VECTUS BIOSYSTEMS LIMITED — Investor Presentation 2021

Aug 29, 2021

CEO PRESENTATION

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OVERVIEW

Fibrosis is the replacement of normal tissue (heart, lung, kidney etc) by scar tissue and can lead to organ failure

Fibrosis is the pathology which underlies:

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HEART FAILURE

LIVER FAILURE

(largest single item on US health care budget ($US32b in 2013)

(liver cirrhosis affects 40% of South Asians and East Asians)

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RESPIRATORY FAILURE (pulmonary fibrosis)

KIDNEY FAILURE (Dialysis and renal transplant costs in the US reached $49.2b in 2011)

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Fibrosis Reversal,
a MAJOR
unmet need
Fibrotic disease
contributes to more
than 40% of
all deaths worldwide
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PATH TO THE CLINIC – VB0004

PHARMA CRITERIA VECTUS Validated Target Platform Technology Transformational Agent Demonstrated Efficacy in Animal Model Demonstrated Safety – IND toxicology IP Covers Composition of Matter Synthesis at Scale Cost of Good Competitive Sufficient Patent Life Phase I Safety Study Human pD (Efficacy) Data

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TARGET VALIDATION

Treatment with VIP reversed cardiac fibrosis in multiple animal models data from one was published in the paper entitled “Vasoactive intestinal peptide reverses existing myocardial fibrosis in the rat” (see right)

https://doi.org/10.1016/j.ejphar.2019.172629

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TARGET VALIDATION

Treatment with VIP was also found to reverse interstitial fibrosis in the kidney in multiple animal models data from one was published in the paper entitled “Vasoactive intestinal peptide infusion reverses existing renal interstitial fibrosis via a blood pressure independent mechanism in the rat” (see right) https://doi.org/10.1016/j.ejphar.2020.172979

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PATH TO THE CLINIC – VB0004

PHARMA CRITERIA VECTUS Validated Target Platform Technology Transformational Agent Demonstrated Efficacy in Animal Model(s) Demonstrated Safety – IND toxicology IP Covers Composition of Matter Synthesis at Scale Cost of Good Competitive IP Covers Composition of Matter Sufficient Patent Life Phase I Safety Study Human pD (Efficacy) Data

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VB0004 & SYSTOLIC BLOOD PRESSURE

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Left: Decrease in SBP from controls in 18 week old SHR treated with VB0004 at 10, 100, 500, 1,000 and 2,500 pmol/kg/min for 4 weeks. Enalapril dose to achieve 7mmHg was 705 pmol/kg/min. SBP continued to decrease with increasing dose to 2,500 pmol/kg/min

Middle: Difference in SBP from control for SHR treated with VB0004 at 2,500 pmol/kg/min at 1, 2, 4, 6 and 8 weeks. The maximal effect of VB0004 in lowering SBP was not reached after 8 weeks treatment

Right: Change in SBP from levels at the commencement of the experiment in Vehicle control for 4 weeks (solid line) SHR treated with VB0004 2,500pmol/kg/min for 2 weeks then vehicle for 2 weeks (dotted line) SBP in increased in parallel with vehicle control after cessation of VB0004

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VB0004 & CARDIAC FIBROSIS

VB0004 has been shown to:

• Rescue cardiac tissue damaged by fibrosis

• Repair existing cardiac damage

• i.e. VB0004 is transformational

14-Week Control

Fibrous tissue (blue staining) is visible around blood vessels and extending between muscle fibres

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• Reduce systolic blood pressure

Treatment with VB0004 at 3 Doses

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At the highest dose (500pmol/kg/min), VB0004 reversed pre-existing fibrosis, while a dose response effect on the level of fibrosis is apparent

5% Ethanol 18-Week Control (Vehicle Control For VB0004)

Fibrosis visible as blue stained tissue is present throughout the section.

Heart At 18 Weeks After 4- week Treatment with VB0004 (500 Pmol/Kg/Min) Minimal fibrosis is visible; normal architecture has been restored.

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VB0004 & KIDNEY FIBROSIS

In the kidney VB0004 has been shown to:

• Reverse renal interstitial fibrosis at all doses

• Restore normal architecture at all doses

• (i.e. VB0004 is considered transformational)

14-Week Control

Fibrosis (blue) partially surrounds some but not all tubules

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Treatment with VB0004 at 3 Doses

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5% Ethanol 18-Week Control (Vehicle Control For VB0004)

Fibrosis has progressed to surround most tubules

Kidney At 18 Weeks After 4- week Treatment with VB0004 (500 Pmol/Kg/Min) No fibrosis visible

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VB0004 & PULMONARY FIBROSIS

In the lung:

• VB0004 reversed fibrosis present 2 weeks after treatment with bleomycin (an anticancer drug)

