Faron Pharmaceuticals Oy · LSE:FARN
Faron Pharmaceuticals Oy — FY2019 Earnings Presentation
26 slides from Faron Pharmaceuticals Oy's earnings presentation, Mar 20, 2020
Slide 1: Faron Pharmaceuticals Full year 2019 Presentation
Faron Pharmaceuticals (LSE AIM: FARN, NASDAQ Helsinki: FARON) Full year 2019 Presentation 20 March 2020
Slide 2: Disclaimer
DISCLAIMER The contents of this presentation have not been approved by an authorised person within the meaning of Section 21 of the Financial Services and Markets Act 2000 (as amended) ("FSMA"). Reliance on the contents of this presentation for the purpose of engaging in any investment activity may
Slide 3: Faron's pipeline is based on receptors regulating immune responses and vascular dysfunctions
FARON’S PIPELINE IS BASED ON RECEPTORS INVOLVED IN THE REGULATION OF IMMUNE RESPONSES & VASCULAR DYSFUNCTIONS Immuno-Oncology ARDS & Organ protection Clevegen® Traumakine® Clever-1 regulates CD73 controls capillary tissue immune status leakage and escalation of inflammation AOC3 escalates inflammati
Slide 4: Key pipeline highlights – all major goals achieved
KEY PIPELINE HIGHLIGHTS – ALL MAJOR GOALS ACHIEVED (including Post Period-end) Clevegen • Switch in immune cell profiles towards increased immune activation confirmed in cancer patients • Dose optimization part completed with good tolerability at all dosing levels • Down regulation of a range of maj
Slide 5: Key financial & corporate highlights
KEY FINANCIAL & CORPORATE HIGHLIGHTS (including Post Period-end) Financial Successfully raised €15.6m gross (€14.5m net) through several fundraises during 2019 Continued tight cash management into 2020 Cash balance of €7.1m on 31 December 2019 (2018: €4.1m) Operating loss of €13.3m (2018: €2
Slide 6: Turn on your immunity
‘i SP SP ir A & Turn on your immunity F (cievecen f?
Slide 7: Macrophages as generals of anti-tumor immunity
MACROPHAGES AS GENERALS OF ANTI-TUMOR IMMUNITY Pro-tumor (M2) Class switching Anti-tumor (M1) IL-10, TGFβ IL-12, TNF⍺ Low MHCII High MHCII M2 macrophages are ... while M1 macrophages immunosuppressive... are immuno stimulatory T-re T-reg T-reg M CD8+ CD8 CD8 7
Slide 8: How does anti-Clever-1 (FP-1305) work?
HOW DOES ANTI-CLEVER-1 (FP-1305) WORK? Release of cancer cell antigenes (cell death) Antigens FP-1305 Clever-1 V-ATPase complex ANTIGEN MHCII PRESENTATION Anitgen complex Antigen Antibody Early phagosome pH 6.2 H+ - acidification Phagolysosome pH 4.5-5.0 - maturation Lysosome pH 4.5 - proteosomal de
Slide 9: Anti-Clever-1 treatment outperforms anti-PD-1 in mouse lung cancer model
Anti-Clever-1 treatment outperforms anti-PD-1 in mouse lung cancer (LLC) model 9
Slide 10: Phase I/II study expansion plan
PHASE I/II STUDY EXPANSION PLAN Dose selection optimization for Part II & III CRC n=10 (initiated Jan’20) Aim & anticipated findings: • Safety ✔ • Cohort selection • Cohort expansion • Surrogate efficacy ✔ • Initial efficacy • Clinical proof of concept Note: New indications added in green 10
Slide 11: Strong immune switch post Clevegen administration
STRONG IMMUNE SWITCH POST CLEVEGEN ADMINISTRATION These changes coincided with metastasis shrinkage of CRC patient tumours Regulatory T-cells CD4-cells CD8-cells 200% 200% 200% % of CD4+CD25+ cells (% from % from predose % from predose 150% 150% 150% 100% 100% 100% predose) 50% 50% 50% 0% 0% 0% Pre
Slide 12: Clevegen clinical summary
CLEVEGEN CLINICAL SUMMARY • FP-1305 has been well tolerated and demonstrated promising clinical anti- tumour activity with partial responses identified in a heavily pre-treated MSS (microsatellite stable) metastatic colorectal cancer patient (see pictures on the right) and a melanoma patient resista
Slide 13: Clevegen downregulates current immuno-oncology checkpoint targets PD-1, PD-L1, CTLA-4
CLEVEGEN DOWNREGULATES CURRENT IMMUNO-ONCOLOGY CHECK POINT TARGETS PD-1, PD-L1, CTLA-4 Clevegen potentiates cell surface biomarkers that indicate heightened anti-cancer activity • Anti-Clever-1 treatment in cancer patients decreases a broad range of checkpoints including PD-1, PD-L1, CTLA-4, OX40, 4
Slide 14: Clever-1, master regulator of immunity
