SG Cowen & Co. 25th Annual Health Care Conference

SG Cowen & Co. 25th Annual Health Care Conference
A focused healthcare company SG Cowen & Co. 25th Annual Health Care Conference Boston, March

Forward-looking statements
This presentation contains forward-looking statements as the term is defined in the US Private Securities Litigation Reform Act of Forward-looking statements provide our expectations or forecasts of future events such as new product introductions, product approvals and financial performance. You can identify these statements by the fact that they do not relate strictly to historical or current facts. They use words such as ‘anticipate’, ‘estimate’, ‘expect’, ‘project’, ‘intend’, ‘plan’, ’believe’ and other words and terms of similar meaning in connection with a discussion of future operating or financial performance. Such forward-looking statements are subject to risks, uncertainties and inaccurate assumptions. This may cause actual results to differ materially from expectations and it may cause any or all of our forward-looking statements here or in other publications to be wrong. Factors that may affect future results include interest rate and currency exchange rate fluctuations, delay or failure of development projects, production problems, unexpected contract breaches or terminations, government-mandated or market-driven price decreases for Novo Nordisk's products, introduction of competing products, Novo Nordisk's ability to successfully market both new and existing products, exposure to product liability and other lawsuits, changes in reimbursement rules and governmental laws and related interpretation thereof, and unexpected growth in costs and expenses. Risks and uncertainties are further described in reports filed by Novo Nordisk with the US Securities and Exchange Commission (SEC) including the company's Form 20-F, which was filed on 23 February Please also refer to the section Risk Management' in the Annual Report Novo Nordisk is under no duty to update any of the forward-looking statements or to conform such statements to actual results, unless required by law. Novo Nordisk has the copyright on the information contained in this presentation. © 2005 Novo Nordisk A/S. 13

Agenda Novo Nordisk – a focused healthcare company
Novo Nordisk in diabetes The metabolic syndrome Liraglutide - The first and only once daily human GLP-1 derivative New treatment modalities Insulin - the ultimate therapy NovoSeven® going forward

… and NovoSeven® is on its way to becoming a blockbuster
A focused healthcare company within attractive therapy areas Existing and new focus areas continue to offer attractive growth rates … … and NovoSeven® is on its way to becoming a blockbuster 250 500 750 1,000 1999 2000 2001 2002 2003 2004 20 15 Cancer 5Y CAGR 31% CNS GI Million USD Diabetes care % CAGR 10 Cardiovascular Arthritis Growth hormone Respiratory 5 Infectious disease 5 10 15 20 Expected % CAGR Source: SG Cowen, IMS/BW and Novo Nordisk 9

The evolution of mankind
2.5 mn years 50 years

Causes of the metabolic syndrome
Overweight/obesity Physical inactivity Genetics Closely associated with insulin resistance Underlying cause of diabetes Reduced HDL-C Elevated triglycerides Hypertension Abdominal obesity Hyper-glycaemia Obesity Dyslipidemia NCEP ATP III. Circulation. 2002;106:

Type 2 diabetes – a complex disease Incl
Genetic Acquired Glucotoxicity Lipotoxicity Insulin deficiency Impaired beta cell function Hepatic glucose production Glucose-induced insulin secretion Post receptor defect Hyperglycemia Tissue response to insulin Glucose uptake Basal hyper- insulinemia Glucose transport Insulin resistance Insulin binding Genetic Acquired Obesity Age

Shortcomings of available treatments
Progressive b-cell failure not counteracted Efficacy of available drugs is not sustained Treatment-related trade-offs Weight gain Hypoglycaemia Complexity of regimens Tolerability issues

Increased insulin response
What is GLP-1? Increased insulin response Key observations 80 A 31 amino acid peptide Cleaved from proglucagon in L-cells in the GI-tract (and neurons in hindbrain/hypothalamus) Secreted in response to meal ingestion (direct luminal and indirect neuronal stimulation) Member of incretin family (GIP, GLP-1 and others) GLP-1 has following effects: 60 Incretin effect IR-insulin (mU/l) 40 What is GLP-1? Glucagon-like peptide-1 (GLP-1) is a 31 amino acid peptide. It is an incretin hormone that is secreted from L-cells in the gastrointestinal system in response to calorie intake, causing the glucose dependent secretion of insulin. Incretins are chemical excitants that promote pancreatic sections (glucose-dependent insulinotropic polypeptide [GIP] is another example). The incretin effect is illustrated by the increased insulin response to glucose loads administered p.o. and i.v. References Nauck et al. Diabetologia 1986;29:46–52 * * * 20 * * * * Glucose-dependently stimulates insulin secretion and decreases glucagon secretion Delays gastric emptying Decreases food intake and induces satiety Stimulates -cell function and preserves or increases -cell mass in animal models –10 –5 60 120 180 Time (min) Insulin response to oral glucose load (50 g/400 ml, ●) and during isoglycaemic i.v. glucose infusion (●) Nauck et al. Diabetologia 1986;29: 46–52, *p ≤ 0.05.

