A Joint Venture Research Agreement

Naturally harvested seafood typically contains high levels of omega-3 fatty acids obtained from their diet, with three of the more important variants in human physiological being linolenic acid (ALA), eicosapentaenoic acid (EPA) and docosahexanoic acid (DHA).1 Humans are incapable of synthesizing these fatty acids, despite their importance in maintaining physiological health, and require regular consumption of these nutrients.2 However, farm-raised seafood requires supplements be fed to the fish to elevate the fatty acid levels to those of naturally-caught seafood.3 The industry researched avenues to supplement fish FA levels, with BASF and CSIRO looking into synthesizing the desired compounds from the canola plant (Brassica napus),4 which could be fed to farm-raised seafood.5 Both BASF and CSIRO looked into introducing enzymes into canola to use alpha-linolenic acid, which was naturally made by the plant, as a starting molecule for EPA and DHA.6

The two companies entered into a joint venture research agreement, allowing analysis of using genes from both companies.7 The year following expiration of the research agreement, BASF developed a canola line capable of synthesizing EPA and DHA, and licensed the technology.8 Shortly thereafter, in the mid-2010’s, CSIRO filed patent applications that claimed priority to provisional applications filed prior to the JV, which it licensed.9 BASF attempted to secure a license from CSIRO, and after negotiations broke down, filed a declaratory action against CSIRO and its licensees,10 arguing that the patents were invalid for lack of written description, or jointly owned based on the research agreement.11

The Court addressed the lack of written description, noting that numerous sections of the specification discussed using canola, specific examples of fatty acid-producing Arabidopsis crops- a commonly accepted model for canola, and scientific rationale supporting the likelihood of canola producing the fatty acids, showing that a skilled practitioner in the field would understand that CSIRO had invented what was claimed.12 The fact that CSIRO did not actually produce the fatty acids until after the provisional filing was dismissed by the court, noting actual reduction to practice is not required, and that the work in the Arabidopsis model as a highly predictive indicator of success in canola, was critical to the written description determination.13 However, the Court also found that claims to a broader group of crops was not supported.

On the issue of joint ownership of the patents, the Court noted the claim relied solely on the research agreement, and analyzed the agreement terms to determine the validity of the claim.14 The Court took a narrow view of the terms, finding that the joint ownership applied only to inventions that include gene constructs from both BASF and CSIRO, information and data that originated from evaluating the BASF-CSIRO gene combinations, and IP that comprises the gene constructs or information above.15 After concluding the CSIRO patents did not claim any combinations of BASF and CSIRO gene combinations, the Court found BASF’s position- that the CSIRO patents were obtained by drawing on the experiments from the joint research, was unreasonable and declined to overrule the finding that CSIRO was the sole owner of its patents,16 highlighting the importance of terms in a contract.

 

1 BASF Plant Science, LP v. Commonwealth Scientific and Industrial Research Organization, No. 2020-1415, p5 (Fed. Cir. Mar. 15, 2022); Hishikawa, et al., Metabolism and functions of docosahexaenoic acid-containing membrane glycophospholipids. FEBS Lett. 2017 Sep; 591(18):2730-2744.

2 Hishikawa, et al. FEBS Lett. 2017.

3 BASF Plant Science, LP, p5.

4 Id. at 6.

5 Id. at 5.

6 Id. at 6.

7 Id. at 7.

8 Id. at 8.

9 Id. at 7,9, 11-12.

10 Id. at 8.

11 Id. at 14.

12 Id. at 26-29.

13 Id. at 30-33.

14 Id. at 35.

15 Id. at 36-37.

16 Id. at 38.

Contract Terms

A recent decision from the Federal Circuit highlights the importance of carefully considering the terms of an agreement prior to signing the document. In Nippon Shinyaku Co., Ltd. v. Sarepta Therapeutics, Inc., the parties entered into a confidentiality agreement with the intention of forming a business relationship.[1] The confidentiality agreement included a provision not to sue that included a provision noting validity challenges before the U.S. Patent and Trademark Office in included in the restrictions,[2] and a separate provision requiring all causes of action be brought in Delaware for a two-year period following the expiration of the agreement.[3]  Upon expiration of the agreement, Sarepta filed numerous IPR proceedings with the U.S. Patent and Trademark Office challenging the validity of Nippon Shinyaku’s patents.[4] The Federal Circuit analyzed the forum selection, noting “all Potential Actions” were required to be filed in the courts of Delaware, which included invalidity challenges.[5] The Court was unpersuaded by arguments that the interpretation of the agreement would effectively eliminate a party’s ability to bring an action before the U.S. Patent and Trademark Office, noting that parties can bargain away rights, such as contracting away IRP challenge rights.[6]

The Federal Circuit’s opinion highlights the criticality of understanding the terms of an agreement prior to signing.  Sarepta’s arguments relating to public policy of permitting a party access to all avenues of action fell flat, and the court countered that the parties were held to the terms that they agreed to, even if those terms restricted one party’s rights. Given the ubiquity of forum selection provisions in contracts- including many licensing agreements, joint ventures, confidentiality agreements, transfer agreements, etc.- parties must understand what they are signing and what rights the party is signing away in its contracts.

