Treating the root cause

TM
of autoimmune disease

Corporate Presentation
30 January 2023
Executive Summary
Disease modifying, multi-target therapeutics for oral treatment of chronic inflammatory disease

• Clinical stage company, founded in 2016, developing oral, disease-modifying

therapeutics for the treatment of chronic inflammatory disease

• First-in-class immunomodulator in Phase 1b for oral treatment of psoriasis

• Promising Phase 1a results demonstrated superior efficacy, safety and durability of effect

• Phase 1b: Formula optimization in 30 psoriasis subjects is underway, readout in Q1 2023

• Phase 2: Determine PASI & IGA scores in 75 subjects for 6-month treatment; design
reviewed by FDA

• Platform-in-a-product using core drugs plus adjuvants to tailor responses against key
cytokine pathways matched to specific diseases. Focusing on (multi-target responses),
including pro-inflammatory NF-kβ, cytokine signaling (TNF-α, IL-17, IL-23), and
promote expansion of Treg cells which suppress autoimmunity

2
PASI: Psoriasis Area and Severity Index; IGA: Investigator's Global Assessment
Leadership Team
Experienced team with over 40 drugs developed, ten prior exits, and over $600M in prior raises

Ira C. Spector, PhD, MBA

CEO, Co-Founder
James Kirwin, MBA
COO, Head of Clinical Operations

Mark Feitelson, PhD

CSO, Co-Founder
Shawn P. O’Brien
Chairman

Alla Arzumanyan, PhD

CDO, Co-Founder
Rob Dickey, IV
CFO

King Lee, PhD

VP, Regulatory Affairs

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SFA Utilizes a Platform to Regulate Key Immunomodulator Pathways
SFA’s patented platform modulates multiple cellular signaling pathways involved in autoimmune diseases
SFA’s platform matches specific
Short Chain Fatty Acids (bacterial
metabolites engineered as small
molecules) to regulate key
cytokines associated with
specific diseases. We are
selecting specific metabolites to
match specific disease profiles.
Adjuvants may also be added to
enhance the effect for specific
diseases. In this way, cytokines
can be upregulated or
downregulated based on the
disease being targeted.
Examples include TNFa, IL-17, IL-
23 and IL-12 (down-regulated)
and IL-10 (up-regulated).

4
SFA Therapeutics Pipeline
Pipeline in autoimmune diseases, liver diseases and oncology

Preclinical Phase 1 Phase 2 Phase 3

Autoimmune Diseases (Psoriasis)

Phase 1b ongoing, 1st cohort enrolled, Phase 2 trial design reviewed by FDA

Oncology (HCC)
FDA Orphan Drug Designation for HCC
NASH (fibrosis)
Phase 1b: IND authorized by FDA for clinical trial in NASH (Q1 2023)

Oncology (CLL & AML Relapse)

CAR-T adjuvant

Other Autoimmune-related Indications

AML: Acute Myeloid Leukemia; CLL: Chronic Lymphocytic Leukemia; HCC: Hepatocellular Carcinoma; NASH: Nonalcoholic Steatohepatitis 5
Autoimmune Disease: The Problem
Treating the Root Cause of Autoimmune DiseaseTM

100% 25% 6-10% 5-11%

Of all Autoimmune Of patients are Of eligible patients CAGR expected in
Diseases target multiple take biologics, orals the next 10 years; a
multiple targets autoimmune huge impact on our
syndrome (MAS) healthcare system

Current therapies 30% of patients fail 100% of current

Current therapies are
have multiple autoimmune therapies only treat
mono or dual target
indications, but therapy the symptoms, with
therapies only
none treat MAS (biologics, orals) major side effects

None of the current therapies have statistically-relevant data in people of color.

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Market Opportunity Exceeds $200B
• Targeted disease prevalence ranges from 4-4.5% of population (350M people)
• High growth disease areas due to unmet needs with CAGRs of 5.5% to 11%
• Current treatments range from $50,000 - $80,000 per year, large healthcare burden
• Majority of patients are >40 years old; aging global populations will further impact
• Current drugs treat symptoms, not the disease
Current Total Market in Top SFA002 Focus Areas:

$40B $121B $20B $28B

Other Autoimmune Liver Disease Select Other
Psoriasis Diseases
(RA, MS, Lupus, AS, Target-mediated
(a front-line immune
Bullous Pemphigoid, disease)
diseases
Uveitis) (AML, CML, ARDS,
Long-Covid)

