First-in-class AD asset to deliver Phase IIa data

Probiodrug 7 September 2016 Outlook

Probiodrug

First-in-class AD asset to deliver Phase IIa data

Corporate outlook

Pharma & biotech

7 September 2016

Price

€20.15

Market cap

€149m

Net cash (€m) at end Q216

14.2

Shares in issue

7.4m

Free float

50%

Code

PBD

Primary exchange

Euronext Amsterdam

Secondary exchange

N/A

Share price performance

%

1m

3m

12m

Abs

(1.7)

6.6

8.4

Rel (local)

(5.1)

2.3

(14.6)

52-week high/low

€26.5

€17.6

Business description

Probiodrug is a German biopharmaceutical company developing its clinical pipeline for the treatment of Alzheimer’s disease. Lead product candidate PQ912 is in Phase IIa. PQ912 is a small molecule inhibitor of glutaminyl cyclase (QC), which is essential for the formation of pGlu-Abeta. Two further products are in preclinical stages.

Next events

Q316 results

10 November 2016

PQ912 first Phase IIa data

End-2016

PQ912 full Phase IIa data

Early 2017

Analysts

Jonas Peciulis

+44 (0)20 3077 5728

Lala Gregorek

+44 (0)20 3681 2527

Probiodrug is a research client of Edison Investment Research Limited

Full results from Probiodrug’s lead Phase IIa SAPHIR trial are expected to be announced early in 2017, which will be a major milestone for the pure-play Alzheimer’s disease (AD) company. The trial investigates the effects of first-in-class PQ912, a small molecule glutaminyl cyclase (QC) inhibitor, on AD patients. The differentiated approach in the AD field and likely sufficient cash position of €14.2m until the readout should be supportive to the share price. We value Probiodrug at €309m or €41.5/share.

Year end

Revenue (€m)

PBT*
(€m)

EPS*
(€)

DPS
(€)

P/E
(x)

Yield
(%)

12/14

0.0

(11.4)

(2.35)

0.0

N/A

N/A

12/15

0.0

(13.5)

(1.96)

0.0

N/A

N/A

12/16e

0.0

(14.2)

(1.91)

0.0

N/A

N/A

12/17e

0.0

(11.0)

(1.48)

0.0

N/A

N/A

Note: *PBT and EPS are normalised, excluding amortisation of acquired intangibles, exceptional items and share-based payments.

H116 update: R&D progress on track

On 30 August, Probiodrug released its H116 report, which showed that the company is on track with the lead Phase IIa trial, with PQ912 to deliver results in coming months. R&D spend in H116 was €4.7m and in line with €4.5m expensed in H115. We keep our full-year R&D cost estimate of €11.1m (€10.2m reported in 2015), as Probiodrug guided that its 2016 net loss may be greater than in 2015 due to increased development activities. G&A expenditure of €1.3m was lower compared to €1.9m in H115, thus indicating good cost management.

Key catalyst approaching; strategy after Phase IIa

Probiodrug’s Phase IIa SAPHIR trial is investigating the effects of PQ912 in AD patients and is due to report first results at end-2016 with the full data to be announced three to four months later. Although primarily a safety and tolerability study, the effect on the pathology of the disease will be assessed by a set of exploratory readouts. Since the treatment duration in Phase IIa is a relatively short three months, development strategy after Phase IIa will depend on the results of the trial. This could lead to a Phase IIb trial or directly to a Phase III trial. Obtaining cognition improvement over such a short term would be a best case scenario, but we do not believe this is a prerequisite to establish an attractive partnership deal before moving into late stage development, as exploratory readout will include a comprehensive set of measures to assess the effects of PQ912.

Valuation: Risk-adjusted NPV of €309m

Our valuation of Probiodrug is slightly increased, from €303m or €40.7/share, to €309m or €41.5/share due to rolling our model forward, which offset the lower cash position of €14.2m. Our model suggests net cash of €14.2m at end H116 should be sufficient to fund operations to mid-2017, by which time the full data from the Phase IIa study would be out. The outcome of the Phase IIa trial is the main catalyst in the near term.

Investment summary

Company description: Differentiated approach for AD

Probiodrug is a German biopharmaceutical company developing therapies for the treatment of AD. The company is employing a differentiated approach targeting the toxic Abeta version of pyroglutamate-Abeta (pGlu-Abeta) with two strategic legs. Lead product candidate small molecule PQ912 prevents the formation of pGlu-Abeta by inhibiting QC, while pGlu-Abeta specific monoclonal antibody (PBD-C06) directly targets pGlu-Abeta leaving non-toxic forms of Abeta untouched. PQ912 is currently recruiting for a Phase IIa study with initial data expected end-2016. An earlier-stage, preclinical AD pipeline include another small molecule QC inhibitor with an optimised pharmacokinetic/pharmaco-dynamic profile.

Probiodrug was founded in 1997, pioneering a new class of anti-diabetics (gliptins) with multiple large pharma partnerships. The company has focused solely on AD since selling the diabetes franchise to OSI Pharmaceuticals for €28.7m (2004) and the Ingenium CDK9 research programme to AstraZeneca for $1m (2013). Probiodrug is based in Halle, Germany, and employs 16 people. Since 2007 it has raised c €114m from investors and management, including gross proceeds of €23.2m from the IPO in October 2014, listing on Euronext Amsterdam at €15.25/share.

Exhibit 1: Product pipeline

Product

Stage

Patent expiry

Mechanism of action

Notes

PQ912

Phase IIa

2030

Small molecule inhibitor of glutaminyl cyclase (QC), the enzyme catalysing the formation of pGlu-Abeta.

SAPHIR study (n=110 with early AD) – first patient enrolled in March 2015. First data expected end-2016 with full results 3-4 months later.

PBD-C06

Preclinical

2029

pGlu-Abeta specific monoclonal antibody. Selectively targets pGlu-Abeta.

Successfully humanised and de-immunised. Manufacturing process optimised in October 2015. Animal toxicology studies in plans.

PQ1565

Preclinical

2034

Small molecule QC inhibitor.

GMP process is being implemented.

Source: Probiodrug, Edison Investment Research. Note: Patent expiries do not include potential extensions.

Valuation

Our Probiodrug valuation is €309m or €41.5/share, based on a risk-adjusted NPV analysis using a 12.5% discount rate. This includes €14.2m net cash reported at end H116 and PQ912 for use in mild AD. We assume PQ912 can achieve peak sales of c €6bn in 2028 (around six years post our forecast 2022 launch). This is based on the assumption that PQ912 will demonstrate disease-modifying benefits, which would be likely to lead to premium pricing, and would be achievable even with only modest penetration of mild AD patients.

