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Accelerating Iga Nephropathy Drug Development

IgA nephropathy presents significant therapeutic challenges, with limited treatment options and a complex pathophysiology that demands innovative drug development strategies. Protheragen stands as a specialized partner in the advancement of IgA nephropathy therapeutics, offering end-to-end preclinical drug development solutions. Our comprehensive services span the entire preclinical spectrum, including target validation, lead optimization, pharmacology, and IND-enabling studies. Backed by a team of scientific experts and leveraging state-of-the-art platforms, Protheragen ensures rigorous evaluation of candidate therapeutics under stringent regulatory standards. Our integrated approach combines deep disease expertise with advanced analytical methodologies, enabling robust data generation and informed decision-making at every stage of development. Protheragen’s commitment to quality and compliance accelerates the pathway from discovery to clinical readiness, minimizing risk and optimizing project outcomes. With a focus on scientific excellence and operational efficiency, Protheragen is dedicated to driving therapeutic breakthroughs in IgA nephropathy. Our mission is to empower our partners with the expertise and resources necessary to bring novel, effective treatments to patients faster and more reliably.

What is Iga NephropathyTargets for Iga NephropathyDrug Discovery and Development ServicesWhy Choose Us

What is Iga Nephropathy

IgA nephropathy, also known as Berger’s disease, is a chronic kidney disorder characterized by the deposition of immunoglobulin A (IgA) in the glomerular mesangium. The disease arises from an abnormal immune response, where galactose-deficient IgA1 acts as an autoantigen, prompting the formation of immune complexes with circulating antibodies. These complexes accumulate in the kidneys, triggering local inflammation, mesangial cell proliferation, and progressive glomerular injury. The condition can develop as a primary renal disorder or secondary to systemic diseases, with genetic predisposition and environmental factors influencing susceptibility. Over time, ongoing inflammation can lead to chronic kidney damage and, in some cases, end-stage renal disease. Clinically, IgA nephropathy presents variably, ranging from asymptomatic microscopic hematuria to recurrent episodes of visible blood in the urine, often following respiratory infections. Proteinuria, hypertension, and declining renal function may develop as the disease progresses. Diagnosis relies on clinical assessment, laboratory tests to evaluate kidney function and proteinuria, and confirmation by renal biopsy demonstrating mesangial IgA deposition. Management focuses on controlling blood pressure and proteinuria, with renin-angiotensin system blockers as first-line therapy. Recently, targeted agents such as iptacopan hydrochloride (a complement inhibitor) and sparsentan (a dual endothelin angiotensin receptor antagonist) have been introduced to reduce proteinuria and slow disease progression.

Launched Drugs

Structure Generic Name CAS Registry Number Molecular Formula Molecular Weight
img-1644670-37-0-free-base2447007-60-3-iptacopan-hydrochloride-rec-innm-usan iptacopan hydrochloride (Rec INNM; USAN) 1644670-37-0 (free base); 2447007-60-3 C25 H30 N2 O4 . Cl H . H2 O 476.993
img-254740-64-2-sparsentan-rec-inn-usan sparsentan (Rec INN; USAN) 254740-64-2 C32 H40 N4 O5 S 592.749

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Targets for Iga Nephropathy

Targets in Clinical or Later Phases of Development

Target Name Gene Symbol
angiotensin II receptor type 1 AGTR1
endothelin receptor type A EDNRA
complement factor B CFB
Complement Complex
nuclear receptor subfamily 3 group C member 1 NR3C1
complement C5 C5
TNF superfamily member 13b TNFSF13B
CD38 molecule CD38
component of inhibitor of nuclear factor kappa B kinase complex CHUK
fms related receptor tyrosine kinase 3 FLT3

IgA nephropathy is driven by a complex interplay of immune and inflammatory processes, with several molecular targets playing central roles in disease pathogenesis. Key among these are components of the complement system such as C3, C5, C5a receptor 1 (C5AR1), and complement factor B (CFB), which mediate glomerular injury through activation of inflammatory cascades and membrane attack complex formation. The renin-angiotensin system, particularly angiotensin II receptor type 1 (AGTR1) and endothelin receptor type A (EDNRA), also contributes to disease progression by promoting glomerular hypertension, fibrosis, and mesangial proliferation. Additionally, immune signaling molecules including spleen associated tyrosine kinase (SYK) and TNF superfamily member 13b (TNFSF13B/BAFF) facilitate immune cell activation, aberrant B cell responses, and the production of pathogenic IgA, further amplifying glomerular inflammation and injury. Therapeutic targeting of these molecules offers promising avenues for disease modification in IgA nephropathy. Complement inhibitors (e.g., pegcetacoplan for C3, eculizumab and avacopan for C5/C5AR1, narsoplimab for MASP2) are under clinical investigation and have shown early benefits in reducing proteinuria and inflammation. Blockade of AGTR1 with angiotensin receptor blockers is already a mainstay of therapy, while endothelin receptor antagonists and BAFF inhibitors are in advanced clinical trials. SYK inhibitors, such as fostamatinib, are also being explored for their capacity to interrupt pathogenic immune signaling. Collectively, these targets represent a shift toward mechanism-based therapies that address both immune-mediated injury and chronic progression in IgA nephropathy.