Because of its short half-life, native GLP-1 has limited clinical value
7 37 9 Lys DPP-IV His Ala Thr Ser Phe Glu Gly Asp Val Tyr Leu Gln Ile Trp Arg i.v. bolus GLP-1 (15 nmol/l) 1000 Healthy individuals Type 2 diabetes Native GLP-1 is rapidly degraded by DPP-IV GLP-1 is stored in intestinal L-cells. As active GLP-1 is secreted from these cells, it is rapidly degraded by the enzyme dipeptidyl peptidase IV (DPP IV) resulting in the inactive, N-terminally truncated form, GLP-1-(9-36)amide. More than 50% of plasma GLP-1 appears to be in this inactive form. Because of its short half-life, native GLP-1 has limited clinical value The rapid degradation of GLP-1 into its inactive form by DPP-IV means that when administered as an i.v. bolus, it has a half-life of just 1.5–2.1 minutes. Combined with rapid clearance, this means that the action of GLP-1 has a very limited time span. References Vilsbøll et al. J Clin Endocrinol Metab 2003;88:220–224 500 Intact GLP-1 (pmol/l) –5 5 15 25 35 45 Time (min) Enzymatic cleavage High clearance (4–9 l/min) t½ = 1.5–2.1 minutes (i.v. bolus 2.5–25.0 nmol/l) Adapted from Vilsbøll et al. J Clin Endocrinol Metab 2003;88: 220–224.

Liraglutide is a long-acting GLP-1 analogue
His Ala Thr Ser Phe Glu Gly Asp Val Tyr Leu Gln Lys Ile Trp Arg C-16 fatty acid (palmitoyl) 7 9 37 Based on natural GLP-1 (97% homology) Liraglutide is a long-acting GLP-1 analogue In creating liraglutide, two modifications to the amino acid sequence of GLP-1 are made: a fatty acid is acylated to lysine at position 26 and the lysine at position 34 is replaced with arginine. These modifications result in increased self-association (which slows absorption from the subcutaneous depot), albumin binding and reduced susceptibility to DPP-IV, which combine to prolong its plasma half-life, protracting its action. Thus, the problem of the short half-life, which is the major clinical drawback of native GLP-1, is overcome. References Knudsen et al. J Med Chem 2000;43:1664–1669 Improved pharmacokinetics: Self-association Albumin binding Slow absorption from subcutis Metabolic stability Long plasma half-life Stability against DPP-IV Knudsen et al. J Med Chem 2000;43:

Plasma glucose (mmol/l)
Once-daily injection of Liraglutide covers 24-h BG profile in type 2 diabetes Placebo 14 Liraglutide (6 µg/kg OD) 12 24-h glucose AUC (mmol/l/h, mean ± SE) 232.3 ± 21.9 187.5 ± (p = 0.01) 10 Plasma glucose (mmol/l) Once-daily injection covers 24 hours in type 2 diabetes The sustained blood glucose lowering action of liraglutide was demonstrated in this study of 13 patients with type 2 diabetes. Patients received 1 week of once-daily subcutaneous liraglutide injections (6 μg/kg) and 1 week of once-daily placebo injections in a double-blind, crossover design. Previous OAD agents were discontinued 2 weeks prior to the study treatment period. Following liraglutide treatment, plasma glucose was consistently lower during a 24-hour test period than following placebo treatment. This observation was borne out statistically in an assessment of area under the curve (AUC; mmol/l/h) for this 24-hour test period (187.5 vs , for liraglutide and placebo, respectively, p = 0.01). References Degn et al. Diabetes 2003;52:498-P Degn et al. Diabetes 2004;53: 8 6 n=13 4 8 12 16 20 24 Time after injection (hours) Injection (08.00) Adapted from: Degn et al. Diabetes 2004;53:

