Two diseases, one unmet need: the IgAN and FSGS landscape

IgA nephropathy (IgAN) and focal segmental glomerulosclerosis (FSGS) are two of the most prevalent primary glomerular diseases driving progression to end-stage renal disease (ESRD), yet neither condition has historically benefited from disease-specific approved pharmacotherapies beyond renin-angiotensin system (RAS) blockade. That gap is now the focal point of an accelerating wave of patent and literature activity across multiple mechanistic pillars.

IgAN is characterised as an immune complex–mediated glomerulopathy driven by aberrantly galactose-deficient IgA1 (Gd-IgA1), its recognition by circulating anti-glycan autoantibodies, and deposition of nephritogenic immune complexes in the mesangium. Patent filings from Chinook Therapeutics identify mesangial PDGF signalling pathways — including PIK3R1, PDGFRA, NFKBIA, PIK3CG, PLA2G4A, TIAM1, PDGFB, NFKB1, and MAP3K1 — as implicated in mesangial cell proliferation and injury. Complement activation via the lectin pathway through MASP-2 is highlighted by University of Leicester filings as a key amplifier of proteinuria and renal fibrosis in IgAN.

FSGS, by contrast, is a podocytopathy characterised by primary podocyte injury and depletion leading to glomerulosclerosis. Multiple patent filings identify soluble urokinase plasminogen activator receptor (suPAR) as a pathogenic circulating factor that activates podocyte β3 integrin, constituting a validated molecular target. Apolipoprotein L1 (APOL1) genetic variants are cited across several filings as increasing ESKD risk in FSGS patients of African ancestry. According to WHO, chronic kidney disease affects approximately 10% of the global population, making the unmet need in these glomerular subtypes a pressing public health concern.

Endothelin receptor antagonists: the most densely patented modality

Endothelin receptor antagonists (ERAs) represent the most densely represented therapeutic modality in the retrieved patent dataset for IgAN and FSGS. Endothelin-1 (ET-1), acting via the ETA receptor, is identified across several ERA-focused patents as a central mediator of renal inflammation, mesangial proliferation, and glomerular hypertension in both conditions.

Atrasentan — a selective ETA receptor antagonist with an ETA Ki of approximately 34 pM — is the subject of multiple active patent families held by Chinook Therapeutics (a Novartis subsidiary) across Japan, Taiwan, China, and the United States. Retrieved filings claim that atrasentan reduces proteinuria, decreases renal inflammation and fibrosis, stabilises eGFR, reduces hematuria episodes, delays ESRD onset, and reduces fatigue in both IgAN and FSGS patients. Japanese filings specify dosing regimens of 0.20 mg to 1.5 mg orally daily, with exclusion criteria — patients not previously diagnosed with diabetic nephropathy, HIV-associated nephropathy, prostate cancer, or acute kidney failure — suggesting these parameters are clinically refined and may surround active clinical trial data.

“FSGS currently has no approved therapy — multiple patent filings from Chinook Therapeutics and Travere/Retrophin explicitly frame atrasentan as addressing a critical unmet need in this indication.”

A biphenylsulfonamide ERA compound, covered in Chinese filings by Travere Therapeutics and Retrophin using the same structural scaffold, is claimed for FSGS and other proteinuric CKD, with mechanistic emphasis on synergistic blockade of both ET-1 and angiotensin II pathways. Supporting rat model data in the filings show ARB plus ERA combinations producing synergistic blood pressure and renal effects. Zibotentan, a separate selective ERA, appears in AstraZeneca filings specifically in the context of a fixed-dose combination with dapagliflozin for high-proteinuria CKD.

SGLT2 inhibitors: from glycaemic control to glomerular protection

SGLT2 inhibitors constitute the second major modality cluster in this patent dataset, with renoprotective mechanisms cited across retrieved filings as independent of glycaemic control — encompassing reduced glomerular hyperfiltration, decreased tubuloglomerular feedback, and anti-inflammatory and anti-fibrotic effects. This mechanistic independence from diabetes underpins the extension of SGLT2 inhibitor claims into primary glomerular diseases.

