Third Quarter 2014 Financial Results
and Corporate Update
1
Safe Harbour
Forward Looking Statement
This presentation contains forward-looking statements about ProMetic’s objectives, strategies and
businesses that involve risks and uncertainties. These statements are “forward-looking” because they
are based on our current expectations about the markets we operate in and on various estimates and
assumptions. Actual events or results may differ materially from those anticipated in these forwardlooking statements if known or unknown risks affect our business, or if our estimates or assumptions
turn out to be inaccurate. Such risks and assumptions include, but are not limited to, ProMetic’s ability to
develop, manufacture, and successfully commercialize value-added pharmaceutical products, the
availability of funds and resources to pursue R&D projects, the successful and timely completion of
clinical studies, the ability of ProMetic to take advantage of business opportunities in the pharmaceutical
industry, uncertainties related to the regulatory process and general changes in economic conditions.
You will find a more detailed assessment of the risks that could cause actual events or results to
materially differ from our current expectations in the Annual Information Form for the year ended
December 31, 2013, under the heading “Risk Factors”. As a result, we cannot guarantee that any
forward-looking statement will materialize. We assume no obligation to update any forward-looking
statement even if new information becomes available, as a result of future events or for any other
reason, unless required by applicable securities laws and regulations. All amounts are in Canadian
dollars unless indicated otherwise.
Copyright notice
The information contained in this presentation (including names, images, logos and descriptions
portraying ProMetic's products and/or services) is the property of ProMetic Life Sciences Inc., of its
divisions and / or of its subsidiaries (“ProMetic”) and is protected by copyright, patent and trademark law
and / or other intellectual property rights. Neither this presentation nor any part may be reproduced or
transmitted in any form or by any means, electronic or mechanical, including printing and photocopying,
or by any information storage or retrieval system without prior permission in writing from ProMetic.
Disclaimer
ProMetic reserves the right to make improvements, corrections and/or changes to this presentation at
any time.
2
AGENDA
Q3 2014 Milestones
Guidance for H2 2014
Q3 financials
Q3 Corporate Update:
- Vanderbilt University Study
- PBI-4547 poster
- Clinical trial for 4050-DKD
Milestones to year end – Outlook for 2015
3
Q3 2014 Highlights
Fibrinogen commercial launch announced for Q4 2014
Development and scale-up of new affinity resin for
multinational client
$20 million follow-on investment from Thomvest
Promotion of Mr. Pritchard to newly created position of COO
Successful Pre-IND FDA meeting for PBI-4050
Inclusion of PLI to S&P/TSX Small Cap Index
Clearance by FDA of plasminogen IND and clearance of pbi4050 CTA by Health Canada (Q4-14 events)
4
H2 2014 GUIDANCE
• PBI-4050 to progress in patients – phase Ib
• To disclose New PBI-4050 data at ASN (American Society of Nephrology
Annual Meeting Nov 12-15)
• To disclose an additional Orphan indication for PBI-4050
• To file the IGIV IND with the FDA
• To disclose 2 additional PPPS™ derived Orphan Rx
• To close partnering deals providing :
• Financial contribution
• Access to market
• Additional manufacturing capacity
• Revenue range for H2 2014 ($15 M - $20 M)
• Subject to revenue recognition on licensing fees
• Revenue significantly higher in Q4
5
Third Quarter 2014
Financial Results
6
Sources of Financial Information
The following information is derived from:
The financial information for the third quarters of 2014 and 2013,
which have been reviewed by Ernst & Young, the Corporation’s
Auditor; and
the audited financial statements for 2013.
All financial information has been prepared in accordance with
International Financial Reporting Standards (IFRS).
Further financial information, including the ProMetic’s Annual
Information Form, is available on SEDAR (www.sedar.com).
All tabulated sums are in CAD 000’s except for “per share”
amounts or where indicated.