• i.e. VB0004 also transformational in the lung

Treatment with VB0004 at 3 Doses

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16-Week Control 20-Week Control VB4-A79 at 20 weeks VB0004 at 20 weeks

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VB0004 THE FIRST NON-PEPTIDE, ORALLY DOSED VIP MIMETIC:

• Decreased systolic blood pressure in a dose dependent manner

SUMMARY

• Reversed pre-existing cardiac fibrosis and restored normal cardiac architecture

• Reversed pre-existing renal interstitial fibrosis and restored normal renal architecture

• Reversed pre-existing pulmonary fibrosis secondary to bleomycin

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PATH TO THE CLINIC – VB0004

PHARMA CRITERIA VECTUS Validated Target Platform Technology Transformational Agent Demonstrated Efficacy in Animal Model(s) Demonstrated Safety – IND toxicology IP Covers Composition of Matter Synthesis at Scale Cost of Good Competitive IP Covers Composition of Matter Sufficient Patent Life Phase I Safety Study Human pD (Efficacy) Data

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DEMONSTRATED SAFETY

Sad And Mad (2 Species)

• Single Ascending Dose (SAD) to 2,000mg/kg no adverse events

• 7 day Multiple Ascending Dose (MAD) to 2,000mg/kg no adverse events

• 28 day MAD to 500mg/kg no adverse events

Mutagenic potential

• In vivo and in vitro tests low to no mutagenic potential

Cardiovascular Safety

• hERG studies - low arrhythmia potential

• Dog cardiovascular safety – No effects on cardiovascular function at maximum dose of 10 grams/day

Metabolism

• Metabolites are the same in human, rat and dog

Respiratory Safety

• rat study no adverse events

Drug Interactions

• No Inhibition of major drug metabolising enzymes (drug interactions less likely)

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PATH TO THE CLINIC – VB0004

PHARMA CRITERIA VECTUS Validated Target Platform Technology Transformational Agent Demonstrated Efficacy in Animal Model(s) Demonstrated Safety – IND toxicology Synthesis at Scale Cost of Good Competitive IP Covers Composition of Matter Sufficient Patent Life Phase I Safety Study Human pD (Efficacy) Data

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FIRST GMP SYNTHESIS BY GLYCOSYN

• Yield increased as scale increased

• VB0004 manufactured to 5kg scale

• Cost efficient at 5kg scale < $(US) 0.05 per mg

• Estimated dose 1-5mg

SYNTHESIS SCALE AND COST

• Stability studies – stable at 2 yrs (long shelf-life)

Second GMP synthesis Assymchem

• Campaign planned to provide 3 validation batches

• Confirm consistency of the synthesis process

• Samples of all 3 will undergo 2 yr stability testing

• Meets FDA requirements for GMP manufacture for Phase 1 and 2 clinical trials

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PATH TO THE CLINIC – VB0004

PHARMA CRITERIA	VECTUS
Validated Target
Platform Technology
Transformational Agent
Demonstrated Efficacy in Animal Model(s)
Demonstrated Safety – IND toxicology
IP Covers Composition of Matter
Synthesis at Scale
Cost of Good Competitive
IP Covers Composition of Matter
Sufficient Patent Life
Phase I Safety Study
Human pD (Efficacy) Data

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VB0004 patent covers

• Compositions of matter

• Methods of use

VB0004 Patent granted in all major jurisdictions

• USA, Europe, Japan, Peoples Republic of China, Republic of South Korea, Russian Federation

INTELLECTUAL PROPERTY

• as well as Australia, Israel, Phillipines, South Africa, Canada, ARIPO

Patent Life

• Priority date September 2014

• 13 years (+5 years on licensing)

VB0004 Method of synthesis patent at National

Phase entry stage

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PATH TO THE CLINIC – VB0004

PHARMA CRITERIA	VECTUS
Validated Target
Platform Technology
Transformational Agent
Demonstrated Efficacy in Animal Model(s)
Demonstrated Safety – IND toxicology
IP Covers Composition of Matter
Synthesis at Scale
Cost of Good Competitive
IP Covers Composition of Matter
Sufficient Patent Life
Phase I Safety Study
Human pD (Efficacy) Data

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• Syneos Health (Nasdaq SYNH) retained to write Investigator Brochure (IB), trial protocol and monitor Phase 1 trial

• Trial design conventional Single Ascending Dose (SAD) and Multiple Ascending Dose (MAD)

• Healthy subjects 14 day MAD

PHASE 1

• Affected individuals 2 groups 28 days 2 doses

• Biomarkers identified

• Includes pharmacokinetic and pharmacodynamic studies

• Expected outcomes – maximum tolerated dose, dose limiting toxicity (if present), pharmacokinetic data and pharmacodynamic data

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HEPATIC CIRRHOSIS (LIVER FIBROSIS)

Causes

• genetic

• infectious (Hep A, B, C)

• alcohol related

• Diabetic

• due to obesity

• cryptogenic (no discernible cause)

Prevalence

• varies to >40% of the

population in countries such as India, Cambodia, Vietnam and China due to endemic Hep B & C.