Financials

Probiodrug reported cash of €14.2m at end H116. Our post-H116 model suggests that this should be sufficient to fund operations until around mid-2017 with the final Phase IIa results due in the beginning of 2017. Existing funding is sufficient to reach the readout, in our view; however, it is uncertain whether the company will be required to repay tax provisions of €2.6m; if it does, the cash reach is likely Q117. In either case, the readout will be imminent or past at that point, which in turn will drive the strategic pathway.

Sensitivities

The main sensitivity for Probiodrug is the outcome of the Phase IIa trial of lead candidate PQ912, with first data expected by end-2016. Although PQ912 has shown efficacy in animal models and proved safe in the Phase I trial, whether this will translate into clinical benefit remains to be seen. Beyond Phase IIa, Probiodrug will need to partner PQ912 to continue its development. Drug development in AD is notoriously perilous, although this could well be justified by the significant size of the market and potential for considerable rewards.

Outlook: Key catalyst approaching

SAPHIR trial: In full swing

Currently Probiodrug is running a Phase IIa SAPHIR trial to investigate PQ912 effects in AD patients, with the first patient enrolled on 9 March 2015 (Exhibit 2). Although primarily a safety and tolerability study, the effect on the pathology of the disease will be assessed by a set of exploratory readouts comprising:

assessment of short-term memory and verbal function (neuropsychological test battery, NTB);

functional assessments by EEG and functional MRI, which will be indicative of changes in synaptic plasticity and neuronal connectivity respectively; and

molecular biomarkers in cerebrospinal fluid (CSF), such as pGlu-Abeta, Abeta oligomers and inflammatory markers.

The first data are expected by end-2016, with the full results due three to four months later.

Exhibit 2: SAPHIR clinical study design

Aim

To determine the safety, tolerability and preliminary efficacy of PQ912 in patients with early AD. Exploratory readouts will be used to look for an efficacy signal to justify advancing to pivotal study.

Summary design

Multicentre (20 sites, seven EU countries), randomised, double-blind, placebo-controlled, parallel-group study.

Design details

n=110. Treatment-naïve patients with mild cognitive impairment due to AD or mild dementia due to AD. MMSE score of 21-30 inclusive, CSF Abeta concentration of < 638 ng/L AND total tau >375 ng/L OR p-tau > 52 ng/L; Tau/Abeta ratio in CSF >0.52; positive amyloid PET if available. Half will receive PQ912, 800mg, twice a day (with an option to decrease the dose if necessary), the other half will receive placebo.

Primary endpoints

Frequency of adverse events and serious adverse events (time frame: 12 weeks, four weeks follow-up).

Exploratory readouts

Assessments of cognitive function and change from baseline in brain functional assessments as brain functional connectivity and synaptic plasticity and molecular biomarker levels in CSF.

Start date

March 2015

Completion dates

Estimated primary completion date end-2016 (first data); full results will be announced three to four months later.

Source: Probiodrug, Edison Investment Research; clinicaltrials.gov. Note: MMSE = mini mental state examination.

Development strategy after Phase IIa

Since the treatment duration in Phase IIa is relatively short at three months, the development strategy after Phase IIa will depend on the results of the trial. Probiodrug could go directly to a pivotal Phase III study if the Phase IIa trial shows clear positive signs of PQ912 clinically improving cognition and neuronal connectivity (measured by EEG, fMRI) or molecular biomarkers. A Phase IIb study to evaluate the efficacy over a longer treatment period is another option if the exploratory readout shows a less clear signal after the three-month treatment.

Green light from chronic animal toxicology data

In April 2016, Probiodrug announced a completion of chronic toxicology studies in the chronic animal toxicology studies confirming a favourable therapeutic margin and further de-risking the lead asset PQ912. PQ912 was tested in rats and dogs for six and nine months, respectively. There were no new findings and no aggravation of the minimal to slight, non-adverse findings compared to the previous shorter one-month and three-month studies conducted in the same animal species. These study results are a regulatory prerequisite and, if approved by the health authorities, allow longer treatment trials with AD patients.

SAPHIR data could trigger a partnership

Probiodrug’s strategy is to establish a partnership to develop PQ912 through late stage studies. If the Phase IIa shows cognition improvements with such a short treatment time as three months, in our view, the company would be in an excellent position to negotiate an attractive partnership deal. Nevertheless, we believe that cognition improvement is not a prerequisite for a partnership, and that a partnership will depend on the detailed data readout.

Phase I details published

Although the headline Phase I data had been published before, in December 2015 Probiodrug announced the publication of the full Phase I results in a peer reviewed journal.1 As a reminder, this was a first-in-man, single and multiple ascending dose study that tested PQ912 in over 200 young and elderly healthy volunteers and assessed the safety, pharmacokinetics (PK, “what the body does to a drug”) and pharmacodynamics (PD, “what a drug does to the body”) of PQ912. Eighty-three subjects received single doses of PQ912 up to 3,600mg and 80 subjects received multiple doses of PQ912 up to 800mg per day. Notably, this study was the first to quantify QC (enzyme that catalyses pGlu-Abeta formation) activity in human plasma and cerebrospinal fluid (CSF). The key findings include:

  I. Lues. A phase 1 study to evaluate the safety and pharmacokinetics of PQ912, a glutaminyl cyclase inhibitor, in healthy subjects. Alzheimer’s & Dementia: Translational Research & Clinical Interventions 1 (2015) 182-195.

PQ912 was safe and well tolerated with most adverse events mild or moderate (GI symptoms, headache) and the maximum tolerated dose was not reached.

Absorption was rapid with maximum plasma concentration reached in 0.5-1.5 hours. The half-life for the concentration decline from maximum concentration to 12 hours post-dose was between two and three hours, but around six hours in CSF (clinically relevant compartment) allowing for a convenient dosing for the patient, while maintaining constant inhibition of QC (the target).

Concentrations of PQ912 in the blood and in CSF correlated well with respective QC inhibition (Exhibit 3). The CSF QC inhibition was estimated at 70% after dosing of 400mg (received in two doses daily) and 90% at 800mg, therefore the latter was selected for the Phase IIa study.

