Merck, Sharpe & Dohme (Australia) Pty Ltd. v Genentech, Inc - [2014] APO 6

IP AUSTRALIA
AUSTRALIAN PATENT OFFICE
Merck, Sharpe & Dohme (Australia) Pty Ltd. v Genentech, Inc. [2014] APO 6

Patent Application: 2003287257

Title:Inhibition of IL-17 production

Patent Applicant:  Genentech, Inc.
Opponent:  Merck, Sharpe & Dohme (Australia) Pty Ltd.
Delegate:  Dr B Akhurst
Decision Date:  6 February 2014
Hearing Date:  12 November 2013, in Canberra
Catchwords:  PATENTS - section 59 opposition - novelty - lack of novelty by inevitable outcome - priority date deferred - lack of novelty over the specification intended for grant in Europe - inventive step - documents would not be ascertained - fair basis - no real and reasonably clear disclosure of a therapeutic method involving testing all subjects to determine they had elevated level of expression of IL-17 prior to treatment - grounds relating to manner of manufacture, useful, clarity, full description and claims define the invention not established

Representation: Patent applicant: Andrew Fox of Counsel, instructed by Dr Stuart Boyer of Griffith Hack, Perth.
Opponent: Matthew Darke of Counsel, instructed by Dr Andrew Blattman and Dr Simon Potter of Spruson & Ferguson, Sydney.

IP AUSTRALIA
AUSTRALIAN PATENT OFFICE
Patent Application: 2003287257

Title:Inhibition of IL-17 production

Patent Applicant: Genentech, Inc.
Date of Decision: 6 February 2014
DECISION
The opposition succeeds. The invention of claims 1-5, 11-12 and 14-33 lacks novelty. Claim 15 and all its dependent claims lack fair basis, insofar as these claims require each individual subject to be tested to determine an elevated level of IL-17 expression prior to treatment with the IL-23 antagonist.
Genentech is allowed 2 months from the date of this decision to file amendments to overcome the deficiencies in the claims.
Costs are awarded according to Schedule 8 against Genentech, Inc.
REASONS FOR DECISION
Background

Patent application 2003287257 was filed by Genentech, Inc. (Genentech) via the PCT on 29 October 2003 claiming priority from provisional application US 60/423,090 filed on 30 October 2002.
After examination, the application was advertised as accepted on 10 December 2009. Merck, Sharpe & Dohme (Australia) Pty Ltd. (MSDA) filed a notice of opposition on 10 March 2010 and served the statement of grounds and particulars on 10 June 2010. After extensions were granted for each evidentiary stage, evidence in support was completed on 29 September 2011, evidence in answer by 2 August 2012 and evidence in reply on 4 February 2013.
Evidence
The evidence in support of the opposition consists of declarations by:
·    Andrew Nathaniel Blattman dated 28 July 2010 with Exhibits ANB-1 to ANB-36
·    Stuart Graham Tangye dated 3 December 2010 (Tangye#1) with Exhibits SGT-1 to SGT-23
·    Stuart Graham Tangye dated 28 June 2011 (Tangye#2) with exhibits SGT-24 to SGT-28
·    Stuart Graham Tangye dated 28 September 2011 (Tangye#3)
The evidence in answer consists of declarations by:
·    Stuart James Boyer dated 2 July 2012 with exhibits SJB-1 to SJB-14
·    Stuart James Boyer dated 31 July 2012 with exhibits SJB-15 to SJB-19
·    Wenjun Ouyang dated 7 March 2012 (Ouyang) with exhibits A to O
The evidence in reply consists of declarations by:
· Stuart Graham Tangye dated 4 February 2013 (Tangye#4) with Exhibits SGT-29 to SGT-30
Amendments to the statement of grounds and particulars and further evidence
The opponent requested amendments to the statement of grounds and particulars on 28 October 2013 and 4 November 2013. The net effect was to add an additional document under the grounds relating to novelty and inventive step. As required by reg 5.9 as in force immediately before April 2013, the applicant was notified of the amendment and had the opportunity to make representations. The amendments were confined to the particulars of the opposition and the Commissioner has no discretion - I allow the amendments.
The first amendment request was accompanied by a declaration by attorney Andrew Blattman and an exhibited document (ANB-39). At the end of the opposition hearing, having heard submissions from both parties in respect of the document, I allowed MSDA’s verbal request to file ANB-39 as further evidence. Genentech advised it did not need additional time to consider the further evidence and declined to file responding evidence.
Grounds of opposition
The statement of grounds and particulars lists the grounds of opposition as: manner of manufacture, novelty, inventive step, usefulness, and section 40 issues.
Standard of proof
The request for examination in this case was filed on 15 August 2007. Therefore, the substantive amendments of the Patents Act brought about by the Intellectual Property Laws Amendment (Raising the Bar) Act 2012, including subsection 60(3A) which allows the Commissioner to refuse a patent application if satisfied on the balance of probabilities that a ground of opposition exists, do not apply to the present application. Instead, the onus of proof in this opposition proceeding lies with the opponent, who must establish that it is clear that a valid patent cannot be granted (F.Hoffman-La Roche AG v New England Biolabs Inc [2000] FCA 283 at [29], [67]; 50 IPR 305; Commissioner of Patents v Sherman [2008] FCAFC 182 at [18], [22]; 79 IPR 426).
I also note that for the same reason, substantive amendments to grounds of opposition which came into effect on 15 April 2013 do not apply to the present opposition. Instead the relevant law to apply to the grounds of opposition is that which stood prior to the amendments.
The subject matter of the specification
The specification is titled “Inhibition of IL-17 production”. Interleukin-17 (IL-17) is a cytokine - a class of soluble proteins that play a role in controlling interactions between different types of immune cells that form the basis of the mammalian immune response. On pages 1-2 of the specification, IL-17 is derived from T cells (T leukocytes, a type of white blood cell) and promotes inflammation by stimulating epithelial, endothelial and fibroblastic cells to produce other inflammatory cytokines and chemotactic cytokines (chemokines); it can synergise with other cytokines to further induce chemokine expression. Another cytokine, IL-23, promotes the proliferation of T cells (page 2 of the specification).
The alternative Th1 and Th2 responses to immune challenge promote cell-mediated or humoral (antibody-based) immune responses for protection against intracellular or extracellular pathogens, respectively. On page 2 of the specification, while the levels of IL-17 had been reported to be significantly elevated in a number of chronic inflammatory conditions, these reports had not identified clear classification of IL-17 within the paradigm of Th1 and Th2 polarized cytokine responses. Furthermore, no correlation had been established between the expression and biological roles of IL-17 and IL-23.
On page 11 of the specification, the invention of the opposed application is based on the recognition that IL-23 induces IL-17 production in activated T cells and that IL-23 antagonists are capable of inhibiting this process. Accordingly, IL-23 antagonists are promising drug candidates for the treatment of inflammatory conditions characterized by elevated levels of IL-17. Conversely, IL-23 agonists are useful to induce protective immune response to various infections.