Significant effect on glucose regulation Continuing weight loss
Liraglutide – a significant effect on both glucose regulation and weight Significant effect on glucose regulation Continuing weight loss Fasting serum glucose mM 2 A reduction of HbA1c of more than 1%-points despite this being only a 5 week trial 1 -1 -2 -3 -4 Mean change in body weight from baseline (%) -1 -2 -3 1 2 3 4 5 p<0.015 Time (weeks) Liraglutide and metformin Glimepiride and metformin Note: Data from the double-blind, double-dummy, randomised, parallel group dose titration phase 2 study including a total of 144 patients with an average HbA1c of %. All changes are from baseline; that is, FSG of mM and an average weight of kg.

Liraglutide selectively reduced calories obtained from candy
Effect on body weight and food intake in rats compared with DPP-IV inhibitor LAF-237 Total cumulated caloric intake was reduced with liraglutide (p=0.009) and unchanged with LAF237 ***p = 12w treatment in obese candy fed rats ***p = ns 35 30 25 Liraglutide, obese n = 10 Preclinical study comparing liraglutide with DPP-IV inhibitor LAF237 in obese rats NOTE: slide and notes based exclusively on what is in the accepted abstract. Particularly important for presenter in Med. Lounge to familiarize themselves with the notes as it is clearly impossible to explain this trial in just one slide. Also, do NOT verbally explain data that is not in the slide/notes. The slide is intended as a “teaser” for LB Knudsens poster. Aim and design: We have studied the difference on food intake and body weight of a long-acting GLP-1 derivative (liraglutide, t½ 12 h in man) and a long-acting DPP-IV inhibitor (LAF237) using obese rats fed a diet of chow and 5 weekly alternating kinds of candy, in order to mimic the excessive caloric intake in obese humans. We used 12 weeks treatment with liraglutide (0.2 mg/kg s.c. bid, n=10) and LAF237 (10 mg/kg p.o. bid, n=10). Results Bodyweight The liraglutide treated rats had a significant reduction in body weight, compared to vehicle treated obese rats (-14.2 ± 4.2 g vs ± 2.5 g, p=0.0001). Liraglutide treatment normalized the bodyweight of the obese rats to the level of a lean control group ( g vs g, p=ns). LAF237 treated rats had a weight gain comparable to vehicle (+24.3 ± 6.0 g vs ± 2.5 g, p=ns) and the body weight at the end of the study was significantly higher than the lean control group (341 ±2.1 g vs 309 ± 4.9 g, p=0.01). Caloric intake Liraglutide significantly (p=0.009) reduced total cumulated caloric intake. This reduction was a selective reduction in calories obtained from candy (p=0.001), since there was actually an increase in calories obtained from chow (p=0.017). No difference was found between LAF237 and vehicle treatment in caloric intake of obese rats. Conclusion: In conclusion, liraglutide normalized the bodyweight of obese candy fed rats and selectively reduced candy-derived caloric intake, whereas LAF237 showed no effect on bodyweight or caloric intake in obese candy fed rats. 20 LAF237, obese n = 9 15 Vehicle, obese n = 14 10 5 Body weight gain (g) Data are mean ± SEM -5 -10 -15 -20 Liraglutide selectively reduced calories obtained from candy Adapted from: Knudsen et al. Diabetes 2004;52(suppl 2):A339.

Effect on -cell glucose sensitivity after a single dose
2 4 6 8 10 12 14 Glucose (mmol/l) Insulin secretion rate (pmol/min/kg) Placebo Liraglutide 7.5 μg/kg Healthy controls Liraglutide restores -cell sensitivity to glucose after a single dose The effect of liraglutide on -cell sensitivity was assessed using a graded glucose infusion protocol, during which glucose is infused to create gradually rising plasma levels from 5–12 mmol/l over 3 hours. Approximately, 9 hours before the graded glucose infusion, patients with type 2 diabetes (n = 10) received a single subcutaneous dose of liraglutide (7.5 μg/kg) or a single dose of placebo in a double-blind, crossover design (3–6-week washout period). A group of healthy controls who did not receive any injections were also included. After an overnight fast and prior to glucose infusion, all groups received a small i.v. bolus of insulin (0.007–0.014 units/kg). This bolus reduced blood glucose to approximately 5 mmol/l in healthy controls, and 6 mmol/l in the liraglutide and placebo groups (this bolus probably explains the horizontal line between the first two measurements). Graded glucose infusion was then initiated and insulin secretion assessed. In all groups, insulin secretion increased concomitantly with increases in glucose concentration. However, after liraglutide dosing, the effect was more pronounced than following placebo, and the secretion rate was similar to that observed in the non-diabetic controls. Thus, a single dose of liraglutide is sufficient to reinstate the insulin response to glucose that is observed in healthy controls. References Chang et al. Diabetes 2003;52:1786–1791 n=10 Data are mean ± SEM. Adapted from: Chang et al. Diabetes 2003;52: 1786–1791.

