IgG-subclass-selective degrader (MoDE)

BHV-1450

An investigational treatment for Pemphigus Vulgaris and Myasthenia Gravis.

Preclinicalby Biohaven
Preclinical
Phase 1
Phase 2
Phase 3
Approved
Drug facts

The same compound appears under different names depending on the context. Here is how to identify BHV-1450 wherever you encounter it, plus the key facts at a glance.

Generic name
BHV-1450
Development codes
BHV-1450, BHV1450
Drug class
IgG-subclass-selective degrader (MoDE)
Manufacturer
Biohaven
How it's taken
Designed as a subcutaneous (under-the-skin) injection, consistent with the rest of the MoDE platform.

An investigational subcutaneous IgG4-selective degrader from Biohaven being developed for autoimmune diseases driven primarily by IgG4 antibodies — most notably pemphigus vulgaris (anti-desmoglein antibodies) and MuSK-positive myasthenia gravis (anti-MuSK antibodies). By targeting the IgG4 subclass rather than all IgG, BHV-1450 is designed to remove disease-causing antibodies while preserving most of the IgG pool that fights infection[3].

How BHV-1450 works

Your immune system makes four types (subclasses) of IgG antibodies: IgG1, IgG2, IgG3, and IgG4. Most antibodies that fight infection are IgG1 and IgG3. But in a small number of autoimmune diseases, the harmful antibodies are the IgG4 type.

Two examples are pemphigus vulgaris, where IgG4 antibodies attack the 'glue' between skin cells and cause painful blisters, and MuSK-positive myasthenia gravis, where IgG4 antibodies block a signaling protein muscles need to contract[5][6]. BHV-1450 is designed to remove specifically the IgG4 antibodies and leave the infection-fighting IgG1/2/3 antibodies alone.

Like the other MoDE drugs, one end of the molecule binds IgG4 in the bloodstream and the other end attaches to a receptor on liver cells, which pulls the antibody inside for disposal. The idea is that patients get the benefit of antibody reduction without as much infection risk as broader IgG-lowering treatments[3].

Mechanism: IgG4-selective extracellular protein degrader (MoDE platform) that removes the IgG4 subclass of antibodies while sparing IgG1/2/3

Side effects and safety

Early trial safety observations

Human safety data for BHV-1450 is limited as of early 2026; the program is in early clinical development. Based on the MoDE platform as a whole, expected side effects include injection-site reactions and mild transient lab changes. Because the drug targets only IgG4, the infection-risk profile should be more favorable than pan-IgG or broad B-cell-depleting therapies — but this needs to be confirmed in clinical studies[3].

This is not a complete list of side effects. Talk to your doctor or pharmacist about what to expect and when to seek medical attention.

Taking BHV-1450

Designed as a subcutaneous (under-the-skin) injection, consistent with the rest of the MoDE platform. Dose and frequency will be established during Phase 1 and early Phase 2.

Clinical trial results

BHV-1450 has not entered human trials. Biohaven's 2025 annual report describes its IgG4-specific degrader as advancing toward candidate nomination, and its August 2026 update says only that it continues advancing degrader candidates for IgG4-mediated disease. Pemphigus vulgaris and MuSK-positive myasthenia gravis are the lead indications[1][2].

Development history

BHV-1450 is part of the broader MoDE portfolio Biohaven licensed from Yale. Rather than building a single pan-IgG drug, Biohaven is developing subclass- and target-selective degraders (BHV-1450 for IgG4-mediated disease, BHV-1400 for Gd-IgA1 in IgA nephropathy, BHV-1420 for anti-PLA2R in membranous nephropathy, BHV-1600 for β1-AR autoantibodies in PPCM) to match the biology of specific autoimmune diseases[3][4].

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Explore Pemphigus Vulgaris and Myasthenia Gravis trials

Other Pemphigus Vulgaris & Myasthenia Gravis treatments

Current care for pemphigus vulgaris centers on systemic corticosteroids plus rituximab (approved 2018 as first-line biologic), with steroid-sparing agents like mycophenolate mofetil and azathioprine[5].

MuSK-positive myasthenia gravis is typically treated with rituximab, corticosteroids, and newer FcRn inhibitors (efgartigimod, rozanolixizumab) or complement inhibitors, though response varies by antibody subtype[6].

BHV-1450 is differentiated by selectively removing the IgG4 subclass that drives both diseases, potentially lowering infection risk compared to broader immunosuppression[3].

Common questions about BHV-1450

▸What is BHV-1450?

An investigational subcutaneous IgG4-selective degrader from Biohaven being developed for autoimmune diseases driven primarily by IgG4 antibodies — most notably pemphigus vulgaris (anti-desmoglein antibodies) and MuSK-positive myasthenia gravis (anti-MuSK antibodies). By targeting the IgG4 subclass rather than all IgG, BHV-1450 is designed to remove disease-causing antibodies while preserving most of the IgG pool that fights infection[3].