Based on the exemplified studies, on page 26 the specification suggests a role for IL-23 in promoting a distinct T cell activation state which expresses IL-17 as an effector cytokine. The function of IL-23 is postulated to be in the promotion of an adaptive immune response to pathogens with IL-17 as a principle effector cytokine.
Structurally, IL-23 is a dimeric protein consisting of a p40 subunit identical to that of the cytokine interleukin-12 (IL-12) and a unique p19 subunit (page 2 of the specification). Interleukin-23 modulatory compounds exert their effect by targeting the p40 or the p19 subunits, or the subunits of the dimeric IL-23 receptor (page 7, lines 13-24).
Claims construction
The principles to be applied in construing a patent specification are well settled in law (Flexible Steel Lacing Company v Beltreco Ltd [2000] FCA 890 at [70] - [81]; (2001) 49 IPR 331 at 347 [70] - [81], Pfizer Overseas Pharmaceuticals v Eli Lilly and Company [2005] FCAFC 224 at [247] - [250]; 68 IPR 1 at 52-54 [247] - [250]).
The specification was accepted with 18 claims. At the hearing, the parties’ submissions were essentially confined to the independent claims and they agreed that the opposition may be determined on this basis. Claims 6-10 and dependent claims defining an in vitro method for identifying an anti-inflammatory agent are not under opposition. The remaining six independent claims are as follows:
1. A method for inhibiting interleukin-17 (IL-17) production by T cells comprising treating said T cells with an antagonist of interleukin-23 (IL-23).
Claim 1 encompasses in vitro and in vivo methods.
4. A method for the treatment of an inflammatory disease characterized by elevated expression of interleukin 17 (IL-17) in a mammalian subject, comprising administering to said subject an effective amount of an antagonist of interleukin-23 (IL-23).
5. Use of an effective amount of an antagonist of interleukin-23 (IL-23) for the treatment of an inflammatory disease characterized by elevated expression of interleukin 17 (IL-17), in a mammalian subject.
Claims 4 and 5 define methods for treating an inflammatory disease characterized by elevated expression of IL-17. In its plain meaning “elevated” expression of IL-17 means that the levels of IL-17 gene products (protein or mRNA) are significantly higher than in an appropriate comparative population, eg. healthy controls.
The Macquarie Dictionary defines the word “characterise” as “to describe the characteristic or peculiar quality of” something. “Characteristic” means a “distinguishing feature or quality”. Applied in this case, the relevant distinguishing feature/peculiar quality of the inflammatory disease specified in claims 4 and 5 is that of an elevated expression of IL-17. Therefore, the phrase “an inflammatory disease characterized by elevated expression of IL-17” encompasses any and all inflammatory diseases in which IL-17 expression is typically elevated.
Genentech submitted that the invention relates to a particular cohort of patients, which exhibit inflammation by reason of the presence of elevated levels of IL-17. However, claims 4 and 5 define the relevant treatment group in terms of the disease, not in terms of the individual subject’s IL-17 levels. These claims encompass all individuals having an inflammatory disease that is characterised by significantly higher IL-17 expression in the patient population as a whole, notwithstanding that any one individual in that group may not exhibit high levels of IL-17 at all times.
There is ambiguity as to which inflammatory diseases fall within the scope of the term “characterized by elevated expression of IL-17”. Resort to the description reveals that the claims encompass at least the target diseases identified on pages 19-20, lines 2-28 as being associated with elevated IL-17 levels, including rheumatoid arthritis (RA), asthma, psoriasis, multiple sclerosis (MS), Crohn’s disease, ulcerative colitis and inflammatory bowel disease. However, the phrase “an inflammatory disease characterized by elevated expression of IL-17” encompasses all inflammatory diseases in which elevated IL-17 is a distinguishing characteristic, and therefore the number of diseases understood to fall within the scope of the claim may expand if more are identified.
14.A method for inducing IL-17 production in a mammalian subject comprising administering to said subject an IL-23 agonist.
Claim 14 is self-explanatory.
15.An antagonist of interleukin-23 (IL-23) when used in a method for treatment of an inflammatory disease in a mammalian subject determined to have an elevated level of expression of interleukin-17 (IL-17) compared with a healthy subject, wherein said antagonist is an anti-IL-23 or an anti-IL-23-receptor antibody.
Claim 15 to the antagonist “when used” in a method of treatment, is a claim to the method of treatment (the obiter of the High Court in Wellcome v Commissioner of Patents 1980 HCA 21 at [21]; 1A IPR 261 at 266, applied).
Claim 15 defines the treatment group in terms of a subject determined to have an elevated level of expression of IL-17. The Macquarie Dictionary defines the word “determine” as “to conclude or ascertain, as after reasoning, observation, etc”. Claim 15 does not specify the means for determining whether IL-17 is elevated. However logically, both observation and reasoning are applicable in this case. The level of IL-17 expression in a subject can be ascertained by actually measuring the level of IL-17 expression in a sample from a subject. Alternatively, where a subject has been diagnosed with an inflammatory disease known to be characterized by elevated expression of IL-17, it is reasonable to infer that the subject exhibits such levels. On this basis, I conclude that the determination step required by claim 15 encompasses both:
(i) actually measuring IL-17 expression in each individual subject prior to treatment; and
(ii) concluding that the subject has elevated IL-17 expression based on a positive diagnosis of an inflammatory disease that has previously been characterized as exhibiting elevated expression of IL-17.
Genentech accepted this construction at the hearing.
34.A method of inhibiting interleukin-17 (IL-17) production by T cells, substantially as hereinbefore described with reference to any one of the examples.
Claim 34 is an omnibus claim limited by reference to the Examples. The specification contains two Examples disclosing in vitro and an in vivo methods of inhibiting IL-17 production by T cells; the former by neutralising IL-23 using an antibody against the p40 subunit prior to its application to mononuclear cells from mouse spleen (Example 1), and the latter by producing an IL-23p19^-/- transgenic mouse, which due to the absence of functional IL-23p19 protein is deficient in IL-23 (Example 2).
Priority date – claim 15
Under sections 43 and 114 of the Patents Act and regulation 3.14(b), as in force immediately before 15 April 2013, where an amendment is allowed to the specification that introduces a claim to matter that was not in substance disclosed in the complete specification before the amendment, the priority date of the amended claim is the date of filing the statement of proposed amendments that resulted in the disclosure.
MSDA submitted that claim 15 was not introduced until 16 October 2009 and the claim is not entitled to an earlier priority date. Responding, Genentech submitted that claim 14 in the specification as filed (identical to accepted claim 4) provides an in substance disclosure of the features of accepted claim 15, and further that a fair reading of the specification makes it clear that the invention relates to treating subjects that have an inflammatory disease that is associated with elevated levels of expression of IL-17.