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Limitations of Current Autoimmune Therapies
Marketed autoimmune therapies are limited by single / dual target approach and safety

Mono / Dual Current therapies are mono or dual targeted, while autoimmune
Targeted diseases (including psoriasis) involve multiple targets

Treats No disease-modifying drugs in the market; available options

Symptoms treat symptoms, SFA-002 has potential to treat disease

Safety Most current therapies for autoimmune diseases (including

Concerns psoriasis) are associated with serious side effects

Current systemic therapies are expensive and not always

High Cost affordable, while SFA-002 has low cost

SOLUTION: SFA-002 is a multi-target therapeutic to address these challenges

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Overview of Lead Program: SFA-002
Potential first-in-class oral therapy with compelling preliminary clinical results in a Phase 1a

Oral, Multi-target
small molecule with proprietary formulation

Immunomodulator
that returns the immune system to normal,
downregulates multiple key psoriasis targets,
including TNF-a, IL-17, IL-23 and IFNg

Disease-Modifying Potential
that targets the root cause of autoimmune
disease and has the potential to treat multiple
autoimmune diseases

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SFA-002 is a Patented Combination of Short Chain Fatty Acids
Activity at receptor sites demonstrates physiological effects important in autoimmune disorders

Formulation science is essential to achieve clinical outcomes

Butyrate promotes histone acetylation at the promoter region of

Foxp3 and CNS1 (Furusawa 2013; Arpaia 2013).
Propionate inhibits HDAC via GPR43 signaling (Smith 2013).
By inhibiting HDAC, SCFA promote expression of FoxP3 essential for
differentiation of Treg(s). Treg(s) express anti-inflammatory IL-10,
block IL-6/STAT3/IL-17 signaling, and suppress autoimmunity.

FoxP3: Transcription factor; CHS1: Conserved Non-coding Sequence 1; GPR43: G Protein Coupled Receptor 43; HDAC: Histone Deacetylase 10
Pathophysiology and SFA-002 Mechanisms in Psoriasis
SFA-002 targets and blocks the key psoriasis pathways and mechanisms
TNFα: butyrate facilitates
degradation of mRNA of TNF-α
(Fukae 2005).

NF-κB: butyrate stabilizes IκBα and

IκBβ (inhibitors of NF-κB) (Qiao
2014; Park 2007).

IFN-γ: IFN-γ acts via STAT1 signaling

(Krause 2006) and promotes IL-23
production. Butyrate inhibits
activation of STAT1 via blocking its
Tyr/Ser phosphorylation, nuclear
translocation, and DNA binding
(Klampfer 2003).

STAT1: Transcription factor; Tyr: Tyrosine; Ser: Serine 11

Overview of SFA-002’s MOA in Psoriasis
SFA-002 works differently than current drugs by targeting multiple validated psoriasis pathways

Summary of MOA
Acts on multiple therapeutic
pathways (multi-target)

Inhibits several pro-inflammatory

cytokines (IL-17, IL-23, TNF-α, and
IFN-y)

Inhibits HDAC to increase Treg

differentiation (thus up-regulates
anti-inflammatory IL-10 and
suppresses autoimmunity)

Acts as an immunomodulator

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SFA-002’s Compelling Preliminary Clinical Results

Superior Efficacy Excellent Safety Durability of Effect

Clinically significant efficacy No adverse events in all 6 Durable response achieved in

compared to current SOC with Psoriasis patients treated in 2 patients who remain
PASI 90 score the Phase 1a trial off treatment

PASI: Psoriasis Area and Severity Index 13

Phase 1a Proof of Activity Data
Data demonstrate significant clearance and no adverse events in all 6 patients, with faster onset
of action and high PASI scores
Subject Characteristics Psoriasis Conditions Study Data
Race / Concomitant Years of Treatment PASI Adverse
Subject Age Sex Co-Morbidities Type Severity
Country Medications Disease Duration Score Events

Caucasian/ LosapPlus1 pill daily Plaque

1 79 F
Ukraine
Unknown
(started in 2016) Psoriasis
Severe 25 >5 years (ongoing) 90 None

Caucasian/ Plaque
2 48 M
Ukraine
None Alcohol
Psoriasis
Severe 15 28 days 80 None

Hypertension,
Caucasian Losap for Plaque
3 72 M
Ukraine
Stage 3 (8 yrs);
hypertension Psoriasis
Mild 15 31 days 80 None
Asthma (12 yrs)