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• Vaccination Hep A, Hep B for prevention

• Abstinence to prevent further damage (EtOH) weight loss

CURRENT THERAPIES

• Diabetes management

• Symptom relief (albumin infusion, ascites removal)

• Sofosbuvir and related agents for Hep C (note this treats the infection but does not prevent progression of the established fibrosis for which lifetime monitoring is required)

• Transplantation

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POTENTIAL THERAPIES

• FXR agonists – Phase 2 reduced liver fat at 6 months, Phase 3 no change in liver fat, decreased fibrosis at 18 months in 18-23% of patients, none achieved resolution of fibrosis. Side effects - itching moderate to severe in intensity in up to 50%

• PPAR-α/δ agonists – Phase 2 decrease in fat and no progression in 19% at 6 months but a reversible loss in renal function. Phase 3 no progression in 20% at 12 months

• Insulin sensitisers – Phase 2b no effect on liver disease, but improved insulin sensitivity

• FGF19 analogues – decrease in liver fat in 74-79% at 12 weeks. High incidence of side effects (93%) including injection site reaction, abdominal pain, diarrhoea, nausea

• PPAR α & γ agonists Phase 2 decrease in ALT at 16 weeks and reduced fat at the highest dose vs placebo. Well tolerated

• THR β agonist Phase 2 decreased ALT, AST and liver fat vs placebo at 12 weeks. SCDI inhibitor- Phase 2b no effect at 12 weeks

• ASK1 antagonists – Phase 2 open label decreased fibrosis at 6 months. Phase 3 discontinued as no decrease in fibrosis without worsening NASH at 12 months

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• No current approved therapy

SUMMARY – LIVER FIBROSIS

• Potential therapies – ineffective and/or high incidence of side effects

• Liver Fibrosis continues to represent an unmet therapeutic need

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VB4-A32 & HEPATIC CIRRHOSIS

VB4-A32 demonstrated ability to:

• reduce peri-portal fibrosis in the liver in a dose dependent manner (right and below)

• Improve liver function tests (below right)

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20-Week Control

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A32 20 Weeks

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PULMONARY FIBROSIS

Causes

• Environmental (e.g. air pollution, diesel particles)

• Occupational (e.g. dusts such as silica, coal, asbestos, cotton dust)

• Infections (e.g. TB, psittacosis, Spanish flu, COVID-19)

• Drugs (e.g. bleomycin, methotrexate)

• Radiation

Essentially, a triggering factor such as coal or silica dust accumulates in the lung which initiates a scarring (fibrotic) reaction to wall off the irritant. However, instead of then turning off once this is achieved the process becomes autonomous and continues to damage the lung even in the absence of continuing exposure. This results in a reduction in the area available for oxygen to exchange across the lungs and manifests as increasing breathlessness.

• Autoimmune diseases (e.g. sarcoid, SLE, scleroderma, Wegener Granulomatosis)

• Idiopathic (no discernible cause) termed IPF

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Two current therapies:

Pirfenidone

CURRENT THERAPIES

regulatory approval approximately 5 years ago. Slows lung function (FVC and 6MWD) decline. Approximately 50% discontinued or reduced dose due to side effects.

Nintedanib

regulatory approval approximately 5 years ago also slows rate of lung function decline. High discontinuation rate due to side effects.

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• Pentraxin 2 analogue – Phase 2 showed significant slowing of the decline in FVC and stabilisation of 6MWD at 6 months

• Anti-CTGF antibodies – Phase 2 slowed decline in FVC and 6MWD (awaiting review)

• Medium Chain Fatty Acid Analogue (PBI4050) – Phase 2 PBI4050, alone or combined with Nintedanib slowed decline or stabilised FVC at 12 weeks. However, in combination with Pirfenidone the rate of decline increased

POTENTIAL THERAPIES

• Autoxin-LPA Inhibitors – Phase 2a ? Halted FVC decline at 12 weeks. Phase 3 underway

• Anti-LOXL.2 Antibodies – No beneficial effect at Phase 2

• Anti-interleukin Antibodies – No efficacy

• Leukotriene Antagonists – Phase 2, no interim results

• Anti-Integrin Antibodies – Phase 2 completed, awaiting data

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Current therapies – slow the decline in lung function compared with placebo, but have a high incidence of unacceptable side effects

VB4-A79: BLOOD PRESSURE

Potential therapies – slow decline or at best stabilise lung function

Pulmonary Fibrosis continues to represent an unmet therapeutic need

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VB4-A79: BLOOD PRESSURE

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Systolic and diastolic blood pressure in 20week SHR following treatment with bleomycin at 14 weeks and randomisation to control, VB0004 or VB4-A79 at 16 weeks.