[1] Nippon Shinyaku Co., Ltd. v. Sarepta Therapeutics, Inc., No. 2021-2369; page 2 (Fed. Cir. February 8, 2022

[2] Id. at pages 2-3.

[3] Id. at page 3.

[4] Id. at page 4.

[5] Id. at pages 9-10.

[6] Id. at page 13.

Invention Disclosures

At some point during a consultation with each patent client, the potential client asks, “So what information do you need from me?” Not only is this a common question, but also a complex one.  The simple answer is taken directly from the rules governing the patent application process- enough for someone in the field to make and use the invention and know exactly what it is you want to protect. Additionally, the application must provide different versions of the invention that the inventor deems covered by the application or wants protection in the application.

However, that answer belies the complexity of patent law, because there is no one way to describe an invention- it depends on the technology and the available information. For devices, the application needs to describe the parts and how those parts work- with one another and to accomplish the end goal of the device. For example, in a bone screw patent application, the way the floating head of the screw connected to the body of the screw, and locked into a set orientation with the body.  For pharmaceutical applications, the synthesis of the compound, animal studies, possible prophetic studies, SAR analysis, metabolism, distribution, dosing regimens, and toxicity can all be helpful or critical to the application.[1]

The prior art must also be considered when determining how much information is needed- because the amount of information needed is not determined in a vacuum.  Prior art is the information known by the field at the time the invention is made.  This includes trade or journal articles (both print and online), web postings, manuscripts, sales documents, and products, though this is not an exhaustive list.  The prior art cuts both ways, since the more information known in the field that relates to the invention means the disclosure needs less information, but also increases the requirement to distinguish the invention from what is already known.

Getting back to the initial question- what is needed for a patent application; the answer is as much information as you can provide, but at a minimum enough information for me to figure out your invention.

[1] For example, the Federal Circuit recently analyzed animal studies and prophetic studies to uphold patent infringement in Novartis Pharma. Corp. v. Accord Healthcare, Inc. No. 2021-1070; p5-7, 10-12 (Fed. Cir. January 3, 2022).

Covid-19 Update

Given the impact of the 2019-nCoV virus (SARS-CoV-2, COVID-19) on everyday life, it made sense to look into what we know about the virus right now and how that knowledge is driving possible treatments and vaccines, to get life moving back to normalcy.  Much of the material was taken from research articles, which are cited at the end, and distilled into a more approachable format.

Scientists working on the 2019-nCoV virus (SARS-CoV-2, COVID-19) have been studying its genome and found a large similarity with the virus responsible for the SARS outbreak of 2003, meaning that the two viruses are related, like cousins.[i]  The virus is a single strand RNA virus that targets the patient’s innate immune system,[ii] and respiratory system.[iii] A fusion spike protein was identified from COVID-19 which binds to proteins on the target cell membrane, angiotensin-converting enzyme 2 (ACE2), resulting in the ejection of a subunit and altering the shape of the fusion spike.[iv]  This allows the virus to merge with the and inject the virus RNA into the cell.[v] ACE2 is a surface enzyme on cells found in the lungs, arteries, heart, kidneys, and intestines,[vi] and is involved in the humoral immune response, recruitment of leukocytes, and generation of reactive oxygen species.[vii]

Once inside a host or patient, the virus is subject to the host’s immune system. However, uncontrolled activation of the host immune response also can cause cytokine release syndrome, where immune response chemicals, cytokines, are over-released into the patient.[viii] Scientists still have an incomplete understanding of cytokine release syndrome, but studies show that activation by an antigen can result in stimulation of secondary cells and non-immune cells, which triggers the humoral and cellular responses, causing further release of immune cytokines that spirals out of control.[ix] Three immune cytokines, IL-6, IL-10, and IFN-γ are the most commonly found in CRS, with IL-6 spiraling the effects of the other cytokines.[x] This can result in fever, hypotension, clotting issues, difficulty breathing, nervous systems dysfunction, fatigue, headache, cough, kidney damage, cardiac dysfunction, neuronal damage which can be mild to severe, such as confusion, hallucinations, difficulty with speech, seizures, and other organ dysfunction.[xi] In COVID-19, the virus attacks cells in the lungs, causing a release on the immune cytokine IL-6.[xii]

COVID-19 has been found to overactivate T-cells,[xiii] which may result in a reduction in T-cells over time.[xiv] In severe COVID-19, immune cytokines can increase even as the T-cell numbers drop.[xv] As such, the effects seen in COVID-19 infection, such as fever, exhaustion, dry cough, aching, nasal congestion, runny nose, sore throat, diarrhea, and difficulty breathing, clotting problems, and septic shock[xvi] may be due to an overactivation of the host immune system.