An important achievement was the fact that the study established a PK/PD correlation between plasma and CSF, which allows for estimation of the target QC inhibition in CSF from blood plasma without the need for CSF collection with lumbar puncture, which requires specialist intervention.

Exhibit 3: PK/PD relationship between PQ912 and QC inhibition in blood and CSF

Source: I. Lues et al. (A) Correlation of PQ912 free plasma concentrations with serum QC inhibition.
(B) Correlation of PQ912 CSF concentration with CSF QC inhibition. Abbreviations: CSF, cerebrospinal fluid; QC, glutaminyl cyclase.

A complementary, earlier-stage pipeline

In addition to PQ912, Probiodrug has an earlier-stage pipeline focused on AD and targeting pGlu-Abeta. This includes PBD-C06, a monoclonal antibody, as well as PQ1565, a follow-on to PQ912. In addition to AD, Probiodrug intends to evaluate the potential of QC inhibitors in other conditions, such as Down’s syndrome and Huntington disease.

PBD-C06

PBD-C06 is a preclinical pGlu-Abeta specific monoclonal antibody, which recognises pGlu-Abeta with very high selectivity and affinity to multiple forms. Preclinical AD animal studies have demonstrated the ability of PBD-C06 to reduce pGlu-Abeta and total Abeta, with consequent rescue of short-term memory deficits and significant improvement of learning and memory after chronic treatment. PBD-C06 has been successfully humanised and de-immunised, so as to avoid detection and attack by the patient’s own immune system. The manufacturing process was optimised in October 2015. Animal toxicology studies are planned for PBD-C06. Probiodrug is currently investigating its potential as a combination therapy with PQ912.

Eli Lilly is also developing a pGlu-Abeta antibody, LY3002813 (Lilly’s internal name is anti-N3pG monoclonal antibody), which is in Phase I. It has announced initial findings from 49 patients (total enrolment of 100 patients is planned according to clinicaltrials.gov) at the Alzheimer’s Association International Conference (AAIC) in July 2016. The patients were with mild cognitive impairment (MCI) due to AD or mild to moderate AD and received single ascending (SAD) and multiple ascending (MAD, monthly) doses. Follow up after the last dose was up to 84 days. Key findings include:

Patients who received the highest dose (10mg intravenously) in the MAD part showed a very significant reduction in Abeta plaques of about 40% measured by positron emission tomography (PET) scans using AD-specific tracer florbetapir (AMYViD, Eli Lilly/Avid Radiopharmaceuticals). Lower doses were ineffective.

The effective dose of 10mg did not induce vasogenic oedema, one of the amyloid related imaging abnormalities (ARIA) and only two asymptomatic microhemorrhages were reported. These adverse events are commonly the dose limiting effects of other plaques-targeting antibodies like aducanumab. No other side effects were reported.

Lilly announced that more details will be given at the 9th Clinical Trials on Alzheimer’s Disease conference in December 2016.

Eli Lilly commented that the half-life of antibodies was unexpectedly short, with four days using the 3mg dose and 10 days with the 10mg dose, while usually antibodies have a half-life of at least 20 days. Another surprising issue was high levels of anti-drug antibodies (patient’s own immune system neutralising the drug). This will need to be further clarified and could be overcome by adjusting the dose. Overall, we view these data as supportive to the concept and worth exploring further. Phase I trials even if performed with AD patients (and not with healthy volunteers) are not designed to capture cognitive effects, while good safety data and plaque-lowering effect in humans seem to support the QC inhibition concept and help Probiodrug guide development of PBD-C06. This also supports the rationale to combine QC inhibitors with anti-pGlu-Abeta antibodies.

PQ1565

PQ1565 is a second small molecule QC inhibitor in preclinical development with further optimised PK/PD characteristics. Probiodrug is currently planning toxicology studies, and is scaling up production.

Combination therapy exploration is rational strategic step

The growing use, and success, of combination therapies with additive and synergistic actions or reducing the dose of the combined drugs for the treatment of cancer has led to the strong rationale that this approach is likely to be successful in AD. In 2014, Eli Lilly reported that a preclinical study of combination therapy with pGlu-Abeta antibody LY3002813, and BACE inhibitor LY2811376 cleared more than 80% of amyloid from the brain of AD mouse models, compared to c 50% clearance each for the respective monotherapies. Combined treatment of Roche’s anti-Abeta antibody, gantenerumab, and a BACE inhibitor also led to enhanced amyloid reduction in AD mouse models in a separate study.

As they act via a different approach, Probiodrug’s candidates would be well suited as part of a combination therapy approach targeting multiple steps in the Abeta cascade. Probiodrug is conducting pre-clinical proof of principle studies for PQ912 in combination with a BACE inhibitor and with PBD-C06. In addition to BACE inhibitors, which act upstream in the Abeta cascade, therapies targeting tau (a misfolded protein that is also a pathological hallmark of AD), acting on the downstream effects, could theoretically be another potential combination partner.

Overview of AD and pGlu-Abeta

The traditional amyloid hypothesis postulates that insoluble plaques of Abeta (a small protein fragment) are the key neurotoxic culprit in AD. In recent years a modified amyloid hypothesis has emerged proposing that not all Abeta is toxic, nor are the plaques themselves toxic. Instead, misfolded soluble Abeta oligomers, or “pre-plaques”, are proposed to be the primary driver of the pathological pathway to AD. These toxic oligomers induce other Abeta molecules to take on the misfolded form and aggregate into plaques.

A specific form of Abeta, pGlu-Abeta, has been shown to trigger the formation of these hypertoxic Abeta oligomers, propagating in a chain reaction-like mechanism.2 This initiates a pathological cascade, with loss of connection between neurons (synaptic dysfunction), tau pathology, neuroinflammation and eventual neuronal death (neurodegeneration) with resultant cognitive decline. Unlike Abeta plaques, which are also seen in cognitively normal individuals, pGlu-Abeta is specific for AD and correlates with the progression of AD pathology.2

  Morawski M, et al. Glutaminyl cyclase in human cortex: correlation with (pGlu)-Amyloid- βload and cognitive decline in Alzheimer’s disease. Journal of Alzheimer’s Disease 39, 385-400 (2014).

