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PROJECT 1

Ion Channel-Targeted Drug Discovery
in Allergic Disease

Identifying the channels. Validating the mechanism. Advancing the candidate.

3

3

16+

IND approvals

Ion channel targets

Years of pipeline

THE PROBLEM

Current therapies work downstream.
We go upstream.

Allergic diseases like atopic dermatitis and allergic rhinitis are driven not by a single pathway, but by converging signals across immune cells, sensory neurons, and epithelial barriers. Conventional therapies — antihistamines, corticosteroids — address symptoms after the fact. We work at the ion channels that initiate and amplify these signals.

Calcium-dependent signaling is the common currency of allergic inflammation. Modulate the channel, and you interrupt the disease at its source.

ORAI1 governs Ca²⁺ influx in T lymphocytes and mast cells. TMEM16A (ANO1) controls Cl⁻ secretion in nasal epithelium. TRPV3 regulates keratinocyte differentiation and skin barrier function. These are our primary targets — and natural compounds are our entry point.

OUR APPROACH

Natural compound screening for multi-target inhibition.

We screen natural compound libraries against ion channel targets using whole-cell patch clamp electrophysiology — the gold standard for measuring channel activity directly. Hits are validated across cell lines and confirmed in disease-relevant animal models.

What distinguishes our strategy is the focus on polypharmacology: natural compounds that inhibit multiple ion channels simultaneously. A single compound that suppresses both ORAI1-driven T cell activation and ANO1-driven epithelial hypersecretion addresses more of the disease than any single-target agent can.

ORAI1

T LYMPHOCYTE

Ca²⁺ release-activated channel mediating store-operated calcium entry in T cells and mast cells

ANO1

NASAL EPITHELIUM

Ca²⁺-activated Cl⁻ channel driving mucus hypersecretion and rhinorrhea in allergic airway disease

TRPV3

KERATINOCYTE

Thermosensitive TRP channel regulating keratinocyte differentiation and skin barrier recovery

PIPELINE

From plant to patient — three approved candidates.

Each candidate emerged from the same pipeline: identify the plant, characterize its ion channel pharmacology by patch clamp electrophysiology, validate in immune and epithelial cell models, and confirm in the OVA-induced murine disease model.

project1_pipeline_v6.jpg

IND APPROVALS

Three candidates. Two diseases. One strategy.

Each candidate emerged from the same pipeline: identify the plant, characterize its ion channel pharmacology by patch clamp, validate in immune and epithelial cell models, confirm in the OVA-induced murine disease model, and advance to IND.

These candidates were developed through a long-term collaboration with Channelopathy Research Center (CRC), Dongguk University College of Medicine, where the laboratory was based for 16 years prior to joining SKKU.

TBF Lotion

IND ✓

Tribulus terrestris (질려자)

Atopic Dermatitis

ORAI1 inhibition · T lymphocyte Ca²⁺ signaling

IND APPROVED · 2019

DSY19 Nasal Spray

IND ✓

IND ✓

Flos Magnoliae (신이)

Allergic Rhinitis

ANO1 · ORAI1 inhibition · Nasal epithelium + T lymphocyte

IND APPROVED · 2019

AP22 Cream

IND ✓

Agrimonia pilosa (짚신나물)

Atopic Dermatitis

TRPV3 activation · ORAI1 inhibition · Keratinocyte + T lymphocyte

IND APPROVED · 2023

Key papers from this program.

REPRESENTATIVE PUBLICATIONS

2025

Biomedicine & Pharmacotherapy

Polypharmacological effects of honokiol on allergic rhinitis: modulation of TMEM16A, TRPV1, and calcium signaling

Phan HTL, Nam YR, Kim HJ, … Nam JH (co-corresponding)

2022

Journal of Ethnopharmacology

In vitro and in vivo anti-allergic effects of magnolol on allergic rhinitis via inhibition of ORAI1 and ANO1 channels

Phan HTL, Nam YR, Kim HJ, … Nam JH (corresponding)

2017

Journal of Dermatological Science

Agrimonia pilosa leaf extract accelerates skin barrier restoration by activation of transient receptor potential vanilloid 3

Nam YR, Kim HJ, … Nam JH (corresponding)

Interested in this program?

Students and collaborators can learn more about our ongoing research or get in touch directly.

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