker) to the existing PGA regimen Second Line and Beyond (2L+) Pharmacologic Treatment in POAG POAG 2L+ Pharmacologic Utilization by Class • The likelihood of progressing past 1L is directl
Slide 70: Potential Future Treatment Paradigm – SBI-100 OE
Potential Future Treatment Paradigm – SBI-100 OE KOLs expect patients will receive SBI-100 OE in 2L in monotherapy • SBI-100 OE has the potential to be used by some physicians as a first line SLT PGA treatment option, but payor access restrictions are expected to limit 1L use to 1L (sporadically use
Slide 71: Market Analysis Summary
Market Analysis Summary Eye care providers: high level of excitement about CB1 agonist and class of drugs Glaucoma still facing significant unmet need UNMET NEED • Patient adherence, improved second-line therapies, novel mechanisms of action and neuroprotective benefits are seen as key unmet needs i
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