While I agree with Genentech’s latter submission, it does not address the key issue. In one embodiment, claim 15 defines a therapeutic method in which the level of IL-17 expression is measured in each individual subject prior to treatment, and the treatment administered to those subjects determined to have elevated levels. Other than the consistory clause introduced with claim 15, the specification contains no disclosure whatsoever of such a method. This conclusion is consistent with Dr Tangye’s evidence that the opposed application does not disclose or suggest that a group of subjects suffering from a relevant inflammatory disease could be classified into subgroups with differing (i.e. normal or high) IL-17 levels (Tangye#3 at [14]; Tangye#4 at [23]).
The specification as filed and provisional application US 60/423,090 from which it ultimately claims priority each disclose a method of treatment applied to subjects having a specified category of disease. Once a subject is diagnosed with a relevant disease, this is sufficient to identify the subject as suitable for treatment with IL-23 inhibitors. The method defined by claim 15 encompasses a distinctly different process.
Dr Ouyang at [25] provides two statements of principle which underpin the difference in scope between accepted claims 4 and 15. Firstly, that certain but not all inflammatory conditions exhibit elevated IL-17 expression. Secondly, that some but not all patients with certain inflammatory diseases have elevated IL-17 expression.
The former principle, embodied in claim 4 at acceptance, was in substance disclosed in the specification as filed and in provisional application US 60/423,090. However, the latter principle embodied in claim 15 was not. The earlier documents do not in substance disclose a therapeutic method in which each subject is individually tested to establish they have elevated IL-17 expression prior to treatment with IL-23 inhibitors.
In view of my findings the priority date of claim 15 and its dependent claims, insofar as these claims require each individual subject to have their IL-17 expression levels tested prior to treatment, is 16 October 2009 - the filing date of the amendment request that introduced this feature.
Manner of Manufacture
Section 18(1)(a) requires that an invention must be a manner of manufacture within the meaning of section 6 of the Statute of Monopolies. Whether a claim defines a manner of manufacture is determined by asking whether the claimed invention lacks the necessary quality of inventiveness on the face of the specification (NV Philips Gloeilampenfabrieken v Mirabella International Pty Ltd [1995] HCA 15 at [9]; (1995) 183 CLR 655).
MSDA submitted that Genentech’s discovery of a link between IL-23 and IL-17 has not been accompanied by any new or useful product or method. Rather, the specification merely identifies the mechanism of action underlying known methods of treatment. Genentech responded that the opponent has not established that the claimed invention is obvious on the face of the specification.
The specification discloses the principle that IL-23 induces IL-17 production by T cells and that as a consequence IL-23 modulatory compounds will also modulate IL-17 expression. The opposed claims relate to the use of IL-23 antagonists or agonists in methods of inhibiting or inducing IL-17 production by T cells in vivo and in vitro, and methods for treating inflammatory diseases associated with elevated expression of IL-17.
It is not apparent on the face of the specification that modulators of IL-23 activity were known to modulate the production of IL-17, nor that IL-23 antagonists could be used to treat IL-17-mediated inflammatory disease. I agree with Genentech; MSDA has not established that the claims do not define a manner of manufacture.
Novelty
The general test for anticipation is the reverse infringement test. The classic formulation of this test is that given by Aickin J in Meyers Taylor Pty Ltd v Vicarr Industries Ltd [1977] HCA 19 at [20]; 137 CLR 228 at 235:
“The basic test for anticipation or want of novelty is the same as that for infringement and generally one can properly ask oneself whether the alleged anticipation would, if the patent were valid, constitute an infringement.”
MSDA opposed claims 1-5 and 11-34 for lack of novelty, although it made no submissions in respect of claim 34.
MSDA accepted that Genentech had discovered the link between IL-23 and IL-17 that established the mechanism of action underlying the therapeutic effect of IL-23 modulators. However, it submitted that prior art methods for treating inflammatory disease involving the administration of IL-23 antagonists would inevitably inhibit the production of IL-17 by the recipient’s T cells. Similarly, administering an IL-23 antagonist to T cells either in vivo or in vitro would inevitably inhibit IL-17 production by those T cells. MSDA submitted that it makes no difference that the skilled addressee was not expressly or implicitly instructed by the relevant prior art to seek to do that which would constitute an infringement of the opposed claims, or even that they did not understand that they would do so.

Responding, Genentech relied on the majority judgement in H Lundbeck A/S v Alphapharm Pty Ltd [2009] FCAFC 70 at [178]-[190]; (2009) 81 IPR 228 (Lundbeck) to argue that in the circumstances of this case, the claims would only lack novelty if the prior art disclosure taught the person skilled in the art all of the features of the claimed invention, including the effect of the IL-23 modulators on IL-17.
Although they disagreed as to its application, both parties accepted the following statement by Justice Bennett in Danisco A/S v Novozymes A/S (No 2) [2011] FCA 282 at [248] as a correct statement of the law:
“A claimed invention is deprived of novelty if it has been given to the public prior to the priority date. One way of this occurring is if a product or a process has been prior used. Another is if information that equates to the claimed invention has been published. To constitute an anticipation, a prior publication must, before the priority date of the claims of the Patent, disclose all of the integers of the claimed invention. There are, however, circumstances in which a prior publication does not expressly make that complete disclosure but still deprives the subsequently claimed invention of novelty … . One example is where the skilled reader understands the disclosures of the prior publication to include a missing integer. Another is where the prior publication contains a direction to use a process that inevitably or inexorably results in something within the claim (General Tire; Lundbeck at [181]–[182]).”
At the hearing, MSDA confirmed that it considered the present case to be analogous to the second example – a prior publication that contains a direction to use a process inevitably or inexorably results in something within the claim. Genentech argued that in that second example, the reasoning in Lundbeck at [173] – [190] establishes that for novelty purposes the prior disclosure must provide the person skilled in the art, not only with a direction that, if followed, would inevitably infringe the invention as claimed, but also with sufficient information that they will understand that they are doing exactly what is claimed.
More recently, in Novozymes A/S v Danisco A/S [2013] FCAFC 6; 99 IPR 417 (Novozymes) the Full Court of the Federal Court considering similar submissions by the parties reviewed the previous law on novelty by inevitable outcome. The majority judgement is that of Justice Jessup (Greenwood and Yates JJ agreeing at [37] and [226], respectively).
Regarding novelty by inevitable outcome, the Full Court in both Lundbeck (at [182]) and Novozymes (at [177]) accepted as a statement of the law in Australia the words of the UK Court of Appeal in The General Tire & Rubber Company v The Firestone Tyre and Rubber Company Limited [1972] RPC 457 at 486 at 485-486; 1A IPR 121 at 138:
“If the prior inventor’s publication contains a clear description of, or clear instructions to do or make, something that would infringe the patentee’s claim if carried out after the grant of the patentee’s patent, the patentee's claim will have been shown to lack the necessary novelty, that is to say, it will have been anticipated. The prior inventor, however, and the patentee may have approached the same device from different starting points and may for this reason, or it may be for other reasons, have so described their devices that it cannot be immediately discerned from a reading of the language which they have respectively used that they have discovered in truth the same device; but if carrying out the directions contained in the prior inventor's publication will inevitably result in something being made or done which, if the patentee’s patent were valid, would constitute an infringement of the patentee’s claim, this circumstance demonstrates that the patentee's claim has in fact been anticipated.