In 2004 Probiodrug’s scientists discovered the key enzyme that is essential for the formation of pGlu-Abeta from Abeta peptides, QC. QC expression has been found to be upregulated in the brains of people with AD correlating with the appearance of pGlu-Abeta and the decline in mini mental state examination (MMSE). Inhibition of QC in animal AD models effectively blocked the production of pGlu-Abeta, prevented the aggregation of all types of Abeta in the brain and demonstrated that QC inhibitors can reduce neurotoxicity, neuroinflammation and restore cognitive function.3 While most new therapies have focused on Abeta formation or the clearance of Abeta plaques, Probiodrug is taking a differentiated approach, focusing on the formation and clearance of pGlu-Abeta specifically.

  Schilling S, et al. Glutaminyl Cyclase inhibition attenuates pyroglutamate Abeta and Alzheimer’s disease-like pathology. Nature Medicine 14(10):1106-11 (2008).

Probiodrug has an extensive patent portfolio, which it believes sufficiently protects its product candidates and the QC target by composition of matter and medical use claims in AD, including combination claims, and also in inflammatory diseases and other indications, such as Down’s syndrome.

Choosing the right AD patient population

Translating preclinical promise into clinical improvement in humans has proved challenging for several therapies targeting Abeta, with a number of pivotal trial failures. It has been proposed that the primary reasons for failure were that the target patient population was too far advanced and, simultaneously, some patients did not have the neuropathology of AD.4 Exhibit 4 illustrates that AD pathology emerges years before onset of clinical symptoms, offering a significant window for interventions that could either delay or prevent symptom onset. Current consensus is that therapies should target the earliest stages of the Abeta pathogenic sequence; in pathological terms ideally before plaques are established, and in clinical terms when there remains a potential for a sufficient cognitive reserve.5 It is also interesting to note that in AD patient brain biopsies pGlu-Abeta emerges at the brink between preclinical and clinical AD stages.6

  Schneider LS, et al. Clinical trials and late-stage drug development for Alzheimer’s disease: an appraisal from 1984 to 2014. J Intern Med. 275(3):251-283 (2014).

  Lemere, C. Immunotherapy for Alzheimer’s disease: hoops and hurdles. Mol Neurodegener. 8:36 (2013).

D. Thal et al. Neuropathology and biochemistry of Aβ and its aggregates in Alzheimer’s disease. Acta Neuropathol (2015) 129:167-182

Exhibit 4: Chronological progression of AD biomarkers according clinical stages

Source: B. Leclerc and A. Abulrob. Perspectives in Molecular Imaging Using Staging Biomarkers and Immunotherapies in Alzheimer’s Disease. Scientific World Journal 2013

Pursuant to this, Probiodrug aims to halt the pathological cascade at its source by preventing toxic oligomer formation. The Phase IIa study of PQ912 is in patients with mild cognitive impairment (MCI) or mild dementia due to AD. The strict screening criteria include three of the four biomarkers recently supported by the FDA to help select early-stage AD patients for clinical trials. Biomarkers and functional assessments will provide the basis for quantitative, objective measures of treatment effect, in addition to the potentially more subjective measures of cognitive function (eg the MMSE).

Preclinical data: PQ912 – a first-in-class QC inhibitor

As QC is essential for pGlu-Abeta formation, it represents an important therapeutic target. In AD animal models, preventive long-term and early therapeutic treatment with PQ912 reduced soluble and insoluble pGlu-Abeta and resulted in improved behaviour (Exhibit 5).

Exhibit 5: PQ912 – efficacy in transgene AD mice

Source: Probiodrug. Note Behavioural improvement assessed using the water maze test (data not shown).

AD R&D landscape highly fragmented

Probiodrug believes its differentiated approach will not only prove successful, but potentially also reduce the risk of side effects associated with generic Abeta approaches. Probiodrug is targeting pGlu-Abeta via two modes of action, which it believes are complementary:

Prevent formation: lead product candidate PQ912, and the preclinical PQ1565, are first-in-class small molecule QC inhibitors discovered by Probiodrug. Inhibition of QC prevents the formation of pGlu-Abeta, targeting the AD pathological cascade at its source.

Capture and clear: PBD-C06 is a preclinical pGlu-Abeta specific monoclonal antibody that aims to selectively clear pGlu-Abeta while leaving non-toxic forms of Abeta untouched.

According to EvaluatePharma there are around 80 companies developing in total c 75 unique compounds with c 40 different mechanisms action in Phase II and Phase III stages with AD patients. Many of these focus on steps in the Abeta cascade, rather than on any specific Abeta subtypes (Exhibit 6). Probiodrug is the only company developing a QC inhibitor as far as we are aware, with the QC target covered by its patent portfolio, which could be a differentiating factor. To our knowledge only Eli Lilly is developing an anti-QC antibody (peer to PBD-C06) with initial Phase I results as described above. Furthermore, given the size of the AD market and the potential for combination therapy, positive developments in the AD field should not preclude successful commercialisation of PQ912, in our view.

Exhibit 6: Probiodrug’s technology is differentiated from competition

Source: Probiodrug

Alzheimer’s disease and the vast target population

The number of people living with dementia worldwide is currently estimated at around 44 million, c 60% of whom have AD. Given the lack of a preventative or curative treatment this number is set to almost double by 2030 and more than triple by 2050 (World Alzheimer Report 2014). In 2015, the direct costs to American society of caring for those with AD will total an estimated $226bn, which is expected to increase to c $1.1trn by 2050 (2015 Alzheimers Disease Facts and Figures). Despite having no disease-modifying ability and limited symptomatic efficacy, the four FDA-approved AD treatments had combined 2015 sales of c $3.8bn globally (EvaluatePharma). Notably, generic donepezil commanded $780m of these sales (21% market share). The Namenda franchise (formerly of Forest Laboratories, now Actavis) had combined revenues of $1.8bn in 2015 (48% market share). Thus, AD not only represents a significant unmet clinical need, it also represents a substantial market opportunity for disease-modifying therapies. As a result, drug development for AD has become a major political, academic and industrial effort, as evidenced by initiatives such as the Global Dementia Discovery Fund and the big pharma collaborations between Biogen and Eisai, AstraZeneca and Eli Lilly. This illustrates the scope and willingness of the industry to support development of novel treatments in AD.

Sensitivities

Probiodrug is subject to the usual risks associated with drug development, including clinical development delays or failures, regulatory risks, competitor successes, partnering setbacks, and financing and commercial risks. The biggest near-term sensitivity for Probiodrug is the success or failure of lead asset PQ912 for AD. PQ912 has already demonstrated in a Phase I trial that it can successfully inhibit QC; however, whether this has any cognitive benefits, as suggested by preclinical models, has yet to be established in humans. Initial Phase IIa data are expected end-2016. Any further delays to the trial as was the case in the beginning of 2016 would mean the need for additional funding. However, we see this as less likely given the unchanged guidance from the company on 30 August and the proximity of the readout data.