Summary of results from preclinical and clinical studies with liraglutide
A 24-hour pharmacodynamic profile Once-daily injection Multiple anti-diabetic actions Increases insulin and lowers glucagon secretion Rapid and sustained glycaemic effect Weight control -cell mass increased in animal models -cell function improved in type 2 diabetes Strictly glucose-dependent actions Very low hypoglycaemia risk (no major and few minor events) Counter-regulatory response to hypoglycaemia not impaired Well-tolerated Mild, transient GI-symptoms; no antibodies (12-week data) Summary: liraglutide key results Liraglutide has a true 24-hour pharmacodynamic profile meaning that it can be administered as a once-daily injection, offering simplicity and flexibility to patients. Liraglutide has multiple anti-diabetic actions: It increases insulin and lowers glucagon secretion It has a rapid and sustained glycaemic effect It is not associated with weight gain and may promote weight loss It has been associated with increase -cell mass in animal models and improved -cell function in patients with type 2 diabetes The effect of liraglutide on pancreatic secretions is strictly glucose dependent This means that it has a very low risk of hypoglycaemia and that the counter-regulatory response to hypoglycaemia is not impaired Liraglutide is well-tolerated The most frequently reported adverse events are related to the gastrointestinal system and are typically transient. Furthermore, liraglutide treatment has not been associated with antibody formation

Key observations from two concepts
Exendin-4 Twice daily Peak Good effect on HbA1c Weight loss Antibodies Historical attempts to prolong GLP-1 action have led to injection site reactions Liraglutide Once daily Peakless Good effect on HbA1c and FBG Weight loss No antibodies No injection site reactions

Stop disease progression Symptomatic treatment
Potential future targets for Type 2 diabetes Possible targets Treatment aspiration Brain: GLP-1 Appetite regulators Liver: Hepatic enzyme inhibitors PPARα Glukokinase Glucagon antagonists PPARδ Cure Disease prevention Stop disease progression Symptomatic treatment Gut: DPP-IV Muscle/Fat: PPARγ Protein tyrosine phosphatase-1b (PTP-1b) PPARδ IkB Kinase AMPK1) 11bHSD12) Hormone Sensitive Lipase Adiponectin3) ß-cell: GLP-1 1) AMPK: Adenosine 5’-MonoPhosphate activated protein Kinase 2) 11bHSD1: 11b-hydroxysteroid dehydrogenase-1 3) Adiponectin: One of the adipocyte-expressed proteins that function in the homeostatic control of glucose, lipid, and energy metabolism.

Beta-cell regeneration e.g.
Examples of potential future type 2 diabetes drug candidates at Novo Nordisk Glucose lowering e.g. Glucagon receptor antagonists Obesity e.g. Histamine H3 receptor antagonists Beta-cell regeneration e.g. Transition Therapeutics, Islet neogenesis therapy

Inappropriate hepatic glucose production in type 2 diabetes
Phosphatase Glucokinase Glucose-6-Phosphate Glycogen phosphorylase Fructose 1-6-bisphosphatase Glucagon Glycogenolysis Gluconeogenesis Glycogen Synthase Glycerol Lactate Amino acids fructose Glycogen PEPCK

Hyperglucagonemia through-out the day in people with type 2 diabetes
Glucagon (pg/ml) Time Time Reaven et al. J. Clin. Endo. & Metab. 1987

Lowered glucose in glucagon receptor knockout mice
Blood glucose (ad lib fed) 25 50 75 100 125 3 6 9 12 15 18 ** *** * Time (min) Blood Glucose (mM) GR+/+ GR-/- 500 1000 1500 AUC IP-GTT GR-/- GR+/+ RW Gelling et al. PNAS 100: , 2003