AstraZeneca’s dapagliflozin accounts for the largest single-assignee patent volume in the SGLT2 cluster, with multiple filings explicitly covering CKD associated with IgAN (Berger’s disease) in patients with and without type 2 diabetes. Critically, these patents explicitly reference the DAPA-CKD trial (ClinicalTrials.gov number NCT03036150) — a published Phase 3 trial that included IgAN-associated CKD — representing the strongest clinical validation signal in this dataset. Boehringer Ingelheim’s empagliflozin is covered in several patents for CKD and related metabolic conditions, including obesity-related glomerulopathy and IgAN. As noted by EMA regulatory guidance, the expansion of SGLT2 inhibitor indications into non-diabetic CKD reflects a broader shift in how these agents are classified therapeutically.

A Taiwan patent held by the National Defense Medical Center identifies SGLT2 protein expression itself as a biomarker for CKD diagnosis and treatment monitoring, specifically in FSGS and IgAN patient cohorts. This dual role — as both pharmacological target and diagnostic marker — distinguishes SGLT2 from other renoprotective targets in this dataset. The patent landscape analysis by WIPO has consistently documented the rapid expansion of SGLT2 inhibitor patent families across multiple therapeutic areas beyond diabetes since 2015.

Complement blockade, suPAR targeting, and emerging biologics

Beyond ERAs and SGLT2 inhibitors, the retrieved patent dataset reveals a mechanistically diverse biologics pipeline targeting IgAN and FSGS through complement pathway inhibition, podocyte-specific signalling, and upstream immune modulation.

Anti-MASP-2 antibodies: clinical signals in IgAN

The University of Leicester, in collaboration with Omeros Corporation, holds a substantial patent family spanning WO, AU, US, SG, MX, CA, and CN jurisdictions covering anti-MASP-2 antibody OMS646 for IgAN. MASP-2 is the initiating enzyme of the lectin complement pathway; its inhibition is claimed to reduce immune complex–driven glomerular inflammation and fibrosis. Patient-level data embedded within these filings describe two IgAN patients achieving proteinuria reductions exceeding 50%, with one patient reaching 325 mg/24 hours from a baseline of 10,771 mg/24 hours by Day 85. Anti-MASP-2 antibody treatment was also reported to enable steroid tapering to ≤5 mg/day. These signals indicate at least early-phase (Phase 1/2) clinical data underpin these filings.

Anti-suPAR biologics: a cross-disease target in FSGS and IgAN

Soluble urokinase plasminogen activator receptor (suPAR) is identified across multiple filings as a pathogenic circulating factor that activates podocyte β3 integrin, directly linking suPAR elevation to podocyte depolarisation and proteinuria in FSGS. Retrieved data indicate suPAR is elevated specifically in FSGS serum versus other primary glomerular diseases, with high pre-transplant suPAR levels predicting post-transplant FSGS recurrence. Walden Biosciences holds 2025 patent filings covering anti-suPAR antibodies and novel uPAR/suPAR-binding molecules for FSGS, IgAN, membranous nephropathy, lupus nephritis, and diabetic nephropathy.

Anti-APRIL antibodies and TGFβ antagonism

Visterra holds a 2025 Chinese patent on antibodies specifically binding APRIL (a proliferation-inducing ligand), a B-cell survival cytokine implicated in the upstream mucosal immune dysregulation driving Gd-IgA1 overproduction in IgAN. Chinook Therapeutics’ 2025 combination filing positions APRIL targeting alongside ERA as a dual-mechanism IgAN strategy — targeting both the upstream immunological driver and downstream hemodynamic/fibrotic effectors simultaneously. Genzyme Corporation (a Sanofi subsidiary) holds Taiwan and Chinese patents claiming that intravenous administration of a TGFβ antagonist treats primary FSGS specifically in patients carrying APOL1 variants, with TGFβ implicated as a profibrotic mediator downstream of podocyte injury.