▸How does BHV-1450 work?

Your immune system makes four types (subclasses) of IgG antibodies: IgG1, IgG2, IgG3, and IgG4. Most antibodies that fight infection are IgG1 and IgG3. But in a small number of autoimmune diseases, the harmful antibodies are the IgG4 type.

Two examples are pemphigus vulgaris, where IgG4 antibodies attack the 'glue' between skin cells and cause painful blisters, and MuSK-positive myasthenia gravis, where IgG4 antibodies block a signaling protein muscles need to contract[5][6]. BHV-1450 is designed to remove specifically the IgG4 antibodies and leave the infection-fighting IgG1/2/3 antibodies alone.

Like the other MoDE drugs, one end of the molecule binds IgG4 in the bloodstream and the other end attaches to a receptor on liver cells, which pulls the antibody inside for disposal. The idea is that patients get the benefit of antibody reduction without as much infection risk as broader IgG-lowering treatments[3].

▸What are the side effects of BHV-1450?

Human safety data for BHV-1450 is limited as of early 2026; the program is in early clinical development. Based on the MoDE platform as a whole, expected side effects include injection-site reactions and mild transient lab changes. Because the drug targets only IgG4, the infection-risk profile should be more favorable than pan-IgG or broad B-cell-depleting therapies — but this needs to be confirmed in clinical studies[3].

▸How is BHV-1450 taken?

Designed as a subcutaneous (under-the-skin) injection, consistent with the rest of the MoDE platform. Dose and frequency will be established during Phase 1 and early Phase 2.

▸Is BHV-1450 FDA approved?

BHV-1450 is currently in preclinical clinical trials for Pemphigus Vulgaris and Myasthenia Gravis. It has not yet received FDA approval.

▸Why target only IgG4 instead of all IgG?

In a small set of autoimmune diseases — pemphigus vulgaris, MuSK-positive myasthenia gravis, and some forms of autoimmune encephalitis — the pathogenic antibodies are almost exclusively IgG4. Most infection-fighting antibodies are IgG1 and IgG3. Selectively removing IgG4 should, in principle, reduce disease activity while preserving most of the immune system's ability to fight infections. This is the core bet behind BHV-1450[5][6].

▸Is BHV-1450 available now?

No. BHV-1450 is in early clinical development and is only available through clinical trials. Pemphigus vulgaris patients should discuss rituximab (first-line biologic) and steroid-sparing options with their dermatologist; MuSK-positive myasthenia gravis patients should discuss rituximab and FcRn inhibitors with their neurologist[5][6].

▸How does BHV-1450 compare to rituximab?

Rituximab depletes B cells, which stops the body from making more antibodies but takes weeks to work and can affect antibody production broadly for months. BHV-1450 is designed to remove existing IgG4 antibodies from the blood directly and quickly, without wiping out B cells. The approaches could eventually be used in sequence or combination, but head-to-head data do not yet exist[5].

▸Could BHV-1450 help other IgG4-driven diseases?

Possibly. IgG4 is the dominant pathogenic subclass in conditions like IgG4-related disease, chronic inflammatory demyelinating polyneuropathy (some subtypes), and certain autoimmune encephalitis syndromes. Biohaven has not publicly committed to all of these, but the biology of an IgG4-selective degrader makes them plausible future indications[3].

Sources and references

Every factual claim on this page is drawn from the public sources listed below. Click any reference to open the original document.

  1. U.S. Securities and Exchange Commission · 2026-03. Biohaven Ltd. Annual Report on Form 10-K for fiscal year 2025. https://www.sec.gov/Archives/edgar/data/1935979/000193597926000020/bhvn-20251231.htm
  2. Biohaven via SEC Form 8-K · 2026-08-10. Biohaven Reports Second Quarter 2026 Financial Results and Recent Business Developments. https://www.sec.gov/Archives/edgar/data/1935979/000193597926000067/a2026q2bhvnearningsprex991.htm
  3. Biohaven · 2025. Biohaven Pipeline — BHV-1450 IgG4 Degrader Program. https://www.biohaven.com/pipeline/
  4. Yale Office of Cooperative Research · 2022. Biohaven Licenses Yale's MoDE Extracellular Protein Degradation Platform. https://ir.biohaven.com/news-releases/news-release-details/biohaven-advances-development-mode-platform-technology-licensed
  5. National Organization for Rare Disorders. Pemphigus Vulgaris. https://rarediseases.org/mondo-disease/pemphigus-vulgaris/
  6. Myasthenia Gravis Foundation of America. MuSK Antibody-Positive Myasthenia Gravis: Diagnosis and Treatment. https://myasthenia.org/

This page is for informational purposes only and does not constitute medical advice. Drug information is sourced from public databases and peer-reviewed literature and may not reflect the most recent updates. Always discuss treatment options with your healthcare provider. Last reviewed: September 2026.

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