Caucasian/ Insulin Resistance Birth control pills, Plaque

4 25 F
USA (unknown duration) Metformin Psoriasis
Mild 7 16 days 95 None

None for >3 months

Plaque &
Caucasian/ Type 2 Diabetes before, during and >2
5 56 M
UAE (unknown duration) months after
Seborrhea Severe 36 45 days 85 None
Psoriasis
investigational treatment
Caucasian/ Plaque Ongoing
6 26 F
USA
None None
Psoriasis
Moderate 1 95 None
photo at 6 months

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SFA-002 Significantly Reduces Psoriasis Lesions
Durable response achieved in severe psoriasis patient
Patient 1 with severe
psoriasis for >25 years
Before SFA-002 ✓ Clinically significant
Treatment reduction of psoriasis
lesions
• PASI 90

✓ No adverse events

✓ Durable response
Off Treatment
>1 Year • Patient remains off
treatment for >1 year
with no return of
symptoms

PASI: Psoriasis Area and Severity Index 15

Compelling Clinical Results in Difficult to Treat Areas
Durable response achieved in patient with hand and scalp psoriasis

Patient 6 with moderate psoriasis,

hand and scalp
Before SFA-002
Treatment ✓ Clinically significant reduction
of psoriasis lesions
• PASI 95

✓ No adverse events

✓ Durable response
SFA-002 Treatment
• Patient remains off
at 6 Months
treatment for >1.5 years with
no return of symptoms

PASI: Psoriasis Area and Severity Index 16

Phase 1b Clinical Trial Design
Two formulations are currently being evaluated for safety and efficacy in 30 subjects

Screening 4- Week Pre-Treatment 12-Week Treatment (Combo 1 or 2) 4-Week Follow-Up

Cohort 1: 15 subjects on Combination 1 from Phase 1a (enrollment completed)

Cohort 2: 15 subjects on Combination 2 with potential for faster onset and higher efficacy (enrolling)
• Cytokine levels are being measured as secondary efficacy markers
• Amendment to Extend Treatment for an additional 3 months filed and pending FDA approval

ClinicalTrials.gov Identifier: NCT05642182 17

Phase 1b Clinical Trial First Read-out
Clinically meaningful changes observed after only 6 weeks in Cohort 1

Before SFA-002
Treatment

SFA-002 Treatment
at 6 weeks

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SFA-002’s Strong Improvement in Murine Psoriasis Model
SFA-002 significantly decreased psoriasis severity in the murine IMQ-psoriasis model

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SFA-002’s Strong Multi-Target Engagement
SFA-002 demonstrated significant response in human ex vivo skin psoriasis model
TNF-α IL-23
• SFA-002 demonstrated
better responses compared
to Otezla

• SFA-002 showed inhibition

across all 6 tested cytokines,
whereas Otezla inhibited 3
IFN-γ IL-17A IL-22 cytokines and was ineffective
for TNF-α, IL-21, and IL-23

• Surprisingly, Otezla
significantly upregulated
TNF-α in comparison to
untreated control

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SFA-002 Downregulated TNF-α in the LPS Murine Model
SFA-002 rapidly reduced plasma TNF-α within 26 hours in the LPS model of acute inflammation

Plasma TNF-α

• SFA-002 showed significant and rapid downregulation

of TNF-α within 26 hours following treatment

• Biologics can take up to 6 months to show clinical

effects in patients, and Otezla can take up to a year

• SFA-002 has the potential to be fast-acting

Plasma TNF-α measured by commercially available ELISA. Data are mean (+/ -) SEM and analyzed by one-way ANOVA with fisher’s 21
uncorrected LSD test (*P<0.05, ***P<0.001, Compared to VEH/LPS group, n=8/group)
SFA-002 Competitive Positioning
SFA-002 is well-positioned to become a first-in-class oral immunomodulatory therapy for psoriasis

Injectable
PASI 75
Oral
Brands / Assets

Stelara
PASI 90-100
BAT2206
AK101
Humira
Biosimilars Remicade
Enbrel
DMB-3116 Cosentyx Skyrizi
ABP-654 SCT-630 Siliq Tremfaya
FYB-202 Taltz
SB-17 Biosimilars: Otezla; Deucravaci- AUR-101; IBI-112 ABY-035
CT-P43 ABP-501 608* Orismilast* tinib (BMS); cedirogant- Mirikizu- AK-111
AVT-04 301s BCD-085 Hemay-005 NDI-034858 (ABBV-157) Ilumya Cimzia CF-101 Jaktinib KBL-697 SCD-044 mab SHR-1314 Bimzelx SFA-002
TNF-⍺