If, on the other hand, the prior publication contains a direction which is capable of being carried out in a manner which would infringe the patentee’s claim, but would be at least as likely to be carried out in a way which would not do so, the patentee’s claim will not have been anticipated, although it may fail on the ground of obviousness. To anticipate the patentee’s claim the prior publication must contain clear and unmistakeable directions to do what the patentee claims to have invented … . A signpost, however clear, upon the road to the patentee’s invention will not suffice. The prior inventor must be clearly shown to have planted his flag at the precise destination before the patentee.”
The reference to “something being made or done” in that passage confirms that the General Tire statement applies to both product and process claims (Novozymes at [146]). It is clear from Justice Jessup’s reasons at [166] and [186] that a finding of lack of novelty based on inevitable outcome may be found in the absence of an explicit or implied disclosure of the inevitable result. In particular at [186], where in carrying out a method a feature of the claim was an inevitable outcome, the fact that this is not disclosed to the skilled addressee by the prior publication does not compromise the case for inevitability.
Justice Jessup provides further guidance on the application of the General Tire principle:
“177 Although General Tire is part of Australian jurisprudence in the relevant area, it must be accommodated to the terms of s 7(1) of the Patents Act, upon which everything depends. That is to say, the inevitability of outcome to which General Tire refers must be such as would arise from recourse to the information referred to in the section. At the expense of repetition, it is here useful to remind ourselves of what the Court of Appeal said in that case ([1972] RPC at 485-486):
… if carrying out the directions contained in the prior inventor's publication will inevitably result in something being made or done which, if the patentee's patent were valid, would constitute an infringement of the patentee's claim, this circumstance demonstrates that the patentee's claim has in fact been anticipated. [Emphasis added]
This proposition is explicitly hypothetical. It is concerned not with what has happened or with what could have happened, but with what would have happened if the directions were carried out. As such, the proposition is in complete harmony with s 7(1), and with every other presently relevant aspect of the jurisprudence in this area. It is not the doing of it, nor even the ability to do it, that amounts to anticipation: it is the content of the information. If the information contains directions which, if carried out, would constitute an infringement of the patent in suit, the invention under the latter is not novel.” [Emphasis in original]
…
187 In my view, the General Tire approach, if taken at all, may be taken only with respect to the whole of any claim asserted to have been anticipated. The “precise destination” at which the flag must have been planted is one which includes every integer of the claim. The approach cannot, in my view, be taken for some integers only, leaving others to be dealt with by reference to the understanding of the skilled addressee. In the present context, what this means is that, to the extent that [a party’s] case is based on General Tire, it is not sufficient that they be able to point to passages in the … patent from which it would appear to the skilled addressee that [a feature of a claim] was contemplated or intended by the earlier inventors. It is necessary that they show that, if [the disclosure relied on] were worked as directed, it would inevitably, as a matter of hard fact, have involved [that feature].”
Consistent with MSDA’s submissions, Novozymes establishes that the reverse infringement test where it applies to inevitable outcome in the General Tire sense does not require the person skilled in the art, before the priority date, to have known that they were performing the method as claimed. All that is necessary is that they would, in fact, have done so.
MSDA relied on the following prior art documents to establish lack of novelty:
Benson, J. et al. (March 2002) FASEB Journal 16(5): A1045 Abstract 759.12
WO 2001/018051 A2 (Schering Corporation) 15 March 2001
WO 2001/085790 A2 (Schering Corporation) 15 November 2001
The European “Text intended for grant” document for application EP 03781490
Genentech’s case for novelty is essentially presented on the basis of its submissions, since its declarant Dr Ouyang did not comment directly on the content of these documents.
Benson et al.
Benson et al. is in evidence as exhibit ANB-2. It is a short abstract titled ‘The role of IL-23 in experimental autoimmune encephalomyelitis’. The entire disclosure is as follows:
“It has previously been demonstrated that neutralisation of IL-12 can ameliorate autoimmune disease. However, studies primarily targeted the p40 subunit, rather than IL-12p35. Interestingly, IL-12p40 is shared by IL-23, a recently described heterodimeric cytokine. Therefore, it was unclear whether the previous findings were due to IL-12 or IL-23 blockade: In this study, our objective was to differentiate the roles of IL-12 and IL-23 in a model of chronic autoimmune disease, relapsing experimental autoimmune encephalomyelitis (EAE). In a side by side comparison, mice were treated with neutralizing monoclonal antibodies specific for either IL-12p35 or IL-12/23p40 after myelin basic protein (MBP) immunization. Antibody concentrations were carefully modified to ensure equivalent in vivo efficacy. Results were analysed by clinical score analysis, histopathology, in vitro proliferation assays, and cytokine profiles. IL-12 specific neutralization had no beneficial effect on the progression of EAE. However, neutralization of both IL-12 and IL-23 effectively ameliorated EAE clinical signs and MBP-specific Th cell responses. These data suggest a dominant role for IL-23 in a model of chronic autoimmune disease.”
Benson et al., discloses a study in which an IL-23 antagonist (a neutralising antibody specific for the IL-12/IL-23p40 subunit) was administered to mammalian subjects (mice) with relapsing experimental autoimmune encephalomyelitis (EAE), and found to be effective in treating the clinical symptoms of the disease (Tangye#1 at [36] - [38]; Tangye#4 at [11]).
Does EAE constitute an inflammatory disease characterized by elevated expression of IL-17? There is no dispute, and the evidence establishes, that EAE is an inflammatory disease (Tangye#1 at [38]; Tangye#4 at [11]; Ouyang at [14]; Exhibit H to Ouyang (the Abstract)). Although published after the priority date the evidence establishes that, as a matter of fact and at all times, EAE is characterized by elevated expression of IL-17 (Exhibit H at Figure 2D; Exhibit L).
Benson et al does not disclose the effect of the IL-23 antagonist on IL-17. However, consistent with the expert evidence (Tangye#2 at [9], [27]; Ouyang at [18]; Tangue#4 at [19]), Genentech accepted that the IL‑23 antagonist that successfully treated the animals would, as a matter of fact, have done so by inhibiting IL-17 production by the animal’s T cells.
I conclude that claim 1 is anticipated by Benson et al. insofar it encompasses the in vivo treatment of a mammalian subject with an IL-23 antagonist. Benson et al also anticipates the therapeutic methods of claims 4-5 and claim 15 insofar as this last encompasses a determination of elevated IL-17 expression based on a positive diagnosis of an inflammatory condition characterized by such levels.
WO 2001/018051 (WO’051)
WO’051 is in evidence as exhibit ANB-5. The document is titled ‘Mammalian cytokines; related reagents and methods’. On page 3 of the document, the invention is based on the association of IL-12p40 subunit with IL-B30 resulting in functional receptor binding and signalling.
