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Allergy

 

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Atopic dermatitis

Atopic dermatitis (eczema) is a condition that makes skin red and itchy. It's common in children but can occur at any age. Atopic dermatitis is long lasting (chronic) and tends to flare periodically. It may be accompanied by asthma or hay fever.

Drug Targeting Immuno pathogenic Pathways of Atopic Dermatitis

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Target

Biologics that target the IL-4 receptor (IL-4-R) alpha subunit can block the signaling of IL-4 and IL-13, both are key mediators of the TH2 immune response and the main driver of AD

The functions of IL-4 and IL-13 overlap, facilitated in part by shared receptor subunits, to trigger TH2.

MOA Mechanism of Action

The functions of IL-4 and IL-13 overlap, facilitated in part by shared receptor subunits, to trigger TH2.

The Mechanism of Action : JAKs inhibitor

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 Janus kinase (JAK)/signal transducer and activator of transcription (STAT)

pathway is a master regulator of immune function.

With a growing movement toward use of targeted therapies, JAK inhibitors are an

important focus of therapeutic research for AD.

M. A. Rodrigues et al., (2020) JAK/STAT inhibitors for the treatment of atopic dermatitis, Journal of Dermatological Treatment, 31:1, 33-40

Solimani et al., Front. Immunol., 03 December 2019

Pathophysiology of Acute and Chronic Atopic Dermatitis

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Atopic dermatitis (AD) is the most common chronic inflammatory skin disease, with a prevalence of 15–20% in developed countries. 

Effects of cytokines on epidermis in AD.

Disrupted epidermal barrier stimulates (KC) keratinocytes to release cytokines and activate (DC) dendritic cells and (LC) Langerhans cells.

Activated DC stimulate Th2 cells to produce IL-4, IL-5, IL-13, IL-31, and IL-33, further leading to cascades of AD symptoms.

Kim J, et al. Allergy Asthma Proc 40:84-92, 2019

Immunopathogenesis and Cytokine Networks of Atopic Dermatitis

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AD is largely driven by CD4+T helper Th2 cells, but other T-cell subsets such as CD4+Th22 cells and Th17 cells are also found

The type 2 cytokines IL-4, IL-5 and IL-13 drive further pathogenesis, including eosinophil and mast cell recruitment and activation, B-cell IgEproduction and IL-31 secretion

TsakokT et al. The British Journal of Dermatology. 180(3):464-474, 2019

AR100DP1 reduces the thickness of skin and eases the symptom in DNCB-induced Atopic dermatitis mice

Naive
Atopic dermatitis

Protopic

(tacrolimus)

AR100DP1-1

AR100DP1-2

AR100DP1-3

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The ARJIL sample treatment on DNCB-induced atopic dermatitis-like phenotypes in BALB/c mice

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The ARJIL sample treatment on DNCB-induced atopic dermatitis-like phenotypes in BALB/c mice

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The expression levels of TSLP in skin by IHC (Immunohistochemical)  staining

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Atopic Dermatitis Animal Experiment - Treatment Results on Mouse Ears

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N: Naïve
S:  Control
SV: Vehicle
Arjil drug A100
Arjil drug V2

 Swelling in the treatment group   was significantly alleviated. 

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 Allergy index (IgE) levels   significantly decreased. 

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Asthma
 

Asthma is a common long-term inflammatory disease of the airways of the lungs. It is characterized by variable and recurring symptoms, reversible airflow obstruction, and easily triggered bronchospasms. Symptoms include episodes of wheezing, coughing, chest tightness, and shortness of breath.

Cell (THP-1) Experiment: ARH007 Active Fraction (ARH007-DS1) Can Suppress Inflammatory Cytokines and Regulate Immune Balance (Th1 and Th2).

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Allergy Clinical Trials of Product
ARH007

Clinical trial hospital: Chung Shan Medical University Hospital

Atopic Dermatitis

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Allergic Rhinitis

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Clinical trial hospital: Chung Shan Medical University Hospital

Allergy clinical trials

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Eosinophil
(inflamed  indicator)

Eosinophil Cationic Protein
(Allergy indicator) 

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AR Drug could suppress mast cell degranulation  in a dose-dependent manner

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AR Drug could suppress TNF-α secretion by dendritic cells  in a dose-dependent manner

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ARJIL Biotech Holding Company

R209, Building A, 4th General Building, NTHU, 101, Sec.2, Kuang-Fu Road, Hsinchu 30013, Taiwan

Business:+8863-573-3608

Primary Contact: Ming-Kun Chen/mkchen@arjilbio.com

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