Once in the patient’s host cells, the virus uses host enzyme, the viral RNA is converted into viral proteins, which are then cut into active parts by viral enzymes, called proteinases.[xvii] The virus uses topoisomerase III-beta, to replicate, akin to Dengue and Zika virus,[xviii] and viral proteins are used to form new virus particles in the cell, eventually resulting in death of the host cell and release of the virus.

 

Work is ongoing on potential treatments for COVID-19, targeting viral access to host cells or replication. Treatment strategies typically revolve around three goals; (1) maintaining an infected patient; (2) stopping virus from entering a cell; and (3) stopping the virus from replicating in the cell.  Strategy (1) includes ventilation,[xix] something that is also seen in cytokine release syndrome (discussed above).[xx] Further, COVID-19 can result the cytokine release syndrome which appears to be similar to other cytokine release syndromes.[xxi] In cancer-based CRS, therapies against IL-6 have been used (toclizumab and siltuximab or clazakizumab, antibodies against the IL-6 receptor and soluble IL-6), as well as immune chemical sponges to remove the cytokines from the patient.[xxii] A such, suggested treatments for COVID-19 include IL-6 inhibitors,[xxiii] low-dose NSAIDs and steroids to control the inflammation and immune response (though ibuprofen was linked to an increase in ACE2 which is used by COVID-19 to enter cells), and immunosuppressants.[xxiv] Strategy (2) includes targeting the fusion spike or covering the virus particle. Initial studies on the fusion spike show that, despite strong similarities between SARS-CoV and COVID-19, antibodies against the SARS-CoV fusion spike did not have significant interaction with the COVID-19 fusion spike.[xxv] However, development is ongoing for antibodies or RNA treatments that target the COVID-19 fusion spike to prevent COVID-19 entry into host cells.[xxvi] Another option is carbohydrate-binding agents that bind to the virus and prevent it from entering a cell.[xxvii] Strategy (3) targets the host cell or enzymes that are used by the virus to commandeer the host. Suggestions include HIV protease inhibitors, chemotherapy to stop cell replication, and stop the virus from using the host cell enzymes to replicate or compounds that prevent the virus from forming new virus particles in the cell.[xxviii]

Hopefully, significant progress is made against COVID-19 through one or more of the therapeutic strategies.  In the meantime, we are doing our best to limit the spread of this pandemic, by having our employees work from home and limit exposure, along with so much of the country.  Stay safe and healthy during these trying times.

[i] https://www.niaid.nih.gov/news-events/atomic-structure-novel-coronavirus-protein, last accessed April 16, 2020; Wrapp, et al., Cryo,EM structure of the 2019-nCoV spike in the prefusion conformation. Science. 2020 Mar 13; 367(6483): 1260-3.

[ii] Steward, Host pathways in coronavirus replication and COVID-19 pre-clinical drug target identification using proteomic and chemoinformatic analysis. Drug Target Review. Mar. 30, 2020, https://www.drugtargetreview.com/article/58628/host-pathways-in-coronavirus-replication-and-covid-19-pre-clinical-drug-target-identification-using-proteomic-and-chemoinformatic-analysis/, last accessed April 16, 2020.

[iii] Yang & Wang, COVID-19: a new challenge for human beings. Cell Mol Immunol. 2020 Mar 31.

[iv] Wrapp, et al., Cryo,EM structure of the 2019-nCoV spike in the prefusion conformation. Science. 2020 Mar 13; 367(6483): 1260-3; https://www.drugtargetreview.com/news/56895/scientists-demonstrate-how-covid-19-infects-human-cells/, last accessed April 16, 2020; https://www.drugtargetreview.com/article/58628/host-pathways-in-coronavirus-replication-and-covid-19-pre-clinical-drug-target-identification-using-proteomic-and-chemoinformatic-analysis/, last accessed April 16, 2020.

[v] Wrapp, et al., Cryo,EM structure of the 2019-nCoV spike in the prefusion conformation. Science. 2020 Mar 13; 367(6483): 1260-3.