Decreased fat mass in glucagon receptor KO mice
+/+ -/- RW Gelling et al. PNAS 100: , 2003

Glucagon receptor antagonists activities
Discovery: Potent, selective, competitive and reversible glucagon receptors antagonists with acceptable pharmacokinetics have been identified The glucagon receptor antagonists improve glucose handling in animal models of type 2 diabetes Development: The glucagon receptor antagonist NN2501 is currently in phase 1 with the aim of evaluating the concept in humans

Islet Neogenesis Therapy
Regeneration of beta cells in animal models of type 1 and type 2 diabetes following Islet Neogenesis Therapy (INT): a combination of the growth factors EGF and Gastrin In a type 2 diabetes animal model Psammomys obesus (Sand rat) In a type 1 diabetes animal model: Non obese diabetic mouse (NOD)

Islet Neogenesis Therapy: proposed mechanism of action
Regeneration of islet cells in the body using two growth factors, Epidermal Growth Factor (EGF) and Gastrin that reproduces fetal development Fetal Development BIRTH Islet Precursor Stem Cell Nesidioblast proliferation Mature Islet Low level Insulin Expression New islet budding from duct EGF Gastrin

Morning blood glucose in Psammomys obesus before, during and after treatment with INT or vehicle
HE LE HE INT Follow-up 20 Vehicle, N=8 Blood glucose in mmol/l 10 INT, N=6 -10 10 20 30 40 50 Days after start of HE diet

Psammomys obesus pancreas after 2 weeks INT
Islet cell mass 150 125 Vehicle INT 100 cell mass mg/kg INT 75 50 25 Vehicle Beta Non Beta

Insulin is the ultimate treatment for type 2 diabetes…
Benefits of the addition of insulin therapy in type2 diabetes Restore postprandial insulin response and improve basal insulin levels to near normal Improve insulin sensitivity in peripheral tissues and reverse insulin resistance Spare beta cells and preserve beta-cell function Prevent development of microvascular complications -Cell function Insulin OADs Diet and exercise Time from diagnosis Source: UKPDS Study Group 1998, Daily G; Clinical Therapeutics/vol 26, no

Out of ‘guideline’ control
HbA1c 50% Real-life insulin initiation 10% It is estimated that more than 2/3 of the patients are not in control 9% 8% ADA Type 2 - slope IDF 7% ADA EASD/AACE 6% -cell function Type 1 – immediate need for insulin Recommended insulin initiation Guideline control Time from diagnosis Note: ADA is American Diabetes Association, IDF is International Diabetes Federation, EASD is European Association for the Study of Diabetes, AACE is American Association of Clinical Endocrinologists Source: Novo Nordisk type 2 diabetes market research, Roper Starch, ADA, EASD, IDF, AACE, Wright A., Burden et al, Diabetes Care 2002; 25:330–336, Turner RC, Cull et al, JAMA 1999; 281:2005–2012

Hypoglycaemia in UKPDS: a problem, also in type 2 diabetes
Around 50% of patients are very worried about the risk of hypoglycaemic events Fear of hypoglycaemia and need for careful blood glucose monitoring contributes to psychological insulin resistance Concerns regarding hypoglycaemia is a barrier to intensifying treatment % patients reporting hypo-glycaemia during treatment with Per year SU Insulin Metf. Any event 17.0 37.0 13.0 Major event*) 0.7 2.3 0.3 *) Requiring 3rd party help 1. UKPDS 16. Diabetes 1995;44:1249– Riddle et al. Diabetes Care 2003;26:3080–3086. 1. Alberti. Pract Diab Int 2002;19:22– Korytowski. Int J Obesity 2002;26(Suppl 3)18– Hunt et al. Diabetes Care 1997;20:292– Leslie et al. Diabetes Spectrum 1994;7:52.