Data from this study will determine subsequent development, with positive data validating the pGlu-Abeta target, opening the doors for partnering and strengthening the case for the remainder of the pipeline. Partnering PQ912 will be key for advancing late-stage development, which can be very costly in AD. We have assumed a deal in our valuation. However, we have limited visibility on the timing and terms of any future deals, although we believe that positive Phase IIa data should help attract and secure a partner.

AD is a substantial market with a large unmet medical need, hence any disease-modifying therapy is likely to generate significant sales. However, development risk is high, with multiple failures in the past, and late-stage trials will be costly. Future pricing and market dynamics are hard to predict, especially if competitors are successful, biomarkers lead to improved diagnosis, and combination therapy emerges as the main focus of development. Our peak sales forecast assumes PQ912 can offer disease-modifying benefit. Our launch timeline assumes that SAPHIR will be positive and can move to Phase III development without the need for an additional Phase IIb.

Valuation

We value Probiodrug at €309.1m or €41.5/share, slightly up from €303.2m or €40.7/share previously, due to rolling our model forward, which offset the lower cash position of €14.2m. The breakdown of our rNPV valuation, which uses a discount rate of 12.5%, is shown in Exhibit 7. Our valuation only includes PQ912, with no value assigned to the preclinical pipeline given its earlier stage of development.

Exhibit 7: Probiodrug rNPV valuation

Product

Indication

Launch

Peak sales (€m)

Value (€m)

Probability

rNPV (€m)

NPV/share (€/share)

PQ912

Alzheimer’s disease

2022

6,200

1,151.7

25%

294.9

39.6

Net cash

14.2

100%

14.2

1.9

Valuation

 

 

 

1,165.9

 

309.1

41.5

Source: Edison Investment Research. Note: Peak sales are rounded to the nearest €100m.

We have forecast peak sales of c €6.2bn in 2028, assuming launch in 2022, for the treatment of mild AD only (c 30% of the total population). This should allow sufficient time to secure a partnership post the Phase IIa readout and conduct an extensive late stage programme. We assume that the partner will cover all development and marketing costs from this point. Our peak sales are based on the assumption that PQ912 proves to be disease-modifying, and therefore able to command a premium price (we assume $35k per year per patient and a 20% discount to that in Europe and RoW). Due to the significant size of the AD market, there is potential for a disease-modifying agent to take a considerable market share in the future.

Our partnering assumptions include a fairly typical deal structure, including an upfront payment, development and sales-related milestones, in addition to royalties on global sales. We conservatively assume a total deal value of €500m (which is below the $820m deal signed in 2011 between Evotec and Roche for EVT 302, a monoamine oxidase type B inhibitor), with 10% for the upfront payment, 50% for development-related milestones and the remainder as sales-related. We include a 15% royalty on global sales, commensurate with an asset out-licensed once proof-of-concept data are available. We risk-adjust the milestone income in line with our assumed probability of success for PQ912. Our success probability was upped from 20% to 25% after the long-term animal toxicity data and is commensurate with the risks associated with AD drug development.

Financials

R&D spend in H116 was €4.7m and in line with €4.5m expensed in H115. We keep our full year R&D cost estimate of €11.1m as Probiodrug guided that 2016 net loss may be greater than in 2015 due to increased development activities. G&A expenditure of €1.3m was lower compared to €1.9m in H115, thus indicating good cost management. We slightly lowered our G&A costs expectations for 2016 and 2017, although the positive effect on the 2016 bottom line was offset by lowered net interest income forecasts. Our other forecasts remain unchanged with slight increase in 2017 EPS.

Probiodrug reported cash of €14.2m at end H116. Our post-H116 model suggests that this should be sufficient to fund operations until around mid-2017. The final Phase IIa results should be released in the beginning of 2017. As per our current estimates, existing funding is sufficient to reach the readout. However, it is uncertain whether the company will be required to repay tax provisions of €2.6m; if it does, the cash reach is likely Q117. In either case, the readout will be imminent or past at that point, which, in our view, in turn will drive the strategic pathway.

We continue to expect that if the trial results are positive, a licensing deal in 2017 is likely given the high profile of Probiodrug’s R&D programme among the larger players in the AD field. Although our valuation includes risk-adjusted milestones from a partner for PQ912 that could be triggered by licensing and the start of Phase III in 2017 (more details in our initiation report), our financial forecasts do not include any such income. Our valuation currently includes risk-adjusted €25m in potential upfront payment in 2017 upon licensing, which could secure the company’s operations without the need for a near term fundraising. In line with our research principles, we do not include this in our financial forecasts, but show €5.9m of illustrative financing added as long-term debt on the balance sheet in 2017. This is based on the cash need that we estimate is required to run the business through to the end of 2017.

Exhibit 8: Summary of the main changes to our Probiodrug financial forecasts

€m

2015

2016e

2017e

Reported

Old

New

% change

Old

New

% change

Revenues

0.000

0.000

0.000

N/A

0.000

0.000

N/A

Gross profit

0.000

0.000

0.000

N/A

0.000

0.000

N/A

Research and development costs

(10.158)

(11.105)

(11.105)

+0%

(7.669)

(7.669)

+0%

Selling, general and administration costs

(3.279)

(3.443)

(3.279)

-5%

(3.615)

(3.443)

-5%

EBITDA

(13.337)

(14.449)

(14.285)

-1%

(11.190)

(11.018)

-2%

Operating Profit (reported)

(13.393)

(14.505)

(14.342)

-1%

(11.242)

(11.070)

-2%

Profit Before Tax (rep)

(13.505)

(14.213)

(14.220)

+0%

(11.176)

(11.053)

-1%

Profit After Tax (rep)

(13.505)

(14.213)

(14.220)

+0%

(11.176)

(11.053)

-1%

EPS (€, rep)

(1.97)

(1.91)

(1.91)

+0%

(1.50)

(1.49)

-1%

Source: Edison Investment Research, Probiodrug accounts

Exhibit 9: Financial summary

€000s

2012

2013

2014

2015

2016e

2017e

Year end 31 December

IFRS

IFRS

IFRS

IFRS

IFRS

IFRS

PROFIT & LOSS

Revenue

 

 

6

0

0

0

0

0

Cost of Sales

0

0

0

0

0

0

Gross Profit

6

0

0

0

0

0

Research and development

(9,255)

(8,004)

(8,008)

(10,158)

(11,105)

(7,669)

EBITDA

 

 

(10,206)

(9,387)

(11,173)

(13,337)

(14,285)

(11,018)

Operating Profit (before amort. and except.)