[vi] https://en.wikipedia.org/wiki/Angiotensin-converting_enzyme_2, last accessed April 16, 2020

[vii] Bernstein, et al., Angiotensin-converting enzyme in innate and adaptive immunity. Nat Rev Nephrol. 2018 May; 14(5): 325-36.

[viii] Xiao, et al., Plasma exchange can be an alternative therapeutic modality for severe cytokine release syndrome after chimeric antigen receptor-T cell infusion: a case report. Clin Cancer Res. 2019 Jan 1; 25(1): 29-34; Zhang, et al., The cytokine release syndrome (CRS) of severe COVID-19 and interleukin-6 receptor (IL-6R) antagonist tocilizumab may be the key to reduce the mortality. Int J Antimicrob Agents. 2020 Mar 29; 105954.

[ix] Shimabukuro-Vornhagen, et al., Cytokine release syndrome. J Immunother Canc. 2018 Jun 15; 6(1):56

[x] Shimabukuro-Vornhagen, et al., Cytokine release syndrome. J Immunother Canc. 2018 Jun 15; 6(1):56

[xi] Xiao, et al., Plasma exchange can be an alternative therapeutic modality for severe cytokine release syndrome after chimeric antigen receptor-T cell infusion: a case report. Clin Cancer Res. 2019 Jan 1; 25(1): 29-34; Shimabukuro-Vornhagen, et al., Cytokine release syndrome. J Immunother Canc. 2018 Jun 15; 6(1):56.

[xii] Zhang, et al., The cytokine release syndrome (CRS) of severe COVID-19 and interleukin-6 receptor (IL-6R) antagonist tocilizumab may be the key to reduce the mortality. Int J Antimicrob Agents. 2020 Mar 29; 105954.

[xiii] Yang & Wang, COVID-19: a new challenge for human beings. Cell Mol Immunol. 2020 Mar 31.

[xiv] Oon, Fighting COVID-19 exhausts T cells. Nat Rev Ummunol. 2020 Apr 6:1

[xv] Zhang, et al., The cytokine release syndrome (CRS) of severe COVID-19 and interleukin-6 receptor (IL-6R) antagonist tocilizumab may be the key to reduce the mortality. Int J Antimicrob Agents. 2020 Mar 29; 105954.

[xvi] https://www.who.int/news-room/q-a-detail/q-a-coronaviruses, last accessed April 16, 2020; Yang & Wang, COVID-19: a new challenge for human beings. Cell Mol Immunol. 2020 Mar 31.

[xvii] Shereen, et al., COVID-19 infection: origin, transmission, and characteristics of human coronaviruses. J Adv Res. 2020 Mar 16; 24:91-8.

[xviii] https://news.fiu.edu/2020/researchers-target-cells-own-machinery-in-fight-against-covid-19

[xix] https://www.aacn.org/education/online-courses/covid-19-pulmonary-ards-and-ventilator-resources, last accessed April 17, 2020.

[xx] Shimabukuro-Vornhagen, et al., Cytokine release syndrome. J Immunother Canc. 2018 Jun 15; 6(1):56

[xxi] Zhang, et al., The cytokine release syndrome (CRS) of severe COVID-19 and interleukin-6 receptor (IL-6R) antagonist tocilizumab may be the key to reduce the mortality. Int J Antimicrob Agents. 2020 Mar 29; 105954.

[xxii] Shimabukuro-Vornhagen, et al., Cytokine release syndrome. J Immunother Canc. 2018 Jun 15; 6(1):56

[xxiii] Zhang, et al., The cytokine release syndrome (CRS) of severe COVID-19 and interleukin-6 receptor (IL-6R) antagonist tocilizumab may be the key to reduce the mortality. Int J Antimicrob Agents. 2020 Mar 29; 105954; Liu, et al., Can we use interleukin-6 (IL-6) blockade for coronavirus disease 2019 (COVID-19)-induced cytokine release syndrdome (CRS)? J Autoimmunity. 2020 Apr 10; 102452; Russell, et al., Associations between immune-supressive and stimulating drugs and novel COVID-19- a systematic review of current evidence. Ecancermedicalscience. 2020 Mar 27; 14:1022.

[xxiv] Russell, et al., Associations between immune-supressive and stimulating drugs and novel COVID-19- a systematic review of current evidence. Ecancermedicalscience. 2020 Mar 27; 14:1022.

[xxv] Wrapp, et al., Cryo,EM structure of the 2019-nCoV spike in the prefusion conformation. Science. 2020 Mar 13; 367(6483): 1260-3.