The Levemir® puzzle: - It all comes together
-0.8 ±2.4 kg 0.1 ±2.0 kg -1 1 p < 0.001 Change in body weight Change in Hb1Ac -0.5 -0.28 0.5 p < 0.001 Predictable Hypos 0.9 2.1 1 3 2 p < 0.001 Nocturnal hypoglycaemia Levemir®/NovoRapid® Human insulin HbA1c 8.6 11.1 5 15 10 p < 0.001 Hypoglycaemia all Weight Source: Diabetologia (2004) 47: Study design: 18-week study, 1:1 randomised, open-labelled, parallel trial, 595 patients with type 1 diabetes mellitus received insulin detemir or NPH insulin in the morning and at bedtime in combination with mealtime insulin aspart or regular human insulin respectively.

Levemir® vs. NPH in treat-to-target trial: HbA1c and hypoglycaemia
9.0 47% risk reduction p < 0.001 NPH + OAD 18 Insulin detemir + OAD 16 8.5 14 8.0 12 HbA1c (%) 7.5 Events per patient per year 10 55% risk reduction p < 0.001 8 7.0 6 6.5 The plot is using arithmetic means (results in previous slides show least square means corrected for baseline). Data V1 V2 V10 V13 Detemir (6.58) NPH (6.46) Already after 12 weeks of treatment patients are achieving a nice level of HbA1c with the treat to target. Getting it closer, +SD HbA1c level 4 2 -2 12 24 Overall Nocturnal Weeks Hypoglycaemia Hermansen et al. EASD Poster 754:PS 64.

Levemir® vs. NPH insulin Treat-to-target trial: HbA1c and weight
9.0 3.5 Insulin detemir + OAD + 2.8 kg 8.5 NPH + OAD 3 2.5 8.0 HbA1c (%) Change in weight from baseline to endpoint (kg) 2 7.5 1.5 + 1.2 kg 7.0 1 The plot is using arithmetic means (results in previous slides show least square means corrected for baseline). Data V1 V2 V10 V13 Detemir (6.58) NPH (6.46) Already after 12 weeks of treatment patients are achieving a nice level of HbA1c with the treat to target. Getting it closer, +SD HbA1c level 6.5 0.5 -2 12 24 Insulin detemir + OAD NPH + OAD Weeks Hermansen et al. EASD Poster 754:PS 64.

Adapted from T. Heise, et al. Diabetes 2004.
The reasoning behind the superior Levemir® profile Clamp-profiles for NPH insulin, insulin glargine and Levemir® NPH Insulin glargine Levemir Adapted from T. Heise, et al. Diabetes 2004.

Analogues supported by strong device portfolio
Novo Nordisk is the only company offering the full range of analogues Analogues supported by strong device portfolio Convenience Novo Nordisk ønsker som ledende diabetes selskab, at kunne imødegå alle disse behov via mage forskellige produkter. Som det ser her er – eller vi inden for en rum tid – være I stand til at møde disse behov med vores analog portefølje. Supperteret at vores stærke leveringssystemer Meeting physiological need for control

Diabetes care pipeline
Compound Type Indication Phase Levemir® (insulin detemir) Insulin Type 1+2 diabetes Being rolled out in EU Filed US Phase 3 JP NovoMix® 50 and 70 Filed EU+JP AERx® iDMS (NN1998) Phase 2 Liraglutide (NN2211) GLP-1 analogue Type 2 diabetes NN344 Phase 1 NN2501 OAD

NovoSeven® - expanding into general haemostasis
Key observations Trauma Regulatory dossier for blunt trauma submitted to EMEA early January 2005 Trial targeting the US to be initiated in Q2 2005 Congenital clotting disorders Bleedings in emergencies High single-dose Trauma FVII deficiency TBI Intracerebral haemorrhage Acquired haemophilia Prophylaxis ICH Regulatory dossier expected to be submitted to EMEA by mid-2005 A global phase 3 trial to be initiated in Q2 2005 Glanzmann’s UGI Variceal bleedings Orthopaedic surgery Our sencond value driver is NovoSeven, which is a recombinant version of the koagulation factor 7a originally developed for treating haemophilia patients with inhibitors towards their traditional treatment. Even since lanch NovoSeven has shown impressive growth rates. Having been on the market since 96 in Europe, 99 in the US we are reaching saturation of the market for the existing indication, hence growth going forward has to be derived for increased investigational use of NovoSeven and eventually new indications. That why we are very pleaseed with the clinical data we have gotten from our NovoSeven expansion programme during the past 6 months, especially the result from the trial on the use of NovoSreven in trauma where we saw a statistically significant reduction in the need for blod transfusions as well as a trend towards lower mortality – a parameter the trial not was designed to show statistical significance on...In terms of upcoming events we will report from the study on the use of NovoSeven in ICH mid 2004. Liver transplantation Cardiac surgery Hepatectomy Current activities ICH data published in NEJM in February 2005 Trauma data to be published in medical journals during 2005 Several studies ongoing Spinal surgery Critical bleedings in elective surgery