Combination strategies and the road to next-generation standard of care

ERA/SGLT2 combinations represent the most commercially advanced convergence point in this dataset, with multiple independent patent families converging on the same mechanistic rationale: simultaneous blockade of endothelin-mediated vasoconstriction and inflammation alongside SGLT2-mediated tubuloglomerular feedback reduction produces additive or synergistic renoprotection in high-proteinuria CKD.

AstraZeneca’s 2024–2025 fixed-dose combination patent for zibotentan plus dapagliflozin targets high-proteinuria CKD defined as UACR greater than 300 mg/g — a population explicitly encompassing IgAN and FSGS. A separate AbbVie filing covers atrasentan combined with an SGLT2 inhibitor for diabetic kidney disease, with claims of additive eGFR protection and BNP reduction, providing mechanistic precedent for ERA/SGLT2 co-targeting in proteinuric nephropathy more broadly. The combination strategy is further supported by the biphenylsulfonamide ERA filings from Travere/Retrophin, which demonstrate synergistic blood pressure and renal effects for ARB plus ERA combinations in rat models — a mechanistic analogy for the ERA/SGLT2 rationale.

Additional combination directions in this dataset include: Chinook Therapeutics’ ERA plus anti-APRIL antibody for IgAN (targeting both upstream immune dysregulation and downstream hemodynamic injury); Resverlogix Corp.’s SGLT2 inhibitor plus BET bromodomain inhibitor for CKD (an epigenetic/metabolic combination); and a 2024 Boehringer Ingelheim filing covering aldosterone synthase inhibitors combined with SGLT2 inhibitors for CKD, adding a mineralocorticoid pathway component. University of Leicester filings also describe anti-MASP-2 antibody use in the peri-transplant setting to prevent IgAN and FSGS recurrence in renal grafts. According to NIH research priorities, combination approaches targeting multiple pathogenic mechanisms simultaneously are increasingly prioritised in CKD drug development.

Strategic implications for IP and drug development teams

The patent landscape described in this dataset carries several actionable implications for IP strategists, drug developers, and clinical development teams working in IgAN and FSGS.

• ERA/SGLT2 combinations are the most commercially advanced convergence strategy. AstraZeneca’s fixed-dose zibotentan/dapagliflozin filing and AbbVie’s atrasentan/SGLT2 combination data together suggest dual ERA/SGLT2 regimens are being actively developed as the next-generation standard of care for high-proteinuria CKD, potentially displacing RAS monotherapy.
• Chinook Therapeutics (Novartis) holds the most concentrated glomerular disease ERA patent estate in this dataset. With at least 8 distinct atrasentan patent records across JP, TW, and CN covering both IgAN and FSGS, IP teams should monitor freedom-to-operate for any ERA development in these indications, particularly given the breadth of method-of-treatment claims including specific exclusion criteria and dosing ranges.
• MASP-2 inhibition provides the only complement-targeted clinical signal in this dataset for IgAN. OMS646 (University of Leicester/Omeros) is mechanistically differentiated from ERA/SGLT2 approaches and may hold particular value in steroid-dependent IgAN given the steroid-tapering signal in embedded patient data.
• suPAR is emerging as a cross-disease biomarker and therapeutic target for both FSGS and IgAN. Walden Biosciences’ 2025 patent estate and the University of Miami’s foundational suPAR/podocyte β3-integrin mechanistic data converge to position anti-suPAR biologics as a precision approach in patients with elevated pre-treatment suPAR levels, particularly relevant in post-transplant FSGS recurrence.
• FSGS remains a high-value regulatory opportunity. The absence of any approved FSGS-specific therapy is explicitly noted in multiple retrieved filings. Atrasentan, suPAR antibodies, TRPC6 inhibitors (Boehringer Ingelheim), and complement/chemokine modulators (ChemoCentryx) are all being positioned to fill this gap, creating a competitive but mechanistically diverse FSGS pipeline.

For teams building IP strategy or competitive intelligence in glomerular disease, the data from EPO and national patent offices across JP, CN, TW, and US jurisdictions will be critical to monitor, given the geographic concentration of active filings documented in this analysis. The PatSnap pharmaceutical intelligence platform provides tools specifically designed for tracking these multi-jurisdictional patent families and their legal status in real time.