Drug Discovery Patent Filings Span Protein Degradation, Ion Channels, and Emerging Targets

Monthly patent reviews spanning April through December 2025 documented thousands of drug discovery IP disclosures, with curated selections highlighting over 150 notable filings per month across oncology, immunology, neurology, and metabolic disease programs.

Targeted protein degradation emerged as a prominent modality across multiple months. Dark Blue Therapeutics disclosed MLLT1/3 degraders in December 2025. Captor Therapeutics filed two patent applications (WO2025233481A1 and WO2025234887A1) disclosing potent CRBN-recruiting NEK7 degraders in November 2025, with both filings describing isoindolinone/glutarimide CRBN-recruiting derivatives differentiated by substituents appended to the isoindolinone core. Across both applications, Captor reported higher potency for the R stereoisomer compared to the S counterpart. In WO2025233481A1, the active stereoisomer (compound X1) drove robust NEK7 degradation with a DC50 of 4.2 nM in PBMCs versus 16.8 nM for the racemate, while the opposite isomer (compound X2) was inactive in the NEK7-HiBiT assay. In WO2025234887A1, the R-piperidin-2-yl stereoisomer (compound A2) was described as approximately 4-fold more potent than the racemate by DC50 comparison.

Captor describes a clinical-stage, multi-target molecular glue compound, CT-01, that degrades GSPT1, NEK7, and SALL4, developed as a prodrug to enhance tissue specificity toward liver and lung cancers. Captor reports efficacy across cell line–derived and patient-derived HCC (hepatocellular carcinoma) xenograft models, along with synergy in combination with everolimus, and has positioned the program to begin a Ph. 1a/b trial (NCT06994572) in HCC, lung cancer, and NET tumors. Captor also lists two NEK7-focused inflammation programs: a brain-penetrant neuroinflammation compound, CT-02B (Parkinson's disease, ALS, MS); and a systemic autoimmunity program compound, CT-02S (e.g., IBD, gout, dermatological diseases).

October 2025 highlights included Amphista's FBXO22-mediated TEAD degraders that expand the targeted protein degradation toolbox. May 2025 disclosures featured CAMKK2 degraders. April 2025 filings included LRRK2 degraders, SARM1 inhibitors, and CK1α degraders. Daiichi Sankyo disclosed SF1 antagonists and SF1–targeting heterobifunctional degraders in November 2025. Xizang/Haisco filed a potent heterobifunctional degrader of PARP1 in July 2025.

Small molecule programs spanned diverse mechanisms and targets. December 2025 filings included KRAS inhibitors from Insilico Medicine with in vivo efficacy against models of mutant KRAS(G12V)-driven cancer, TRPM2 antagonists from Biohaven for pain, and LINE-1 RT inhibitors from Rome Therapeutics, employing anti-viral scaffolds to target cancer via the human "dark genome".

November 2025 disclosures included SiteOne's NaV1.8 pain IP with substituted cycloalkyl and heterocycloalkyl inhibitors, and Lilly's expansion of its IP footprint in small-molecule amylin and/or calcitonin receptor agonism. Kymera broadened its STAT6 strategy with small molecule inhibitors alongside a leading oral degrader program.

October 2025 highlights featured non-peptide PTH1R agonists from Septerna, Kyorin's first MRGPRX2 antagonist patent application following its recent deal with Novartis for indications in the mast cell/allergy space, and Rigel's dual IRAK1/4 inhibitor chemotype designed to deepen TLR and IL-1R pathway suppression in inflammatory and myeloid disease settings.

September 2025 filings covered boronic acids as guanidine mimics for dual ARG1/2 inhibition (AZ), epoxides as covalent warheads for modulating mRNA (Arrakis Therapeutics), multiple filings targeting the orphan receptor GPR17 for multiple sclerosis (Roche, Myrobalan Therapeutics), ion channel inhibitors for neuromuscular disease (NMD Therapeutics), and glutaminase 1 inhibitors from Sitryx Therapeutics for immunology applications.

August 2025 patent applications spanned immunology, antibacterials, and synthetic lethality in MTAP-deleted tumors. July 2025 disclosures included macrocyclic small molecule GLP-1R agonists (Insilico Medicine), CNS-penetrant NLRP3 inflammasome inhibitors (Ventus), prodrug strategies for oncology programs (GSK), and scaffolds that potently inhibit PLA2G15, a new target for neurodegenerative diseases (Scenic).

May 2025 featured PKR activators, 17β-HSD13 inhibitors, and Kv7.2/7.3 activators among over 150 notable disclosures. April 2025 filings included antiviral agents and multiple targeted protein degradation programs.

Mechanistically, NEK7 inhibition has often been framed as a complementary approach to blocking NLRP3 inflammasome activation, supported by foundational work identifying NEK7 as a key mediator of NLRP3 assembly/activation downstream of cellular potassium efflux. However, more recent data complicate a simple model that posits NEK7 as being necessary for NLRP3 activation. At least one report using a NEK7-directed molecular glue degrader describes full NEK7 degradation but only partial and variable inhibition of NLRP3-dependent IL-1β release in human immune cells and whole blood, with effects that can depend on donor and stimulation conditions. Separately, additional work suggests NEK7 can accelerate inflammasome activation, while being dispensable for NLRP3 activation in some experimental settings. Together, these findings argue that the NEK7–NLRP3 relationship is likely context-dependent.