A Singular Disclosure Requirement Is Necessary For Patent Law

The Court of Appeals for the Federal Circuit’s recent jurisprudence on 35 U.S.C. § 112 has selectively and severely curtailed innovation in the fields of pharmaceuticals and biotechnology. Specifically, the Federal Circuit’s shifting position on 35 U.S.C. § 112 and their evolving jurisprudence to combine expanding the application and scope of the written description requirement with a separate, heightened standard for enabling claims directed to innovation in a genus of therapeutic antibodies, or a genus of compounds having functional limitations, has caused havoc in the biopharmaceutical industry. Federal Circuit jurisprudence on how to interpret the disclosure requirements of the 35 U.S.C. § 112 contravenes the statute and Supreme Court precedent by mandating two separate disclosure requirements in place of one, namely that patent applications not only “enable” but also separately “describe” inventions. This recently developed and reactively evolving judge made approach raises the bar exceedingly high for obtaining any meaningful patent protection for new biomedical discoveries, goes against many decades of patent practice, and is proving to be a powerful impediment to the investment necessary for developing new and lifesaving medicines. This article examines patent law’s current disclosure requirements to highlight a failing judicial trajectory and proposes a return to a single 35 U.S.C. § 112(a) standard. By doing so, the great shock that has singled out and disrupted the biopharmaceutical industry will be removed and the law can once again encourage, in a technology-neutral manner, the private sector to innovate in all fields of endeavor, including encouraging the biopharmaceutical industry to develop new lifesaving medicines and treatments

Eviscerating Patent Scope

The scope of patent claims directed to inventions in the field of pharmaceuticals and biotechnology has been stumped by the Court of Appeals for the Federal Circuit’s recent jurisprudence on 35 U.S.C. § 112. Specifically, the application of a heightened test for enablement of claims to a genus of compounds with functional limitations or a genus of therapeutic antibodies, coupled with an increasingly broader application of the written description doctrine, has resulted in considerable uncertainty in the biopharmaceutical industry. The Federal Circuit’s shift in interpreting 35 U.S.C. § 112 contravenes the statute and Supreme Court precedent by splitting the singular standard of § 112(a) into two separate requirements, namely “enablement” and “written description”, and by going a step further to treat enablement as a question of law when no such distinction was ever envisaged by Congress or held by the Supreme Court. This judicially created approach in recent years has set aside over a century of patent practice to now make it exceedingly difficult to obtain meaningful patent protection for biopharmaceutical innovations and as a result has impeded investment and progress for developing lifesaving treatments. This article examines this legal scheme and highlights why changes to current patent disclosure laws and a return to a single 35 U.S.C. § 112(a) standard is necessary to avoid disrupting and inhibiting future innovation in the essential fields of pharmaceuticals and biotechnology

Patent Eligibility of Disease Diagnosis

The U.S. Supreme Court effectively redefined the scope of patent eligible subject matter when it decided Mayo.1 This decision focused on medical diagnostic technology and has had a profound effect on the biotechnology and personalized medicine industries in the United States. Subsequent back-to-back decisions by the Supreme Court in Myriad2 and Alice3 have made it unequivocally clear that there is now wholesale broadening of the judicially created exceptions to statutory laws governing patent eligible subject matter. This has caused havoc in the biopharmaceutical industry by not only making it a near impossibility to obtain a patent in certain fields, but also by vastly increasing the number of medical diagnostic patents being invalidated based on Section 101 of Title 35 of the U.S. Code. This major change in law has had unintended consequences, discouraging research and development necessary for new medical diagnostic and therapeutic methods to come to market. This article analyzes the patent eligibility legal landscape and focuses on emerging medical diagnostic technologies to explain why the Supreme Court’s recent rulings were made in error. I end by discussing how Congress could either abolish, as unnecessary, the non-statutory, Supreme Court-created, exceptions to Section 101, or to amend the statute. Only by doing so can our laws once again encourage and reward creative thinkers and entrepreneurs who take risk and innovate new medical diagnostic technologies in the U.S

The Patent Law Clinic at NYLS Helps a Nonprofit’s Efforts to Change Lives in Central Africa

https://digitalcommons.nyls.edu/community_news/1021/thumbnail.jp

Killing Rarity

On May 22, 2019, Botswana decided after many years to lift its ban on hunting elephants and in February 2020 held its first auctions for the right to hunt elephants. This turnaround change in their law coincides with a rapidly changing legal landscape in the United States related to the practice of trophy hunting of rare, intelligent animals, including elephants. This Article analyzes the fluid legal landscape surrounding this uncommon form of hunting of rare animals and possible ways of using the Administrative Procedures Act and the Federal Advisory Committee Act as a means of challenging the government’s rapidly changing position. This Article also explores the legal status of rare animals in the context of our property rights and humanity’s cultural heritage, urges Congress to take action to limit this form of hunting, and ends by offering both international trophy hunters and conservationists alike four innovative and practical solutions to consider. In December 2021, the British government announced a ban on importing hunting trophies of rare animals into the UK; the United States government should do likewise in 2022

Platelets stop us leaking

In this issue of Blood, Welsh and colleagues determine how platelet thrombi limit the loss of plasma-borne proteins from the microvasculature. 1 The concept that platelets prevent leakage from blood vessels following a penetrating injury will come as little surprise to most readers, but exactly how platelets physically contribute to this process is not well understood. Such injuries result in the loss of blood cells and plasma into the surrounding tissues, and both forms of loss must be halted quickly. Platelets are believed to form the first line of defense in such situations, forming a thrombus that is capable of plugging the hole and supplying molecules that contribute to localized inflammation and wound healing

Glycoprotein Ib-V-IX, a Receptor for von Willebrand Factor, Couples Physically and Functionally to the Fc Receptor y-Chain, Fyn, and Lyn to Activate Human Platelets

The adhesion molecule von Willebrand factor (vWF) activates platelets upon binding 2 surface receptors, glycoprotein (GP) Ib-V-IX and integrin aIIbb3. We have used 2 approaches to selectively activate GP Ib using either the snake venom lectin alboaggregin-A or mutant recombinant forms of vWF (DA1-vWF and RGGS-vWF) with selective binding properties to its 2 receptors. We show that activation of GP Ib induces platelet aggregation, secretion of 5-hydroxy tryptamine (5-HT), and an increase in cytosolic calcium. Syk becomes tyrosine phosphorylated and activated downstream of GP Ib, and associates with several tyrosinephosphorylated proteins including the Fc receptor g-chain through interaction with Syk SH2 domains. GP Ib physically associates with the g-chain in GST-Syk-SH2 precipitates from platelets stimulated through GP Ib, and 2 Src family kinases, Lyn and Fyn, also associate with this signaling complex. In addition, GP Ib stimulation couples to tyrosine phosphorylation of phospholipase Cg2. The Src familyspecific inhibitor PP1 dose-dependently inhibits phosphorylation of Syk, its association with tyrosine-phosphorylated g-chain, phosphorylation of PLCg2, platelet aggregation, and 5-HT release. The results indicate that, upon activation, GP Ib is physically associated with FcR g-chain and members of the Src family kinases, leading to phosphorylation of the g-chain, recruitment, and activation of Syk. Phosphorylation of PLCg2 also lies downstream of Src kinase activation and may critically couple early signaling events to functional platelet responses