The evidence establishes that the IL-12 p40/IL-B30 dimer described by WO’051 is, in fact, IL-23. Interleukin-12p40 is identical to IL-23p40 and IL-B30 is an alternative name for the IL-23p19 subunit (Tangye#1 at [42], [47] and Exhibit ANB-22 at [0040]). In the following text, where WO’051 refers to the IL‑12p40/IL-B30 complex, I have substituted IL-23.
WO’051 describes the treatment of inflammatory diseases with IL-23 antagonists (Tangye#1 at [45]). WO’051 does not exemplify the therapeutic use of IL-23 antagonists or agonists. However, MSDA drew my attention to passages that it submitted describe the use of antagonists against IL‑23 for treating a range of inflammatory conditions.
The information on page 30, that the invention provides reagents with significant commercial and/or therapeutic potential that “will … be useful in the treatment of conditions associated with abnormal physiology or development, including inflammatory conditions” does not identify the relevant inflammatory diseases with any degree of precision.
A number of passages disclosing that IL-23 antagonists or agonists “may” be useful to treat immune disorders or chronic inflammation (page 12; page 31, lines 9-11, 29-32), even where relevant inflammatory disorders are explicitly identified (page 32, lines 26-29), are more in the nature of an invitation to investigate further; they fall short of a clear and unmistakeable direction so to use it.
More specific information on the use of IL-23 antagonists is provided at page 31 at lines 34-37:
“Particular targets for therapeutic application include, e.g., lung conditions, both asthma and fibrosis, in EAE models …, diabetes and gut inflammations.”
A reasonable construction of that sentence is that it directs the reader to use IL-23 antagonists for treating the identified conditions. However, does it constitute a direction which, if followed, would necessarily constitute an infringement of the combination of features in the opposed claims (if valid)?
The terms “lung fibrosis” and “diabetes” each encompass a broader field than idiopathic pulmonary fibrosis, chronic pulmonary inflammatory disease and autoimmune diabetes identified in the opposed specification as being associated with elevated IL-17. Similarly, it can be inferred from Dr Ouyang’s evidence at [24] that the term “gut inflammation” encompasses more than ulcerative colitis, Crohn’s disease and inflammatory bowel disease. Since MSDA has not established that the alternative conditions encompassed by these terms are associated with elevated IL-17 expression, I cannot conclude that the direction to treat these broadly defined conditions would inevitably result in something within the opposed claims.
Nevertheless, WO’051 does identify asthma and EAE as candidates for treatment; both of which are identified in the opposed specification as being associated with elevated IL-17 levels. However, even if it were applied to these conditions, the evidence before me does not establish that the mosaic of passages MSDA relies on provides a clear and unmistakable direction to perform a method that would necessarily constitute an infringement of the opposed claims.
WO’051 broadly describes potential agonists and antagonists, including antibodies against IL-23 (page 21-23), the dose and formulation for effective therapy is left to the user to optimise based on a number of factors, including the other medicaments administered (page 33, line 22 to page 34, line 23). At page 31 and claim 13, WO’051 teaches that IL-23 antagonists may be combined with existing therapeutics including modulators of inflammation. As one example of my concerns, it is not clear that if an IL-23 antagonist was administered in combination with other anti-inflammatory compounds as directed, that it would be in a sufficient amount to inhibit IL-17 expression.
The opponent also relied on claims 33-37 of WO’051 to establish lack of novelty. Independent claim 33 defines a method of modulating the inflammatory response in an animal, comprising contacting cells of the animal with a therapeutic amount of an agonist or antagonist of IL-23p19 protein.
Insofar as claim 33 recites an agonist, I consider it to provide a clear and unmistakeable direction to the method of opposed claim 14. It is not in dispute that the physiological effect of IL-23 is to induce IL-17 production and it is clear from the opposed specification and evidence that a “therapeutic amount” of an IL-23 agonist sufficient to modulate the inflammatory response in a mammalian subject would necessarily involve induction of IL-17 (Figures 2, 3 of the opposed specification; Ouyang at [15], last sentence). It follows that claim 14 is not novel.
However, I have insufficient information on which to conclude that the reverse would be true and opposed claim 1 necessarily infringed by claim 33 of WO’051. It appears that a “normal” or baseline level of IL-17 expression product (protein or mRNA) may be indistinguishable from zero (see Figs 2 and 3 of the opposed specification; Exhibit H, Fig 2D; Exhibit N, Fig 5). In this situation, it is reasonable to conclude that IL-17 production could not be inhibited (repressed) further by the application of an IL-23 antagonist. On this basis, I could only make a finding that IL-17 expression would be inhibited where the cytokine is present at elevated levels prior to treatment with an antagonist. However, neither claim 33 nor its dependent claims identify any target population with sufficient specificity to ensure that performing the invention as claimed would necessarily involve the treatment of subjects with elevated expression of IL-17.
In summary, claim 14 is anticipated by WO’051. However, MSDA has not established that WO’051 contains a clear and unmistakable direction to use IL-23 antagonists in a manner that would inevitably, as a matter of fact, infringe claims 1, 4-5 and 15, if valid.
WO 2001/085790 (WO’790)
WO’790 is in evidence as exhibit ANB-6. Its title is ‘Mammalian receptor proteins; related reagents and methods’. On pages 2-3, the invention relates to the cytokine receptor subunit DCRS5, which is in fact a subunit of the IL-23 receptor (page 3 lines 2-4 of the specification, bearing in mind that the p40/IL-B30 ligand is IL-32). The ligand-receptor pairing is said to provide insight into indications for use of agonists and antagonists of the receptor subunits.
On the basis of Dr Tangye’s evidence, MSDA submitted that WO’790 discloses IL-23 antagonists as effective agents for the treatment of a range of autoimmune inflammatory diseases (Tangye#1 at [39] - [42]; Tangye#4 at [13]).
On pages 5-6, WO’790 teaches that the therapeutic uses of the receptor agonists and antagonists include methods of modulating the physiology or development of a cell by contacting a cell with the antagonist or agonist. Suitable antagonists are soluble receptor subunits, or antibodies or antisense nucleotides directed against the receptor subunits. Agonist antibodies bind the receptor complex. On page 6, in one embodiment, an antagonist is administered to a cell from a host that exhibits signs or symptoms of, relevantly, MS, RA or psoriasis. Conversely, an agonist is administered to a cell from a host that, among other things, suffers from a tumour, viral or fungal growth; receives a vaccine; or suffers from an allergic response.
Claims 21-23 of WO’790 are similar in scope to their consistory statements summarised above but are ambiguous as to whether they encompass in vivo as well as in vitro methods. This is resolved by pages 39-40 of the description which discloses the therapeutic utility of the invention in treating diseases and disorders.
Claim 22 directs the reader to perform a method comprising contacting a cell, in vivo or in vitro, with a sufficient amount of an antagonist of IL-23 to modulate the physiology or development of the cell where the cell is from a host exhibiting signs or symptoms of, relevantly, MS, RA or psoriasis, all of which are disclosed in the opposed application as inflammatory diseases characterized by elevated expression of IL-17.