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Drug Discovery and Development Services

In Vitro Efficacy Testing ServicesIn Vivo Model DevelopmentPK/PD Study ServicesIn Vivo Toxicity Assessment ServicesBiomarker Analysis Services
In Vitro Efficacy Testing Services

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Our In Vitro Efficacy Testing Service accelerates IgA nephropathy drug discovery by providing robust, sensitive platforms for compound screening and mechanistic profiling. We utilize advanced cell-based, biochemical, and biophysical assays—including flow cytometry, ELISA, radioligand displacement, and surface plasmon resonance—to evaluate effects on key molecular targets such as complement factors, angiotensin II, and inflammatory mediators. Critical pharmacological parameters like IC-50, Ki, and Kd are precisely measured, enabling quantitative assessment of potency and selectivity. Our tailored approach delivers actionable data for lead optimization, supporting informed decision-making and de-risking therapeutic development for IgA nephropathy.

Angiotensin Ii Receptor Type 1 Cd38 Molecule
Complement C3 Complement C5
Complement C5A Receptor 1 Complement Factor B
Endothelin Receptor Type A Heme Oxygenase 1
Mbl Associated Serine Protease 2 Peroxisome Proliferator Activated Receptor Gamma
Spleen Associated Tyrosine Kinase Tnf Superfamily Member 13B

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Why Choose Us

Choosing Protheragen as your partner in IgA nephropathy drug development means entrusting your project to a team with deep, specialized expertise in this complex disease area. At Protheragen, our scientific and technical teams are dedicated to advancing research and developing innovative therapeutics for IgA nephropathy, supported by state-of-the-art technology platforms and a robust infrastructure. We pride ourselves on a proven track record of delivering reliable, high-quality preclinical drug development services, consistently meeting the rigorous demands of our clients and the industry. Our processes are governed by strict quality standards and full regulatory compliance, ensuring that every project is managed with the utmost professionalism and integrity. Above all, Protheragen is committed to driving progress in IgA nephropathy treatment, working closely with partners to bring new hope to patients. By choosing Protheragen, you benefit from our unwavering dedication, scientific excellence, and a reliable partnership focused on achieving meaningful outcomes in IgA nephropathy therapeutics.

FAQs for Our Services

Q: What are the main challenges in preclinical research for developing new drugs to treat IgA nephropathy?

A: Preclinical research in IgA nephropathy faces several challenges, including the lack of fully representative animal models that accurately mimic human disease pathology. Additionally, the heterogeneity of IgA nephropathy in patients complicates the translation of preclinical findings to clinical outcomes. Our company addresses these challenges by utilizing a combination of established and innovative in vivo and in vitro models, as well as leveraging advanced biomarker discovery platforms to better predict clinical efficacy.

Q: What are the key regulatory considerations when developing drugs for IgA nephropathy?

A: Regulatory agencies such as the FDA and EMA require robust preclinical data demonstrating both safety and efficacy before approving clinical trials for IgA nephropathy therapies. This includes comprehensive pharmacokinetics, toxicology, and mechanism-of-action studies. Our team is experienced in designing preclinical programs that meet global regulatory standards, ensuring thorough documentation and compliance with GLP (Good Laboratory Practice) to facilitate smooth IND/CTA submissions.

Q: What technical expertise is required for preclinical research in IgA nephropathy?

A: Technical expertise in IgA nephropathy research involves proficiency in immunological assays, renal histopathology, and molecular biology techniques for biomarker analysis. Our scientists are skilled in developing and validating disease-relevant animal models, performing kidney function and injury assessments, and utilizing advanced imaging and omics technologies to elucidate drug mechanisms and therapeutic effects.

Q: What are the typical timeline and cost considerations for preclinical drug development in IgA nephropathy?

A: Preclinical drug development timelines for IgA nephropathy typically range from 12 to 24 months, depending on the complexity of the program and the required regulatory studies. Costs can vary significantly, but generally range from $2 million to $8 million for a comprehensive preclinical package, including efficacy, safety, and toxicology studies. Our company offers tailored project management and budget optimization strategies to ensure efficient and cost-effective preclinical development.

Q: What are the key success factors in preclinical drug development for IgA nephropathy?

A: Key success factors include selecting appropriate disease models, identifying reliable biomarkers of efficacy and safety, and ensuring rigorous study design and execution. Early engagement with regulatory authorities and integration of translational endpoints are also critical. Our company’s multidisciplinary team collaborates closely with clients to design and execute preclinical programs that maximize the likelihood of clinical and regulatory success.

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