7
Year‐To‐Date Revenues: $M
16
14
12
8,8
5,1
10
8
6
4
6,8
7,3
YTD 2013
YTD 2014
2
0
Product Sales
Service & Licensing Revenues
8
Third Quarter 2014: Results
Quarter ended September 30
2014
2013
CAD 000s
CAD 000s
Revenues
Cost of Goods Total Research & Development Costs
Administration & Marketing
Finance Costs
Fair Value adjustment on Warrants
Gain on revaluation of Equity Investment
Purchase Gain on Business Combination
Net Loss
Net Loss per share (basic)
EBITDA*
YTD ended September 30
2014
2013
CAD 000s
CAD 000s
2,315
5,960
12,464
15,566
867
7,846
3,006
774
10,420
‐
‐
1,547
4,618
1,981
467
2,622
‐
‐
4,659
23,397
7,883
1,825
12,432
(24,258)
(8,065)
4,667
12,409
4,570
1,128
2,622
‐
‐
(20,677)
(5,303)
(5,919)
(9,896)
(0.04)
(0.01)
(0.01)
(0.02)
(7,668)
(1,738)
(19,688)
(5,006)
*EBITDA is a non‐GAAP measure, employed by the Corporation to monitor its performance. Therefore it is unlikely to be comparable to similar measures presented by
other companies. The Corporation calculates its EBITDA by subtracting from Revenues, its Cost of Goods Sold, its Research and Development Expenses Rechargeable
and Non‐Rechargeable as well as its Administration and Marketing Expenses and excluding depreciation of capital assets and licenses, amortization of licenses and
patents and share‐based payments.
9
Comparison of Key Financials : Balance Sheet
30 September 2014
CAD 000s
10,383
31 December 2013
CAD 000s
17,396
4,928
14,172
12,893
9,631
104,743
4,663
Trade & Other Payables
6,098
7,877
Deferred Revenues
1,536
984
Warrant Liability
21,743
9,311
Long –term Debt (Thomvest)
22,291
6,217
‐
3,040
42,400
18,638
137,955
49,872
Selected information
Cash
Accounts Receivable
Capital Assets
Intangible Assets
Long‐term Debt Provided by Shareholders
Total Equity Balance Sheet Total Assets
10
10
Third Quarter 2014
Corporate Update
11
Vanderbilt University Study
PBI‐4050 protects against the development of diabetic nephropathy (DN) in db/db eNOS‐/‐ mice
Raymond C. Harris, Ming‐Zhi Zhang
Vanderbilt University School of Medicine
12
Vanderbilt University Study
db/db eNOS knockout Mouse model
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
Dramatic albuminuria
GFR  , SCr 
Hypertension (vs. db/db)
Mesangial expansion 
Mesangiolysis
Nodular glomerulosclerosis
Arteriolar hyalinosis
Macrophage infiltration
Glomerular fibrin & hyaline
deposition
GBM thickening
Tubulointerstitial injury
Normal aorta, no atherogenic
lesions
Hyperinsulinemia, large islets
Lower plasma glucose levels
13
Vanderbilt University Study
Proteinuria is significantly increased in
db/db mice with eNOS-/*
*
albumin/creatinine (g/mg)
1500
BKS
eNOS-/db/db
db/db/eNOS-/-
1250
1000
750
500
250
16 weeks of age
24 weeks of age
14
Vanderbilt University Study
15
Vanderbilt University Study
16
Vanderbilt University Study
Late treatment with PBI-4050 protects against diabetic
nephropathy in db/db eNOS-/- mice
PBI-4050
Outer
medulla
Corte
x
Vehicle
Masson’s trichrome staining: original magnification: 160 X
Selectively colors collagen in blue
17
Vanderbilt University Study
Late PBI-4050 treatment reduces kidney fibrosis (collagen 1) in db/db eNOS-/- mice
Vehicle
PBI-4050
Collagen I
Collagen I staining. X400.
18
Vanderbilt University Study
Late PBI-4050 treatment reduces kidney fibrosis (collagen IV) in db/db eNOS-/- mice
Vehicle
PBI4050
Collagen IV
Collagen IV staining. X400.
19
Vanderbilt University Study
Late PBI-4050 treatment reduces myofibroblasts in db/db eNOS-/- mice
Vehicle
PBI-4050
α-SMA, a marker of myofibroblasts. X160.