Dr Tangye states that where a subject responded in a positive manner to an IL-23 antagonist, the treatment would inhibit IL-17 production by the subject’s T cells (Tangye#2 at [27]). Although this evidence refers to an antagonist of the IL-23 ligand and WO’790 to an antagonist of the IL-23 receptor, since the downstream effects of the compounds are the same, I consider Dr Tangye’s evidence to be equally applicable in both situations. Dr Tangye’s evidence at Tangye#2 [28]-[29] and Tangye#4 [19] supports my conclusion.
I find WO’790 to provide clear and unmistakable directions to perform a method that would inevitably result in claims 1 and 4-5 being infringed, in addition to claim 15 insofar as this last encompasses a determination of elevated IL-17 expression based on a positive diagnosis of an inflammatory condition characterized by such levels.
Claim 23 of WO’790 provides clear and unmistakeable directions to the method of opposed claim 14. It is not in dispute that the physiological effect of IL-23 is to induce IL-17 production. Claim 23 requires an IL-23 agonist to be administered in a sufficient amount of to modulate the physiology and development of a cell. For similar reasons as provided at [68] above, I consider that this would necessarily involve induction of IL‑17.
The “Text intended for grant” document for related application EP03781490.
Exhibit ANB-39 consists of collated documents from the opposition proceedings in Europe in respect of related patent EP 1576011. At the hearing, MSDA relied only on the “Text intended for grant” (TIFG) document, a “marked-up” copy of the accepted application. At the hearing, I told the parties that I considered the publication date of this document to be 20 February 2009, the day it was made publically available on the EPO website.
I have found above that the priority date of claim 15, insofar as it relates to testing each individual subject to determine they have elevated levels of IL-17 expression, is 16 October 2009. The TIFG document is a single document that has been made publicly available prior to this date, and consequently, for this embodiment of claim 15 it forms part of the prior art base for novelty purposes under section 7(1) of the Act.
Claim 20 of the TIFG document is substantially the same as opposed claim 15 - the only difference being that the antagonist is defined as “for use” in the method, while Australian claim 15 recites “when used”, consistent with the jurisdictional differences in the construction of these terms. At the hearing Genentech accepted that if the priority date of claim 15 were deferred, claim 15 is anticipated by the TIFG document. I agree.
In summary, I have found that the documents raised by MSDA anticipate independent claims 1, 4, 5, 14 and 15. The parties agreed that the opposition could be heard on the basis of the independent claims, with the dependent claims falling the same way. On this basis, dependent claims 2-3, 11-12, 16-33 also lack novelty.
Inventive step
Under the provisions of subsections 7(2) and 7(3) of the Patents Act 1990, an invention is taken to involve an inventive step when compared with the prior art base unless it would have been obvious to a person skilled in the art. Obviousness is assessed in the light of the common general knowledge as it existed in the patent area before the priority date, either on its own, or together with information in a document or a combination of documents that the person skilled in the art could, before the priority date of the relevant claim, be reasonably expected to have ascertained, understood and regarded as relevant and where necessary combined. “Obvious” means “very plain” (Lockwood Security Products Pty Ltd v Doric Products Pty Ltd(No 2) [2007] HCA 21 at [51]-[52]; 72 IPR 447).
The test for obviousness is whether it would have been a matter of routine to proceed to the claimed invention.
“The test is whether the hypothetical addressee faced with the same problem would have taken as a matter of routine whatever steps might have led from the prior art to the invention, whether they be the steps of the inventor or not.” (Aicken J in Wellcome Foundation Ltd v VR Laboratories (Aust) Pty Ltd [1981] HCA 12 at [45]; 148 CLR 262 at 286)
MSDA relied on the following prior art:
Benson, J. et al. (March 2002) FASEB Journal 16(5): A1045 Abstract 759.12
WO 2001/018051 A2 (Schering Corporation) 15 March 2001
WO 2001/085790 A2 (Schering Corporation) 15 November 2001
The “Text intended for grant” document for application EP03781490
The usual approach to obviousness is the problem-solution approach. Once the problem has been formulated, and the common general knowledge or prior art base have been determined, the question of whether the claimed solution is obvious must be addressed.
The problem
On page 1 of the specification, produced by activated T cells, the proinflammatory cytokine IL-17 stimulates epithelial, endothelial and fibroblastic cells to produce other inflammatory cytokines and chemotactic cytokines (chemokines), and synergises with other cytokines to further induce chemokine expression. On page 2, the specification reveals that elevated IL-17 expression had been reported in a number of chronic inflammatory diseases, although there was no clear classification of IL-17 into the cytokine profiles typical of the Th1- or Th2-polarised immune responses.
On page 1 and 2a, relevant to the opposed claims, in one aspect the invention concerns a method for inhibiting IL-17 production by T cells. In other aspects the invention concerns methods for treating inflammatory diseases associated with elevated expression of IL-17 and for inducing IL‑17 production in a mammalian subject using IL-23 antagonists and agonists.
Although the specification does not explicitly identify a problem or need in the art before the priority date, it is clear that it does teach that IL-17 is elevated in a number of inflammatory diseases and identifies the source and proinflammatory nature of the cytokine. Therefore, the problem that can be derived from the specification is that addressed by the first aspect identified above, which is the provision of a method for inhibiting IL-17 production by T cells. The solution to that initial problem underpins the later claims to methods of identifying an anti-inflammatory agent (which are not opposed) and the therapeutic methods involving modulation of IL-17 expression.
At the hearing, MSDA identified the problem addressed by the specification as the provision of effective methods for treating inflammatory diseases characterised by high expression of IL-17, or patients with high expression of IL-17. The focus on IL-17 in that statement is consistent with the more fundamental formulation of the problem I have arrived at above. The expert evidence does not identify any alternative problem or need in the art before the priority date.
Having determined that the problem is the provision of a method for inhibiting IL-17 production by T cells, the next question is whether the cited prior art documents would have been ascertained, understood and regarded as relevant by person skilled in the art faced with this problem.
Ascertained, understood, regarded as relevant
Dr Tangye states that he had searched patent databases in the past and that he had the capacity to access each of Benson et al, WO’051 and WO’790 before October 2002 (Tangye#1 at [28], and [32] - [34]). I will accept that these documents could have been ascertained.
Of more importance is the fact that none of Benson et al, WO’051 and WO’790 refer to IL-17. Although Dr Tangye states that it was known that IL-17 expression was increased in inflammatory diseases (Tangue#2 at [14]), his evidence does not establish that IL-17 was known before the priority date to be a desirable target for therapeutic intervention in these diseases, or that IL-23 antagonists would work for this purpose. Therefore, on the basis of the evidence before me, I cannot conclude that the person skilled in the art seeking information with a view to providing a method for inhibiting IL-17 production by T cells would regard these documents as relevant.