CLEVER-1, MASTER REGULATOR OF IMMUNITY Anti-Clever-1 treatment downregulates all major checkpoints on T cells Activation Marker Activation Marker * P < 0.05 Activation Marker ** P < 0.01 *** P < 0.001 Conclusion: Clevegen could outperform markers current immune check point treatments (anti-PD-1, P
Slide 15: Focused clinical development strategy initiated with CRC
FOCUSED CLINICAL DEVELOPMENT STRATEGY INITIATED WITH CRC Standalone in solid Indications in MSS mCRC and 1st registration in MSS tumors (MATINS) other solid tumors (last line) mCRC last line Phase I/II MSS Efficacy Registration in MSS Safety mCRC SOC+FP- Phase III MSS mCRC SOC+FP-1305 as 1st line mC
Slide 16: High Clever-1 expression predicts poor prognosis in several tumour types
HIGH CLEVER-1 EXPRESSION PREDICTS POOR PROGNOSIS IN SEVERAL TUMOUR TYPES MAKING THEM IDEAL FOR CLEVEGEN TREATMENT Low-grade glioma Ovarian carcinoma Invasive breast carcinoma Low (n=76) Low (n=164) High (n=74) High (n=163) Survival probability P = 6,7x10-7 P = 0,002 Low (n=301) High (n=298) P = 0,00
Slide 17: Clevegen value drivers
CLEVEGEN VALUE DRIVERS Provides stand-alone or combination therapies to combat cancer Novel mode of action to remove immune suppression around tumours • Targets unique immune switch molecule Clever-1 on the surface of tumour associated type 2 macrophages (TAM-2) • No expected toxicities or abnormali
Slide 18: Next Clevegen steps
NEXT CLEVEGEN STEPS Clevegen: Accelerate MATINS regulatory pathway by • Expanding study sites in Europe and US for Part II and III (cohort expansions) • Accelerate expansion cohorts, initiated with CRC • Expanding clinical indications to other expansion cohorts • Seeking regulatory end of phase II a
Slide 19: Interferon-beta treatment of ARDS and other ischaemic reperfusion injuries
INTERFERON-BETA TREATMENT OF ARDS AND OTHER ISCHAEMIC REPERFUSION INJURIES
Slide 20: Acute respiratory distress syndrome (ARDS)
ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) A leading driver of mortality in influenza, pneumonia, sepsis, and major trauma ARDS is an inflammatory lung injury leading to vascular leakage filling the lungs with fluid – “drowning from within” The burden of ARDS • Over 300,000 cases annually in EU & US
Slide 21: Phase I/II proof of concept trial results
PHASE I/II PROOF OF CONCEPT TRIAL RESULTS Reduction in ICU stay from 28 to 16 days, less need for dialysis between groups Primary endpoint: significant drop in mortality1 Traumakine® treated (n=37, APACHE II of 22) Mortality 8% P = 0.01 (28 day) Control group, standard treatment (n=59, APACHE II of
Slide 22: Phase III trial (INTEREST study): design & results
PHASE III TRIAL (INTEREST STUDY): DESIGN & RESULTS Multi center, double blind, 1:1 randomized, pan-European trial1,2 N=301 (296 dosed) FP-1201-lyo 10 μg Eligible patients • ≥18 years All-cause All-cause Primary FDA required Dosing • Receiving regimen analysis: endpoint: mortality mortality mechanica
Slide 23: Concomitant corticosteroid use increases mortality
CONCOMITANT CORTICOSTEROID USE INCREASES MORTALITY Post hoc propensity-matched analysis of INTEREST trial data base of the active arm(1) Patients without concomitant steroid use Patients with concomitant steroid use(1) (1) Steroids reduce the efficacy of Traumakine by reducing its inferior-beta acti
Slide 24: Future Traumakine steps
FUTURE TRAUMAKINE STEPS Traumakine: Finalising next steps • Finalise new study plans post FDA acceptance • Initiate preparations for pilot INTEGRITY part • Study initiation post external funding • Continue interactions with key ICU opinion leaders to minimize corticosteroid use in ARDS patients • Se
Slide 25: Key investment highlights
KEY INVESTMENT HIGHLIGHTS 1 • Advancing promising first-in-class immuno-oncology program, Clevegen, which appears to reactivate the Lead IO Program, Clevegen immune system against immunosuppressive tumors (FP-1305), is Potentially • Clevegen targets CLEVER-1 positive Tumor-associated Macrophages (TA
Slide 26: Thank You
Thank You “Our world is built on biology. Once we begin to understand our biology, it then becomes a technology” Footnotes