(10,521)

(9,675)

(11,241)

(13,363)

(14,311)

(11,044)

Intangible Amortisation

(37)

(26)

(26)

(30)

(30)

(26)

Exceptionals

0

0

0

0

0

0

Other

0

0

0

0

0

0

Operating Profit

(10,558)

(9,701)

(11,267)

(13,393)

(14,342)

(11,070)

Net Interest

(314)

(106)

(170)

(112)

122

17

Profit Before Tax (norm)

 

 

(10,835)

(9,781)

(11,411)

(13,475)

(14,190)

(11,027)

Profit Before Tax (FRS 3)

 

 

(10,872)

(9,807)

(11,437)

(13,505)

(14,220)

(11,053)

Tax

(656)

0

0

0

0

0

Profit After Tax (norm)

(11,491)

(9,781)

(11,411)

(13,475)

(14,190)

(11,027)

Profit After Tax (FRS 3)

(11,528)

(9,807)

(11,437)

(13,505)

(14,220)

(11,053)

Average Number of Shares Outstanding (m)

4.1

4.3

4.9

6.9

7.4

7.4

EPS - normalised (€)

 

 

(2.84)

(2.30)

(2.35)

(1.96)

(1.91)

(1.48)

EPS - normalised and fully diluted (€)

 

(2.84)

(2.30)

(2.35)

(1.96)

(1.91)

(1.48)

EPS - (IFRS) (€)

 

 

(2.85)

(2.30)

(2.35)

(1.97)

(1.91)

(1.49)

Dividend per share (€)

0.0

0.0

0.0

0.0

0.0

0.0

Gross Margin (%)

N/A

N/A

N/A

N/A

N/A

N/A

EBITDA Margin (%)

N/A

N/A

N/A

N/A

N/A

N/A

Operating Margin (before GW and except.) (%)

N/A

N/A

N/A

N/A

N/A

N/A

BALANCE SHEET

Fixed Assets

 

 

996

425

186

140

84

32

Intangible Assets

67

101

82

56

26

0

Tangible Assets

926

321

101

81

55

29

Investments

3

3

3

3

3

3

Current Assets

 

 

9,009

5,856

21,294

21,726

8,271

3,787

Stocks

18

0

0

0

422

422

Debtors

5

0

0

0

0

0

Cash

7,726

4,421

20,920

21,361

7,484

3,000

Other

1,260

1,435

374

365

365

365

Current Liabilities

 

 

(3,570)

(9,320)

(4,580)

(4,911)

(4,656)

(4,343)

Creditors

(3,570)

(3,974)

(4,580)

(4,911)

(4,656)

(4,343)

Short term borrowings

0

(5,346)

0

0

0

0

Long Term Liabilities

 

 

(1,070)

(1,265)

(929)

(822)

(822)

(6,688)

Long term borrowings

0

0

0

0

0

(5,866)

Other long term liabilities

(1,070)

(1,265)

(929)

(822)

(822)

(822)

Net Assets

 

 

5,365

(4,304)

15,971

16,133

2,877

(7,212)

CASH FLOW

Operating Cash Flow

 

 

(12,090)

(8,477)

(10,540)

(12,149)

(13,998)

(10,367)

Net Interest

22

9

(54)

0

122

17

Tax

28

9

5

2

0

0

Capex

(64)

(4)

(2)

(6)

0

0

Acquisitions/disposals

0

0

0

0

0

0

Financing

9,516

(188)

32,436

12,594

0

0

Dividends

0

0

0

0

0

0

Net Cash Flow

(2,588)

(8,651)

21,845

441

(13,877)

(10,351)

Opening net debt/(cash)

 

 

(10,314)

(7,726)

925

(20,920)

(21,361)

(7,484)

HP finance leases initiated

0

0

0

0

0

0

Other

0

0

0

(0)

0

0

Closing net debt/(cash)

 

 

(7,726)

925

(20,920)

(21,361)

(7,484)

2,866

Source: Edison Investment Research, Probiodrug accounts

Contact details

Revenue by geography

Probiodrug AG
Weinbergweg 22
06120 Halle/Saale
Germany
+49 345 555 9900

www.probiodrug.de/

N/A

Contact details

Probiodrug AG
Weinbergweg 22
06120 Halle/Saale
Germany
+49 345 555 9900

www.probiodrug.de/

Revenue by geography

N/A

Management team

Chairman of the management board and CEO: Konrad Glund, PhD

CFO: Hendrik Liebers, PhD

Konrad Glund, co-founder of Probiodrug, left to join (OSI) Prosidion in 2004 as COO and VP of business and corporate development. He returned to Probiodrug in 2006 as CEO. Dr Glund holds a PhD in biochemistry; he is the author of more than 60 publications and is co-inventor on more than 10 patents.

Hendrik Liebers joined Probiodrug as CFO in 2007. Before this he spent a number of years with several private equity and venture capital firms, including IBG and Corporate Finance Holding, and has held numerous board seats in biotech companies. He holds diplomas in economics and biology and a PhD.

CDO: Inge Lues, PhD

Inge Lues joined Probiodrug as R&D adviser in 2008 and has been CDO since 2013. From 2007 to 2013 she was also an adviser to other biotech companies and public research institutions. Before this, Dr Lues was head of global drug discovery and non-clinical development pharma at Merck KGaA (2002-07).

Management team

Chairman of the management board and CEO: Konrad Glund, PhD

Konrad Glund, co-founder of Probiodrug, left to join (OSI) Prosidion in 2004 as COO and VP of business and corporate development. He returned to Probiodrug in 2006 as CEO. Dr Glund holds a PhD in biochemistry; he is the author of more than 60 publications and is co-inventor on more than 10 patents.

CFO: Hendrik Liebers, PhD

Hendrik Liebers joined Probiodrug as CFO in 2007. Before this he spent a number of years with several private equity and venture capital firms, including IBG and Corporate Finance Holding, and has held numerous board seats in biotech companies. He holds diplomas in economics and biology and a PhD.