PEG-TNF-⍺
IL-17A

PDE-4

IL-23A

JAK 1/2

S1P1a

IL-23A

IL-17A
TYK2

RORγt

IL-17F, IL-17A
IL-12, IL-23

A3AR agonist

IL-17A, IL-23,
Lactobacillus

TNF-⍺, IFN-γ
gasseri

TNF-α,
SFA-002 is the only oral immunomodulatory therapy with the potential to achieve PASI 90 - 100
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SFA-002 vs. TYK-2s in Psoriasis – Clinical Comparisons
SFA-002 has faster onset, superior efficacy and better safety

Asset MOA ROA Efficacy Safety Onset Dosage

Endpoint (weeks)
SFA-002 IL-17A, IL-23, TNF-α, IFN-γ Oral PASI 90 No AEs 6 QD
SOTYKTU™ (deucravacitinib), BMS TYK-2 Oral PASI 75 • Upper respiratory 16 QD
infections
• Increased CPK
• Elevated liver enzymes
NDI-034858, Nimbus (Takeda) TYK-2 Oral PASI 75 • TBC 12 QD

SFA-002 targets and blocks the key psoriasis pathways and mechanisms

Above represent data in label for approved drugs. US only. Adult PsO only.
• SFA-002 uses core drugs plus adjuvants to tailor responses against key cytokine pathways matched to specific diseases. Multi-target responses, including pro-
inflammatory NF-kβ, cytokine signaling (TNF-α, IL-17, IL-23), and promotes expansion of Treg cells which suppress autoimmunity
• SOTYKTU Efficacy: PASI 90 36%, PASI 100 14% - at 16w. Safety: AEs in >1% of subjects; upper respiratory tract infection (19.2%), blood creatine phosphokinase increase
(2.7%), Herpes simplex (2%), mouth ulcers (1.9%), folliculitis (1.7%), acne (1.4%); infections occurred in 29% of the SOTYKTU group (pneumonia, covid-19); lab
abnormalities included increased CPK, liver enzyme elevations (ALT, AST) in 22 subjects, decreased GFR in 4 subjects, lipid elevations
• Nimbus (acquired by Takeda); Ph2 efficacy results not yet available.
• TYK2 mediates IFN-α/β, IL-12, IL-23, IL-10, IL-22, and IL-6 signaling (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9488612/figure/f0002/) 23
Intellectual Property and CMC
Robust patent portfolio including composition of matter and methods of use

IND authorized in 2020 following strong in vivo and in vitro data

Drug manufacturer under contract and analytical methods developed

Phase 1b is underway and Phase 2 protocol has been reviewed by FDA

Global patent strategy includes 9 issued and 39 pending patents in 12

countries (US patent coverage through 2041)

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Key Investors and Collaborators
Industry validating investors and academic partnerships

Investors Academic Partnerships

ASYMMETRY

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SFA-002 Development Plan, Timeline and Use of Proceeds
SFA is seeking a $25 M raise to accelerate the clinical development of SFA-002

2021 2022 2023 2024 Budget Estimates

Phase 1B Studies1 Funded

Phase 2 Study2 $3 M

Two-Species Tox Study $1 M

Formulation Optimization $1 M

Manufacturing / Analytic Methods $1 M

Bioequivalence & Dose-Ranging $1 M

Commercial Development Program $1 M

Other Costs (i.e., IP protection, milestone payments, reserves, Phase 3 estimate) $17 M
1 Phase 1B Studies (data readout mid-2023): 30 subjects to optimize formulation, 2 cohorts of 15 subjects
2 Phase 2 Study (data readout early 2025): 75 subjects over 6 months, designed to determine PASI & IGA scores 26
Investment Opportunity
Treating the Root Cause of Autoimmune DiseaseTM

Differentiated First-in-class Initial Clinical

Multi-Targeting Platform Therapeutic Potential Proof of Concept

Patented small molecule Disease-modifying potential Compelling efficacy and

drugs that act on multiple for treating psoriasis and safety data in early
therapeutic pathways numerous other clinical trials and
autoimmune diseases preclinical models