Regarding the EP0378149 text intended for grant document, Genentech argued that it would not have been ascertained. MSDA made no submissions on this point. I agree with Genentech. This document was published only on the European Patent Office file documenting the prosecution of application EP0378149 in Europe. While this makes the document publicly available, there is no evidence to suggest that the person skilled in the art would search such files. MSDA has not established that this document would have been ascertained.
Since I have found that the documents relied on by MSDA would not have been ascertained or regarded as relevant, I conclude that the claimed invention involves an inventive step.
Useful
The requirements for utility in a claimed invention under section 18(1)(c) were provided by the Full Court of the Federal Court as follows:
“If the claimed invention does what it is intended by the patentee to do and the end result obtained is itself useful, the invention is useful within the meaning of s 18(1)(c) … As to the first aspect, the invention as claimed must attain the result promised by the patentee” (Ranbaxy Australia Pty Ltd v Warner-Lambert Co LLC [2008] FCAFC 82 at [141]; 77 IPR 449)
“A claim is bad if it covers means that will not produce the desired result, even if a skilled person would know which means to avoid. That is to say, everything that is within the scope of a claim must be useful, otherwise the claim will fail for inutility.” (H Lundbeck A/S v Alphapharm Pty Ltd [2009] FCAFC 70 at [81], [217]; 81 IPR 228)
MSDA submitted that claims such as 4, 5 and 15 which relate to the treatment of diseases characterized by, or patients determined to have, elevated expression of IL-17, lack utility.
Essentially, MSDA’s argument is that these claims cannot be put into practice because the specification does not disclose how such diseases or patients are to be identified and this is not part of the common general knowledge in the art. Relying on the judgement of Justice Whitford in the UK High Court in American Cyanamid Company v Berk Pharmaceuticals Limited [1976] RPC 231, MSDA argued that a skilled addressee seeking to apply the claims might identify the wrong inflammatory diseases or the wrong patients and for this reason the claims lack utility.
Genentech submitted that this present situation is distinguished from American Cyanamid because elements of the description in that case were found to be “likely to lead to the wrong result; at best it is likely to be hopelessly ambiguous”. I agree with Genentech’s submission that the phrase “elevated expression of IL-17” can be construed in its plain meaning and is far from being hopelessly ambiguous. I have found elsewhere in this decision that the words of the claims are clear and that the person skilled in the art could identify the relevant diseases.
MSDA has produced no evidence to establish that the claimed methods of treatment will not work, and consequently it has not established that claims 4, 5 and 15 lack utility.
Section 40
Section 40(2) of the Patents Act relevantly requires that a complete specification must (a) describe the invention fully, including the best method known to the applicant of performing the invention and (b) end with a claim or claims defining the invention. Section 40(3) requires that the claim or claims in a patent specification must be clear and succinct and fairly based on the matter described in the specification.
Section 40(2)(a): Full Description
The High Court in Kimberly-Clark Australia Pty Ltd v Arico Trading International Pty Ltd [2001] HCA 8 at [25]; (2001) 207 CLR 1 at 17 explained the test for full description as:
“The question is, will the disclosure enable the addressee of the specification to produce something within each claim without new inventions or additions or prolonged study of matters presenting initial difficulty?”
MSDA submitted that the specification does not provide sufficient information to delineate the outer boundaries of the claim, or to enable the person skilled in the art to do so. Relying on Dr Tangye’s evidence, MSDA argued that the opposed specification contains no guidance or parameters to enable the person skilled in the art to determine whether a given inflammatory disease is characterised by elevated expression of IL-17 (Tangye#2 [32] - [34]; Tangye#3 [18]; Tangye#4 at [24]). In particular there is no guidance as to “normal” levels of IL-17 or the level by which IL-17 expression must increase in humans for it to be considered elevated (Tangye#2 at [35], [45]; Tangye#3 [18(iii)]; Tangye#4 [26]).
In its plain meaning “elevated” expression of IL-17 means that the IL-17 gene is expressed at a higher level than in a relevant comparative group. I agree with Genentech’s submission that the person skilled in the art at the priority date would understand the phrase “elevated levels of X” to mean that the levels were elevated compared to something such as a base level or “normal” level, in the present case a subject that does not have an inflammatory disease.
Critically, although he considers the specification deficient, Dr Tangye does not say that the person skilled in the art at the priority date could not determine whether an individual has, or if a disease is characterized by elevated levels of IL-17 expression products. Rather, his evidence is that performing the work to determine the whole scope of the claim would require a lot of work (Tangye#2 at [37], [44]; Tangye#3 at [16]), for example:
“A person of ordinary skill in the art would be required to conduct significant population studies on numerous mammalian species to ascertain what could potentially constitute an “elevated” range of IL-17 expression in diseased individuals across the full range of mammals and diseases within the scope of the claims. This would be a considerable undertaking and subject to many uncertainties. For example, in mammalian species there can be significant variation in levels of IL-l7 production in individuals with a given inflammatory disease. Cytokines such as IL-17 are known to act locally which introduces further variability when sampling diseased and non-diseased mammalian populations. In addition, IL-l 7 expression may be increased in mammals without inflammatory diseases. For example, bacterial and fungal infections common in many mammalian populations potentially cause elevated IL-17 levels independently of inflammatory disease. In my opinion, these and other factors would make it difficult to determine what constitutes an “elevated” range of IL-17 expression across the full range of mammals and diseases within the scope of the claims.” (Tangye#2 at [37])
The opposed specification refers to measuring IL-17 protein or mRNA (both gene expression products) in samples of body fluids, cells or tissues from a subject (page 20, lines 2-19). It refers to the use of the generic methods ELISA, immunostaining and quantitative RT-PCR to measure the levels of IL-17 protein and mRNA (page 3, line 19; page 20, line 4). What constitutes a “normal” or baseline level of IL-17 for any given clinical situation can be established by measuring the levels in a relevant sample from a comparable group of healthy subjects or any other relevant control group. The specification at page 20 lines 2-3 and 8-9 reports two such studies.
Dr Tangye states at several points in his evidence that it was “well known before the priority date that inflammatory diseases are associated with elevated expression of IL-17” (see for example Tangye#1 at [66]; Tangye#2 at [14], [22], [26]). This fact can only have been established if the person skilled in the art before the priority date had been able to measure the level of IL-17 expression in subjects with an inflammatory disease and determine that the levels were higher than those in a relevant comparative group. I note that the opposed specification on page 20 cites four studies finding that particular inflammatory diseases are associated with elevated expression of IL-17, supporting the view that reliable identification of such diseases is not beyond the person skilled in the art. Therefore, I agree with Genentech that the specification provides sufficient information to enable the person skilled in the art to determine whether a disease is characterized by elevated expression of IL-17 or to determine whether an individual subject has an elevated level.
I find that the specification satisfies the requirement to fully describe the invention in that it provides sufficient information to enable the person skilled in the art to produce something within each claim without new inventions or additions or prolonged study of matters presenting initial difficulty.