Factor VII first filings of patent applications by Novo Nordisk
NovoSeven® - Novo Nordisk keeps expanding the IP rights Factor VII first filings of patent applications by Novo Nordisk Key observations More than 80 patent filings so far Major patent expirations are US end 2010 EU early 2011 Japan 2008 Our sencond value driver is NovoSeven, which is a recombinant version of the koagulation factor 7a originally developed for treating haemophilia patients with inhibitors towards their traditional treatment. Even since lanch NovoSeven has shown impressive growth rates. Having been on the market since 96 in Europe, 99 in the US we are reaching saturation of the market for the existing indication, hence growth going forward has to be derived for increased investigational use of NovoSeven and eventually new indications. That why we are very pleaseed with the clinical data we have gotten from our NovoSeven expansion programme during the past 6 months, especially the result from the trial on the use of NovoSreven in trauma where we saw a statistically significant reduction in the need for blod transfusions as well as a trend towards lower mortality – a parameter the trial not was designed to show statistical significance on...In terms of upcoming events we will report from the study on the use of NovoSeven in ICH mid 2004.

Taking NovoSeven® beyond patent expiration - an example
Clot Firmness Build on rFVIIa mechanism of action to provide fast and efficient local haemostasis Same activity as rFVIIa when bound to tissue factor Increased activity when bound to the activated platelet Time (s) Our sencond value driver is NovoSeven, which is a recombinant version of the koagulation factor 7a originally developed for treating haemophilia patients with inhibitors towards their traditional treatment. Even since lanch NovoSeven has shown impressive growth rates. Having been on the market since 96 in Europe, 99 in the US we are reaching saturation of the market for the existing indication, hence growth going forward has to be derived for increased investigational use of NovoSeven and eventually new indications. That why we are very pleaseed with the clinical data we have gotten from our NovoSeven expansion programme during the past 6 months, especially the result from the trial on the use of NovoSreven in trauma where we saw a statistically significant reduction in the need for blod transfusions as well as a trend towards lower mortality – a parameter the trial not was designed to show statistical significance on...In terms of upcoming events we will report from the study on the use of NovoSeven in ICH mid 2004. FVIIa – 25 nM (90 µg/kg) FVIIa – 200 nM (720 µg/kg) Analogue-1 – 25 nM Analogue-2 – 25 nM Analogue-3 – 25 nM

Taking NovoSeven® beyond patent expiration
Extensive preclinical activities ongoing Formulations Ready-to-use device Alternative formulation Heat stable Analogues Various analogues Derivatives Long-acting derivative Combinations FXIII combination therapy Our sencond value driver is NovoSeven, which is a recombinant version of the koagulation factor 7a originally developed for treating haemophilia patients with inhibitors towards their traditional treatment. Even since lanch NovoSeven has shown impressive growth rates. Having been on the market since 96 in Europe, 99 in the US we are reaching saturation of the market for the existing indication, hence growth going forward has to be derived for increased investigational use of NovoSeven and eventually new indications. That why we are very pleaseed with the clinical data we have gotten from our NovoSeven expansion programme during the past 6 months, especially the result from the trial on the use of NovoSreven in trauma where we saw a statistically significant reduction in the need for blod transfusions as well as a trend towards lower mortality – a parameter the trial not was designed to show statistical significance on...In terms of upcoming events we will report from the study on the use of NovoSeven in ICH mid 2004.

Investor information Investor Relations contacts Novo Nordisk A/S Investor Relations Novo Allé, DK2880 Bagsværd Fax (+45) Mogens Thorsager Jensen Tel (direct): (+45) Palle Holm Olesen Tel (direct): (+45) In North America: Christian Kanstrup Tel (direct): (+1) Share information Novo Nordisk’s B shares are listed on the stock exchanges in Copenhagen and London. Its ADRs are listed on the New York Stock Exchange under the symbol ‘NVO’. For further company information, visit Novo Nordisk on the internet at

SG Cowen & Co. 25th Annual Health Care Conference

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