CDO: Inge Lues, PhD

Inge Lues joined Probiodrug as R&D adviser in 2008 and has been CDO since 2013. From 2007 to 2013 she was also an adviser to other biotech companies and public research institutions. Before this, Dr Lues was head of global drug discovery and non-clinical development pharma at Merck KGaA (2002-07).

Principal shareholders

(%)

BB Biotech AG

14.13

IBG Group

13.46

Edmond de Rothschild Investment Partners

13.24

AVIVA

10.84

HBM Healthcare Investments

8.86

LSP

7.88

TVM

7.50

JP Morgan Asset Management

5.15

Founder/Management

4.30

Biogen Idec

3.66

LBBW

3.15

Supervisory Board

2.34

Others

5.49

Companies named in this report

Biogen (BIIB US), AstraZeneca (AZN LN), Eli Lilly (LLY US), Roche (ROG VX)

Edison, the investment intelligence firm, is the future of investor interaction with corporates. Our team of over 100 analysts and investment professionals work with leading companies, fund managers and investment banks worldwide to support their capital markets activity. We provide services to more than 400 retained corporate and investor clients from our offices in London, New York, Frankfurt, Sydney and Wellington. Edison is authorised and regulated by the Financial Conduct Authority. Edison Investment Research (NZ) Limited (Edison NZ) is the New Zealand subsidiary of Edison. Edison NZ is registered on the New Zealand Financial Service Providers Register (FSP number 247505) and is registered to provide wholesale and/or generic financial adviser services only. Edison Investment Research Inc (Edison US) is the US subsidiary of Edison and is regulated by the Securities and Exchange Commission. Edison Investment Research Limited (Edison Aus) [46085869] is the Australian subsidiary of Edison and is not regulated by the Australian Securities and Investment Commission. Edison Germany is a branch entity of Edison Investment Research Limited [4794244]. www.edisongroup.com

DISCLAIMER
Copyright 2016 Edison Investment Research Limited. All rights reserved. This report has been commissioned by Probiodrug and prepared and issued by Edison for publication globally. All information used in the publication of this report has been compiled from publicly available sources that are believed to be reliable, however we do not guarantee the accuracy or completeness of this report. Opinions contained in this report represent those of the research department of Edison at the time of publication. The securities described in the Investment Research may not be eligible for sale in all jurisdictions or to certain categories of investors. This research is issued in Australia by Edison Aus and any access to it, is intended only for "wholesale clients" within the meaning of the Australian Corporations Act. The Investment Research is distributed in the United States by Edison US to major US institutional investors only. Edison US is registered as an investment adviser with the Securities and Exchange Commission. Edison US relies upon the "publishers’ exclusion" from the definition of investment adviser under Section 202(a)(11) of the Investment Advisers Act of 1940 and corresponding state securities laws. As such, Edison does not offer or provide personalised advice. We publish information about companies in which we believe our readers may be interested and this information reflects our sincere opinions. The information that we provide or that is derived from our website is not intended to be, and should not be construed in any manner whatsoever as, personalised advice. Also, our website and the information provided by us should not be construed by any subscriber or prospective subscriber as Edison’s solicitation to effect, or attempt to effect, any transaction in a security. The research in this document is intended for New Zealand resident professional financial advisers or brokers (for use in their roles as financial advisers or brokers) and habitual investors who are “wholesale clients” for the purpose of the Financial Advisers Act 2008 (FAA) (as described in sections 5(c) (1)(a), (b) and (c) of the FAA). This is not a solicitation or inducement to buy, sell, subscribe, or underwrite any securities mentioned or in the topic of this document. This document is provided for information purposes only and should not be construed as an offer or solicitation for investment in any securities mentioned or in the topic of this document. A marketing communication under FCA Rules, this document has not been prepared in accordance with the legal requirements designed to promote the independence of investment research and is not subject to any prohibition on dealing ahead of the dissemination of investment research.
Edison has a restrictive policy relating to personal dealing. Edison Group does not conduct any investment business and, accordingly, does not itself hold any positions in the securities mentioned in this report. However, the respective directors, officers, employees and contractors of Edison may have a position in any or related securities mentioned in this report. Edison or its affiliates may perform services or solicit business from any of the companies mentioned in this report. The value of securities mentioned in this report can fall as well as rise and are subject to large and sudden swings. In addition it may be difficult or not possible to buy, sell or obtain accurate information about the value of securities mentioned in this report. Past performance is not necessarily a guide to future performance. Forward-looking information or statements in this report contain information that is based on assumptions, forecasts of future results, estimates of amounts not yet determinable, and therefore involve known and unknown risks, uncertainties and other factors which may cause the actual results, performance or achievements of their subject matter to be materially different from current expectations. For the purpose of the FAA, the content of this report is of a general nature, is intended as a source of general information only and is not intended to constitute a recommendation or opinion in relation to acquiring or disposing (including refraining from acquiring or disposing) of securities. The distribution of this document is not a “personalised service” and, to the extent that it contains any financial advice, is intended only as a “class service” provided by Edison within the meaning of the FAA (ie without taking into account the particular financial situation or goals of any person). As such, it should not be relied upon in making an investment decision. To the maximum extent permitted by law, Edison, its affiliates and contractors, and their respective directors, officers and employees will not be liable for any loss or damage arising as a result of reliance being placed on any of the information contained in this report and do not guarantee the returns on investments in the products discussed in this publication. FTSE International Limited (“FTSE”) © FTSE 2016. “FTSE®” is a trade mark of the London Stock Exchange Group companies and is used by FTSE International Limited under license. All rights in the FTSE indices and/or FTSE ratings vest in FTSE and/or its licensors. Neither FTSE nor its licensors accept any liability for any errors or omissions in the FTSE indices and/or FTSE ratings or underlying data. No further distribution of FTSE Data is permitted without FTSE’s express written consent.