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Thank You
Appendix
SFA-002 Phase 1b Clinical Trial Design
Two combinations currently being evaluated for safety and efficacy in 30 subjects

Cohort 1: 15 subjects on Combination 1 from Phase 1a (enrollment completed)

Cohort 2: 15 subjects on Combination 2 with potential for faster onset and higher efficacy (enrolling)
Cytokine levels will be measured as efficacy markers

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Preclinical Data in Liver Disease Formed the Basis for the Platform
Data showing major effects at validated disease targets provides major platform opportunity

Microarray analysis
of several cancer related pathways and
immune molecules associated with the
pathogenesis of HCC.
Among mice developing cancer, tumor
pathways known to be activated in HCC are
strongly down-regulated. Inflammatory
pathways were identified as another
potential area for drug development.

Included in US 10,143,669 B2

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Microarray Analysis of SFA SCFA Liver Disease Formulation in mice
Scientific Pathways Have Been Elucidated and Are Understood
A “Master Switch” for Inflammation and Carcinogenesis

Proteomics
analysis showed
down-regulation
of molecules
critical for
inflammation and
carcinogenesis
Included in US
11,065,217 B2

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SFA-001 Delays Onset and Progression of Liver Cancer
HBxTg Transgenic Mice Treated with SFA001 Showed Delayed Onset and Progression of HCC

In mice bred with the gene for liver cancer, 50% of the treated
mice developed no tumors, the other 50% treated mice had
fewer and smaller tumors

Untreated Mouse Livers

SFA001 + - Reduction
No of total tumors 14 31 55%
No of mice 12 9 66%
No of tumors/
1.2 3.4 66.5
mouse
Ave. tumor
0.31 0.66 53%
diameter

Treated Mouse Livers

HBx transgenic mice (HBxTg) progressively develop hepatitis
and steatosis (4-6 mo), dysplasia/microscopic HCC (8-10 mo),
and multinodular macroscopic HCC (11-12mo)

33
SFA-001 Reduces Tumor Growth and Cancer Cell Viability
SFA-001 Blocks Human Xenograft Liver Cancer Growth and Reduced Viability of Cancer Cells
SFA001 Treated Mouse Control Mouse
A B • Immunocompromised nude mice
were subcutaneously injected with
human liver cancer cells (Huh7X)

• SFA-001-treated (with low and high

doses) mice (A) had slower tumor
growth compared to controls (B)

Percent cell viability

Tumor volume*102MM3

• SFA-001 reduced viability of cancer

cell lines (Huh7X and Hep3BX) but
not viability of primary human
hepatocytes
Weeks of treatment SFA001 concentration

SFA-001 Received FDA Orphan Drug Designation for HCC

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Advisory Team
Scientific and business advisors with deep expertise in psoriasis and other disease markets
Scientific Advisors Business Advisors
Sylvia Hsu, MD Professor and Chair, Dermatology, Temple University Craig Kenesky, JD, PhD IP Counsel, Wilson Sonsini Goodrich
& Rosati
Senior Consultant at Princeton Dermatology Corporate Counsel, DLA-Piper
Andrew Gilbert, JD
Daniel Sauder, MD Associates, Prior Chair, Dept. Dermatology at John
Hopkins and University of Toronto
Jordan Warshafsky, MBA Business/HR Advisor, Ashton Tweed
Director, Professor of Dermatology and
Epidemiology, Vice Chair of Clinical Research,
Joel Gelfand, MD, MSCE Medical Director of Clinical Studies Unit in the Angela Lynch, PhD Scientific Advisor, Toxicology
Department of Dermatology, UPenn
Raxit Mehta, M.C.E Formulation Advisor
Chris Gallen, MD, PhD CEO, WEX Pharmaceuticals

Joseph Camardo, MD
Satdarshan Monga, MD
CMO, ADC Therapeutics; Chair, Board of MaliHealth Kate Hermans, MBA Commercialization Planning
Member of Scientific Advisory Committee at DNDi
Director, Vice Chair, and Chief, Pittsburgh Liver Sri Sriadibhatla, PhD Ben Franklin Technology Partners,
Research Center, Division of Experimental Pathology, Board Observer
University of Pittsburgh

Todd Abrams, PhD Director, New Ventures and

Brent Korba, PhD Professor, Georgetown University Medical Center
Business Development, Temple
University, Board Observer
35
DNDi: Drugs for Neglected Diseases initiative