20
Vanderbilt University Study
Late PBI-4050 treatment reduces kidney macrophage infiltration in db/db eNOS-/- mice
Vehicle
PBI-4050
Dark spots are
Macrophages
Infiltrating the
kidney
F4/80 staining, a marker of macrophages. 160 X
21
Vanderbilt University Study
Late PBI-4050 treatment reduces kidney oxidative stress in db/db eNOS-/- mice
Vehicle
PBI-4050
Nitrotyrosine staining, a marker of oxidative stress. X100.
22
Vanderbilt University Study
Late PBI-4050 treatment reduces kidney CTGF in db/db eNOS-/- mice
Vehicle
PBI4050
CTGF staining, a pro-fibrotic mediator. x160
23
Vanderbilt University Study
Late PBI-4050 treatment increased kidney autophagy in db/db eNOS-/- mice
Vehicle
PBI-4050
Up‐regulation of
autophagy is very
important in the
self‐repair process
LC3A staining, a marker of autophagy. x160
24
Vanderbilt University Study
Plasma insulin levels (ng/ml)
A
7
A: In untreated mice, plasma insulin levels decrease
gradually. * P < 0.05 vs. 8 wk; †P < 0.05 vs. 16 wk.
6
5
B: Early treatment with PBI-4050 (8 to 20 wks) prevents the
decline of plasma insulin concentration. * P < 0.05 vs. vehicle.
4
3
*
2
1
0
8
†
16
C: Late treatment with PBI-4050 (16 to 24 wks) not only
prevents the further loss of pancreas function, but restores
pancreas function to that seen at 8 wk of age. ** P < 0.01 vs.
vehicle; † P < 0.05 vs. baseline at 16 wk of age.
24
Age (week)
C
7
Vehicle
PBI-4050
*
6
5
4
3
2
1
8
week
20
week
Plasma insulin levels (ng/ml)
Plasma insulin levels (ng/ml)
B
6
Vehicle
PBI-4050
**†
5
4
3
2
†
1
0
16
week
Insulin
24
week
25
Vanderbilt University Study
26
Vanderbilt University Study
27
PBI‐4547
Oral treatment with PBI-4547, a novel first-in-class anti-diabetic and anti-fibrotic compound,
improves blood glucose level and kidney function in the diabetic db/db mouse model
Lyne Gagnon, Kathy Hince, Liette Gervais, François Sarra-Bournet, Mikaël Tremblay, Marie-Pier Cloutier,
Shaun Abbott, Jean-Simon Duceppe, Boulos Zacharie, Pierre Laurin and Brigitte Grouix
PROMETIC BIOSCIENCES INC., LAVAL, QUÉBEC
PBI-4547 reduces blood glucose level
Photomicrographs
expansion (X100)
tissue
showing
mesangium
F)
0.4
db/db
30
20
10
NX C57BL/6
NX db/db
Day 0
B)
NX db/db +
PBI-4547
(10 mg/kg)
Day 42
db/db + PBI-4547 (50 mg/kg)
Histological Score
10
5
Day 0
Day 42
Day 42
D)
p = 0.006
0
NX C57BL/6
NX db/db
p = 0.008
NX db/db + NX db/db +
PBI-4547
PBI-4547
(10 mg/kg) (50 mg/kg)
Glucose/Insulin Ratio
p = 0.09
5
Day 105
35
20
10
NX db/db
NX db/db + NX db/db +
PBI-4547
PBI-4547
(10 mg/kg) (50 mg/kg)
PBI-4547 reduces mesangium lesions
1.0
0.5
p=0.0001
p=0.0001
p=0.0001
NX C57BL/6
NX db/db
NX db/db + NX db/db +
PBI-4547
PBI-4547
(10 mg/kg) (50 mg/kg)
Day 105
25
15
p=0.068
0.1
0.0
NX db/db +
PBI-4547
(50 mg/kg)
PBI-4547 reduces insulin resistance (Day 42 and Day 105)
30
p=0.035
function
1.5
15
NX db/db +
PBI-4547
(10 mg/kg)
kidney
0.2
G)
db/db + PBI-4547 (10 mg/kg)
20
C)
p=0.016
Day 105
25
NX db/db
increases
0.3
NX C57BL/6
PBI-4547 maintains or normalizes insulin level
NX C57BL/6
PBI-4547
(GFR)
0.0
NX db/db +
PBI-4547
(50 mg/kg)
30
25
20
15
10
p = 0.0002
p = 0.0003
p = 0.0003
5
0
NX C57BL/6
NX db/db
PBI-4547 reduces blood triglyceride
level
300
NX db/db + NX db/db +
PBI-4547
PBI-4547
(10 mg/kg) (50 mg/kg)
Triglycerides (mg/dl)
Glucose (ng/ml)
kidney
40
0
Glucose/Insulin Ratio
of
C57BL/6
50
0
Total nephrectomy of the right kidney
was performed on day 0 and animals
were treated with vehicle or PBI-4547
(10 and 50 mg/kg, oral once a day) from
day 1 through 104. Kidney function (GFR)
and kidney mesangium lesions were
examined (PAS staining).