As previously VB0004 significantly decreases both systolic and diastolic pressure while VB4-A79 had no effect.

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VB4-A79 PULMONARY FIBROSIS

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Pulmonary fibrosis in 16-week controls (two weeks after Bleomycin administration) and at 20 weeks after 4 weeks treatment in VB0004, A79 and vehicle control rats. VB0004 and VB4-A79 were administered at 500pmol/kg/min in the drinking solution (5% ethanol) vehicle control is drinking solution alone.

• p<0.001 vs 20 week control, # p<0.01 vs 16-week control.

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VB4-A79 HISTOLOGY

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16-Week Control 20-Week Control VB4-A79 at 20 Weeks VB0004 at 20 Weeks
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Lung sections in bleomycin treated rats after 2 weeks of control drinking solution (left), after 6 weeks of control drinking solution (centre) and after 2 weeks of control drinking solution followed by 4 weeks treatment with A79 or VB0004 (500pmolkg/min). Scar or fibrous tissue appears blue / cyano in these sections. In the controls 2 weeks after bleomycin administration fibrous tissue has thickened many alveoli (air sac) walls but not yet obliterated small blood vessels (capillaries), which appear as red dots which are individual red blood cells. By 6 weeks in the control rats fibrous tissue is evident causing thickening of all of the alveoli walls and replacing many of the thin walled blood vessels (capillaries) which would normally surround the alveoli allowing gas exchange. In VB4-A79 treated rats alveoli walls are thinner and capillaries are more numerous.

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• 3 first in class assets addressing major unmet therapeutic needs

• VB0004 – entering Phase1, addressing Systolic Hypertension, cardiac, renal and pulmonary fibrosis, possible orphan indication for scleroderma

VECTUS IN SUMMARY

• VB4-A32 – addresses liver fibrosis, restored normal liver architecture in NASH/ASH models

• VB4-A79 – addresses pulmonary fibrosis from all causes except scleroderma where BP lowering probably required, revered existing fibrosis due to bleomycin

• Exceptional patent portfolio encompassing a library of > 1,000 compounds

• Successful raising of $7 million by Gleneagle and Morgans (Scone)

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• VB0004 – Phase 1

USE OF FUNDS

• VB4-A32 – undertake GMP synthesis (Assymchem), with IND toxicology studies to follow

• Laboratory – further work on detailed mechanisms of action for VB4-A32, VB4-A79

• Diversify to encompass other areas of unmet therapeutic need and investigate therapies from Vectus extensive library e.g. develop cellular models for Alzheimer’s disease and investigate efficacy of potential candidates

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WHY ALZHEIMERS

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Accumulation of B-amyloid in the brain causes formation of plaques, which disrupt neuronal connections and cause accumulation of Tau proteins, which are dissociated from microtubules within neurones causing tangle formation, a precursor to neuronal cell death.

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PATENT PORTFOLIO

• VIP patents for heart, kidney and aortic fibrosis – granted all jurisdictions

• VIP fragment patents compositions and methods of use for –

• hypertension, cardiac, renal and aortic fibrosis granted most jurisdictions

• VB0004 compositions and methods of use for hypertension, cardiac and renal fibrosis – granted Russian Federation, Israel, Singapore, ARIPO, Canada, Philippines, South Africa, Ukraine, Vietnam, Nigeria, Mexico , accepted in Indonesia

• VB0004 library of approx. 70 related compounds compositions and methods of use for treatment of hypertension, cardiac and renal fibrosis – granted US, Australia, China, Europe, Japan, Korea, Russia, Ukraine, Hong Kong, Vietnam, Singapore, accepted in South Africa, ARIPO, Brazil, accepted Mexico

• VB4-P5 and library of related compounds compositions and methods of use for treatment of renal cell death, renal fibrosis and hepatic fibrosis – granted US, China, Australia, South Africa, accepted Europe, Japan, Russia, Israel

• GMP method of synthesis VB0004 – granted USA, Australia, India, accepted Europe, China

• VB4-A79 and related compounds compositions and use for treatment of pulmonary fibrosis – granted Australia, China, accepted USA, Europe, Mexico

• VB0001 and related compounds compositions and use –

• for management of hypertension and fibrotic disease PCT application

• VB4-A32 and library of related compounds compositions and methods of use for treatment of hepatic, cardiac and renal fibrosis – granted US, Europe, Australia, South Africa

• VB0002, VB0003 and VB0005 and related compounds compositions and use for management of hypertension and fibrotic disease – national phase

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Comparable Transactions

• Successful Phase 1/1b would place Vectus at the point where many transactions have been completed

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VIP AGONISTS – T BENCHMARK FOR ANTI-FIBROTICS

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