Section 40(3): Fair Basis
Section 40(3) requires that the claim or claims in a patent specification be fairly based on the matter described in the specification.

As the test for fair basis, the High Court in Lockwood Security Products Pty Ltd v Doric Products Pty Ltd [2004] HCA 58 at [69]; (2004) 217 CLR 274 at 300 [69] approved the words of Gummow J in Rehm Pty Ltd v Websters Security Systems (International) Pty Ltd (1988) 81 ALR 79 at 95:
“… the question is whether there is a real and reasonably clear disclosure in the body of the specification of what is then claimed, so that the alleged invention as claimed is broadly, that is to say in a general sense, described in the body of the specification.”
The High Court in Kimberly-Clark v Arico [2001] HCA 8 at [15]; (2001) 207 CLR 1 at [15] and Lockwood v Doric [2004] HCA 58 at [57]; (2004) 217 CLR 274 at [57], approved the principle provided by Barwick CJ in Olin Corporation v Super Cartridge Co Pty Ltd [1977] HCA 23 at [6]; (1994) 180 CLR 236 at 240:
“The question whether the claim is fairly based is not to be resolved, in my opinion, by considering whether a monopoly in the product would be an undue reward for the disclosure. Rather, the question is a narrow one, namely whether the claim to the product … as expressed, travels beyond the matter disclosed in the specification.”
MSDA submitted that the claims lack fair basis insofar as they relate to the treatment of diseases characterized by, or subjects determined to have, elevated levels of IL-17. It contended that the specification does not disclose that IL-17 expression is elevated for some inflammatory diseases but not others; or that a group of subjects suffering from any one inflammatory disease could be classified into subgroups exhibiting normal or elevated levels of IL-17 expression.
Claims 4-5 - inflammatory diseases characterized by elevated expression of IL-17
I have found above that the specification provides sufficient information to enable the person skilled in the art to determine whether any given inflammatory disease is characterized by elevated IL-17 expression. Applying the same reasoning, I find that the specification provides a real and reasonably clear disclosure of a number of diseases that are characterized by elevated IL-17 expression and the means by which others could be investigated and successfully identified.
Claim 15 - subjects determined to have an elevated level of expression of IL-17
In considering the priority date of claim 15, I have found there was not an in substance disclosure in the specification as filed or its priority document of the feature requiring IL-17 expression to be measured in each individual subject prior to treatment and determined to be elevated prior to treatment with an IL-17 antagonist. For similar reasons I consider claim 15 to lack fair basis.
The specification as a whole describes an invention in which the presence of a relevant inflammatory disease/disorder/condition in the subject drives the selection for treatment, not the individual subject’s IL-17 levels. A number of passages in the specification support this view (page 10, lines 10-12; page 11, lines 7-11; pages 19-21; page 20, lines 20-22 and page 27, lines 11-13).

Although a consistory statement was introduced into the specification with claim 15, this alone does not provide fair basing for the claim because the statement does not reflect the description of the invention in the specification as a whole (Lockwood Security v Doric Products [2004] HCA 58 at [87]; 217 CLR 274 applied).
I conclude that insofar as it requires each subject to be tested to determine they have an elevated level of IL-17 expression prior to treatment, the subject matter of claim 15 travels beyond the matter described in the specification and lacks fair basis. The parties agreed to the opposition being determined on the basis of the independent claims with the independent claims falling the same way. Therefore, I find claim all claims dependent on claim 15 also lack fair basis.
Section 40(2)(b): Claims define the invention
The requirement in section 40(2)(b) that a complete specification for a standard patent shall end with a claim or claims defining the invention is simply that there must be a claim or claims and that they should define the monopoly for which the application has been made (AMP Inc v UtiluxPty Ltd (1971) 45 ALJR 123 at 128). In this regard, while the nature of the invention is to be determined from the specification as a whole including the claims, the absence of a central feature of the invention from a particular claim will result in it not defining the invention (the Deputy Commissioner in Sabre Inc v Amadeus Global Travel Distribution SA [2004] APO 21).
MSDA’s submissions for section 40(2)(b) were the same as those for other section 40 grounds; that insofar as they relate to the treatment of diseases characterized by, or subjects determined to have, elevated levels of IL-17, the claims fail to define the invention. MSDA relied on Colgate-Palmolive Co v Cussons Pty Ltd 26 IPR 311 at [351], in which Justice Sheppard said:
“If the invention is not described, or if there is uncertainty about what it is that has been invented, … the claims will not perforce define the invention”
MSDA argued that since the meaning of the expressions “diseases characterized by”, “subjects determined to have”, and “elevated levels of IL-17” are not clear and can’t be resolved, the claims do not define the invention.
I have found that these expressions can be given a meaning. The nature of the invention in this case is identified on pages 1 and 2a-2b of the specification. Relevant to the opposed claims, the invention concerns inhibition of the production of the proinflammatory cytokine IL-17 by T cells using an IL-23 antagonist and the use of IL-23 antagonists in the treatment of inflammatory diseases characterized by elevated IL-17 expression. The invention also relates to a method for inducing IL-17 production by administering an IL-23 agonist.
The claims define the invention in similar terms and as a consequence they define the invention for which the application has been made.
Section 40(3): Clarity
A claim is lacking in clarity if a third party could not ascertain whether an act would fall within the scope of the claim (Monsanto Co v Commissioner of Patents (1974) 48 ALJR 59 at 60). However, a claim does not lack clarity because it uses inexact language or is difficult to construe, as long as it provides a “workable standard” suitable to the intended use (Minnesota Mining & Manufacturing Co v Beiersdorf (Aust) Ltd [1980] HCA 9 at [46]; (1980) 144 CLR 253 at 274).
MSDA submitted that insofar as the claims relate to the treatment of “diseases characterized by” and “subjects determined to have” elevated levels of IL-17 the meaning of these phrases is not clear and cannot be resolved. In particular, the term “elevated expression of IL-17” is not defined in the specification, and “normal levels” are not known from the prior art or the common general knowledge in the art. As such, the scope of the claims is uncertain.
I have found above that the claims can be given a meaning, and that the person skilled in the art would be able to determine an elevated level of IL-17 and the diseases characterized by such levels. As such I find the claims are clear.
Conclusion
The opposition is successful. I have found independent claims 1, 4-5 and 14-15 lack novelty and with them claims 2-3, 11-12 and 16-33. Claim 15 and all claims dependent on claim 15 lack fair basis insofar as these claims encompass testing each individual subject to determine they have elevated IL-17 expression levels prior to treatment, lack fair basis.
It is possible to overcome the deficiencies I have identified by amendment of the claims. I therefore allow Genentech 2 months from the date of this decision to propose such amendments.
Costs
Both parties submitted that costs should follow the event. Merck, Sharpe & Dohme (Australia) Pty Ltd. have been successful in their opposition. I award costs according to Schedule 8 against Genentech, Inc.
Dr B Akhurst
Delegate of the Commissioner of Patents