[xxvi] Wrapp, et al., Cryo,EM structure of the 2019-nCoV spike in the prefusion conformation. Science. 2020 Mar 13; 367(6483): 1260-3.

[xxvii] Russell, et al., Associations between immune-supressive and stimulating drugs and novel COVID-19- a systematic review of current evidence. Ecancermedicalscience. 2020 Mar 27; 14:1022.

[xxviii] Russell, et al., Associations between immune-supressive and stimulating drugs and novel COVID-19- a systematic review of current evidence. Ecancermedicalscience. 2020 Mar 27; 14:1022.

Lego Suit

The toy industry is in a tumultuous time, with many industry experts concerned physical toys are being replaced by digital ones.1  In fact, one of the largest building toy manufacturers, Lego A/S, which manufactures around 75 million bricks each year, suffered an 8% drop in revenue in 20172  Likely as a result of the competition in the toy industry, Lego has been asserting its intellectual property against competitors. One such example reached the Federal Circuit, whom just issued a nonprecedential opinion in Lego A/S v. Zuru Inc.3

Lego obtained patents on its traditional bricks in 1961 (U.S. Pat. 3,005,282) and began facing competition in the 1980’s when its patent expired.  Since then, Lego has used a combination of copyrights, trademarks, and patents to protect its business. Among its copyrights are two pertaining to the Lego figurines, i.e. minifigures.4

Similarly, Lego obtained trademarks on its minifigures and the heads of the minifigures;5

Zuru, a Chinese company, began selling building bricks having a similar structure to the known Lego brick, and included figurines in some of the building kits.  The Zuru figurines were largely as seen below;6

Lego sued Zuru for copyright and trademark infringement of the minifigure copyrights and trademarks.  In part of the suit, Lego successfully sought an injunction to prevent Zuru from selling its figurines.7 During appeal, the Federal Circuit found that the copyright infringement test (where the case was handled) required a finding

[of whether an] ordinary observer, unless he set out to detect the disparities, would be disposed to overlook them, and regard [the] aesthetic appeal as the same.” … The fact-finder must examine the works for their “total concept and feel.”8

The Court, upon looking at the facts, agreed with the trial court that the look and feel was sufficiently similar to justify the injunction.9

The Federal Circuit then addressed Lego’s claims of design patent infringement of patents D688,328, D641,053, and D614,707.  The design patents cover the following ornamentation of brick structures, respectively;

The alleged infringement was due to the sale of building block kits, such as the one depicted below;10

The preliminary injunction issued by the trial court for the bricks was challenged by Zuru, who argued that there was no irreparable harm caused from the further sale of the bricks.11 The Federal Circuit analyzed whether there was irreparable harm to Lego if an injunction were not issued immediately, and found arguments pertaining to forcing Lego to license its brick designs was insufficient and circular, and loss of market share due to those specific bricks were speculative and lacked any evidence.12 However, this will likely be a small victory for Zuru, whom did not challenge many of the findings leading to the injunction and will likely be enjoined at a later date by the trial court.

These results are not surprising, given the claims brought by Lego. However, it does showcase an interesting strategy of Lego, and its use of various types of intellectual property in securing its marketplace. On the other side, what does this mean for Zuru?  Absent a license from Lego, it appears the company’s building block line will be pulled from Walmart shelves and no longer sold in the U.S.  The company does offer various other toy lines,13 and given its extra-U.S. status might still manufacture building toys destined for locations outside the U.S., where Lego lacks IP protection.


1https://www.forbes.com/sites/karstenstrauss/2013/03/15/breaking-rules-in-the-toy-business/#7280a0fd3717, last accessed Jan. 16, 2020.
2https://www.bbc.com/news/business-43298897, last accessed Jan. 16, 2020.
3See, Lego A/S v. Zuru Inc., No. 2019-2122 (Fed. Cir. Jan. 15, 2020).
4Lego A/S, slip opinion at 6; U.S. Copyright Regs. VA0000655230 and VA0000655104
5U.S. Trademark Regs. 4,903,968; 4520327
6Taken from Lego A/S, slip opinion at 7.
7Lego A/S, slip opinion at 5-6.
8Lego A/S, slip opinion at 11.
9Lego A/S, slip opinion at 12, 14.
10https://www.walmart.com/ip/MAX-Build-More-Building-Bricks-Value-Set-759-Bricks-Major-Brick-Brands-Compatible/364375176, last accessed Jan. 16, 2020 (image cropped).
11Lego A/S, slip opinion at 15.
12Lego A/S, slip opinion at 16-17.
13See, https://zuru.com/product-list/?brand=brand&category=category&is_new=false&language=en, last accessed Jan. 16, 2020.