Frankfurt +49 (0)69 78 8076 960

Schumannstrasse 34b

60325 Frankfurt

Germany

London +44 (0)20 3077 5700

280 High Holborn

London, WC1V 7EE

United Kingdom

New York +1 646 653 7026

245 Park Avenue, 39th Floor

10167, New York

US

Sydney +61 (0)2 9258 1161

Level 25, Aurora Place

88 Phillip St, Sydney

NSW 2000, Australia

Wellington +64 (0)48 948 555

Level 15, 171 Featherston St

Wellington 6011

New Zealand

Frankfurt +49 (0)69 78 8076 960

Schumannstrasse 34b

60325 Frankfurt

Germany

London +44 (0)20 3077 5700

280 High Holborn

London, WC1V 7EE

United Kingdom

New York +1 646 653 7026

245 Park Avenue, 39th Floor

10167, New York

US

Sydney +61 (0)2 9258 1161

Level 25, Aurora Place

88 Phillip St, Sydney

NSW 2000, Australia

Wellington +64 (0)48 948 555

Level 15, 171 Featherston St

Wellington 6011

New Zealand

Edison, the investment intelligence firm, is the future of investor interaction with corporates. Our team of over 100 analysts and investment professionals work with leading companies, fund managers and investment banks worldwide to support their capital markets activity. We provide services to more than 400 retained corporate and investor clients from our offices in London, New York, Frankfurt, Sydney and Wellington. Edison is authorised and regulated by the Financial Conduct Authority. Edison Investment Research (NZ) Limited (Edison NZ) is the New Zealand subsidiary of Edison. Edison NZ is registered on the New Zealand Financial Service Providers Register (FSP number 247505) and is registered to provide wholesale and/or generic financial adviser services only. Edison Investment Research Inc (Edison US) is the US subsidiary of Edison and is regulated by the Securities and Exchange Commission. Edison Investment Research Limited (Edison Aus) [46085869] is the Australian subsidiary of Edison and is not regulated by the Australian Securities and Investment Commission. Edison Germany is a branch entity of Edison Investment Research Limited [4794244]. www.edisongroup.com

DISCLAIMER
Copyright 2016 Edison Investment Research Limited. All rights reserved. This report has been commissioned by Probiodrug and prepared and issued by Edison for publication globally. All information used in the publication of this report has been compiled from publicly available sources that are believed to be reliable, however we do not guarantee the accuracy or completeness of this report. Opinions contained in this report represent those of the research department of Edison at the time of publication. The securities described in the Investment Research may not be eligible for sale in all jurisdictions or to certain categories of investors. This research is issued in Australia by Edison Aus and any access to it, is intended only for "wholesale clients" within the meaning of the Australian Corporations Act. The Investment Research is distributed in the United States by Edison US to major US institutional investors only. Edison US is registered as an investment adviser with the Securities and Exchange Commission. Edison US relies upon the "publishers’ exclusion" from the definition of investment adviser under Section 202(a)(11) of the Investment Advisers Act of 1940 and corresponding state securities laws. As such, Edison does not offer or provide personalised advice. We publish information about companies in which we believe our readers may be interested and this information reflects our sincere opinions. The information that we provide or that is derived from our website is not intended to be, and should not be construed in any manner whatsoever as, personalised advice. Also, our website and the information provided by us should not be construed by any subscriber or prospective subscriber as Edison’s solicitation to effect, or attempt to effect, any transaction in a security. The research in this document is intended for New Zealand resident professional financial advisers or brokers (for use in their roles as financial advisers or brokers) and habitual investors who are “wholesale clients” for the purpose of the Financial Advisers Act 2008 (FAA) (as described in sections 5(c) (1)(a), (b) and (c) of the FAA). This is not a solicitation or inducement to buy, sell, subscribe, or underwrite any securities mentioned or in the topic of this document. This document is provided for information purposes only and should not be construed as an offer or solicitation for investment in any securities mentioned or in the topic of this document. A marketing communication under FCA Rules, this document has not been prepared in accordance with the legal requirements designed to promote the independence of investment research and is not subject to any prohibition on dealing ahead of the dissemination of investment research.
Edison has a restrictive policy relating to personal dealing. Edison Group does not conduct any investment business and, accordingly, does not itself hold any positions in the securities mentioned in this report. However, the respective directors, officers, employees and contractors of Edison may have a position in any or related securities mentioned in this report. Edison or its affiliates may perform services or solicit business from any of the companies mentioned in this report. The value of securities mentioned in this report can fall as well as rise and are subject to large and sudden swings. In addition it may be difficult or not possible to buy, sell or obtain accurate information about the value of securities mentioned in this report. Past performance is not necessarily a guide to future performance. Forward-looking information or statements in this report contain information that is based on assumptions, forecasts of future results, estimates of amounts not yet determinable, and therefore involve known and unknown risks, uncertainties and other factors which may cause the actual results, performance or achievements of their subject matter to be materially different from current expectations. For the purpose of the FAA, the content of this report is of a general nature, is intended as a source of general information only and is not intended to constitute a recommendation or opinion in relation to acquiring or disposing (including refraining from acquiring or disposing) of securities. The distribution of this document is not a “personalised service” and, to the extent that it contains any financial advice, is intended only as a “class service” provided by Edison within the meaning of the FAA (ie without taking into account the particular financial situation or goals of any person). As such, it should not be relied upon in making an investment decision. To the maximum extent permitted by law, Edison, its affiliates and contractors, and their respective directors, officers and employees will not be liable for any loss or damage arising as a result of reliance being placed on any of the information contained in this report and do not guarantee the returns on investments in the products discussed in this publication. FTSE International Limited (“FTSE”) © FTSE 2016. “FTSE®” is a trade mark of the London Stock Exchange Group companies and is used by FTSE International Limited under license. All rights in the FTSE indices and/or FTSE ratings vest in FTSE and/or its licensors. Neither FTSE nor its licensors accept any liability for any errors or omissions in the FTSE indices and/or FTSE ratings or underlying data. No further distribution of FTSE Data is permitted without FTSE’s express written consent.

Frankfurt +49 (0)69 78 8076 960

Schumannstrasse 34b

60325 Frankfurt

Germany

London +44 (0)20 3077 5700

280 High Holborn

London, WC1V 7EE

United Kingdom

New York +1 646 653 7026

245 Park Avenue, 39th Floor

10167, New York

US

Sydney +61 (0)2 9258 1161

Level 25, Aurora Place

88 Phillip St, Sydney

NSW 2000, Australia

Wellington +64 (0)48 948 555

Level 15, 171 Featherston St

Wellington 6011

New Zealand

Frankfurt +49 (0)69 78 8076 960

Schumannstrasse 34b

60325 Frankfurt

Germany

London +44 (0)20 3077 5700

280 High Holborn

London, WC1V 7EE

United Kingdom

New York +1 646 653 7026

245 Park Avenue, 39th Floor

10167, New York

US

Sydney +61 (0)2 9258 1161

Level 25, Aurora Place

88 Phillip St, Sydney

NSW 2000, Australia

Wellington +64 (0)48 948 555

Level 15, 171 Featherston St

Wellington 6011

New Zealand

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