Statistics: Student’s t-test
E)
60
Insulin (ng/ml)
STUDY DESIGN
RESULTS
A)
GFR (ml/min/gBW)
RATIONALE
Worldwide, 171 million people have
diabetes, and a number of complications
are associated with poorly controlled
hyperglycemia. Diabetic nephropathy is
one of the most common complications
of diabetes. Research points towards a
multifactorial etiology and complex interplay of several pathogenic pathways that
can contribute to the declining kidney
function in diabetes. Obese and diabetic
db/db mice exhibit a consistent mesangial
matrix expansion. The aim of this study
was to investigate the effect of PBI-4547
on blood glucose and insulin levels, and
kidney function in uninephrectomized (NX)
diabetic (db/db) mice.
200
p = 0.0024
100
0
p = 0.0002
NX C57BL/6
NX db/db
NX db/db + NX db/db +
PBI-4547
PBI-4547
(10 mg/kg) (50 mg/kg)
28
CONCLUSIONS
PBI-4547:
 Reduces blood glucose level
 Maintains or normalizes insulin level
 Reduces insulin resistance (glucose-insulin
ratio)
 Reduces blood triglyceride level
 Increases kidney function (GFR)
 Reduces mesangium lesions
PBI-4547 offers the potential as a novel
therapy for regulation of glucose metabolism
and reduction of diabetic nephropathy.
PBI‐4050 Clinical Program
PBI-4050: Clinical Program
H2 2014
Phase Ib
Multiple doses DKD patients
Safety & PK
(Canada) 2015
Phase Ib / II DKD patients
Multi center Study
Placebo controlled – double blind
(Canada & USA)
Phase Ib / II Idiopathic Pulmonary Fibrosis (IPF) patients
Multi center Study
Open Label
(Canada & UK)
Phase Ib / II Orphan condition (TBA)
Multi Center study
Open label
(Canada & UK & USA)
Objectives of the program:
Primary end points:
• Safety & tolerability in patients
• Effects on biomarkers for fibrosis in blood & urine
• Effects on diabetes (when applicable)
• Tissue analysis / biopsies (when applicable)
Information on dosing
Set the stage for phase II/III
29
Milestones to year‐end
• To disclose an additional Orphan indication for PBI-4050
• To file the IGIV IND with the FDA
• To disclose 2 additional PPPS™ derived Orphan Rx
• To close partnering deals providing :
• Financial contribution
• Access to market
• Additional manufacturing capacity
• Revenue range for H2 2014 ($15 M - $20 M)
• Subject to revenue recognition on licensing fees
• Revenue significantly higher in Q4
30
2015 Outlook
Development and Regulatory Milestones
In 2015, the Company expect to
• have 4 plasma‐derived Biopharmaceuticals in phase III
• file a BLA for plasminogen
• generate PBI‐4050 proof of concept data in humans (via multiple phase Ib/II)
• advance 2 new small molecules to be ready to enter clinical program in Q1 2016
• Secure multiple Orphan Drug Designations
Partnering
Multiple partnerships with drugs in clinical stage to provide:
• complementary expertise and financial contribution
• Access to market Revenue Growth
Increasing supply of Bioseparation affinity resins
Sales of plasma‐derived proteins
Expect strong H1 2015
31
Q&A
32