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adx 102 (TargetMol)

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TargetMol adx 102

<t>ADX-102</t> and bronchial epithelial cell viability. Medium release of lactate dehydrogenase (LDH) was measured and expressed as % viability in BEAS-2B cells ( A ) or LDH activity in 16HBE cells ( B ) after 24 h treatment with 0.1 µM to 10 mM ADX-102 in M-199 with 10% serum (Media). An equal number of cells were sonicated for maximum LDH release (Lysed). Positive assay control (+) was provided by a manufacturer. * p < 0.05 and ** p < 0.01 vs. 10 µM ADX-102; **** p < 0.0001 vs. 0–100 µM ADX-102. Bars represent SEM of biological n of three with three technical replicates. ns = not significant.

Adx 102, supplied by TargetMol, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/adx 102/product/TargetMol
Average 90 stars, based on 1 article reviews

adx 102 - by Bioz Stars, 2026-04

90/100 stars

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1) Product Images from "Aldehyde Trapping by ADX-102 Is Protective against Cigarette Smoke and Alcohol Mediated Lung Cell Injury"

Article Title: Aldehyde Trapping by ADX-102 Is Protective against Cigarette Smoke and Alcohol Mediated Lung Cell Injury

Journal: Biomolecules

doi: 10.3390/biom12030393

ADX-102 and bronchial epithelial cell viability. Medium release of lactate dehydrogenase (LDH) was measured and expressed as % viability in BEAS-2B cells ( A ) or LDH activity in 16HBE cells ( B ) after 24 h treatment with 0.1 µM to 10 mM ADX-102 in M-199 with 10% serum (Media). An equal number of cells were sonicated for maximum LDH release (Lysed). Positive assay control (+) was provided by a manufacturer. * p < 0.05 and ** p < 0.01 vs. 10 µM ADX-102; **** p < 0.0001 vs. 0–100 µM ADX-102. Bars represent SEM of biological n of three with three technical replicates. ns = not significant.

Figure Legend Snippet: ADX-102 and bronchial epithelial cell viability. Medium release of lactate dehydrogenase (LDH) was measured and expressed as % viability in BEAS-2B cells ( A ) or LDH activity in 16HBE cells ( B ) after 24 h treatment with 0.1 µM to 10 mM ADX-102 in M-199 with 10% serum (Media). An equal number of cells were sonicated for maximum LDH release (Lysed). Positive assay control (+) was provided by a manufacturer. * p < 0.05 and ** p < 0.01 vs. 10 µM ADX-102; **** p < 0.0001 vs. 0–100 µM ADX-102. Bars represent SEM of biological n of three with three technical replicates. ns = not significant.

Techniques Used: Activity Assay, Sonication

ADX-102 and bronchial epithelial cell migration. Circular wounds in monolayers of BEAS-2B cells were measured for cell migration into the wound area in the presence of 0–100 µM ADX-102 over time ( A ). Positive control for wound closure was M-199 with 10% serum (FBS). In panel ( B ), BEAS-2B cells were wounded in the presence of 5% cigarette smoke extract (CSE) and in the presence of 0–100 µM ADX-102, and % wound closure was measured. * p < 0.05 vs. 0 µM ADX-102. Bars represent SEM of n = 5, each with three replicates.

Figure Legend Snippet: ADX-102 and bronchial epithelial cell migration. Circular wounds in monolayers of BEAS-2B cells were measured for cell migration into the wound area in the presence of 0–100 µM ADX-102 over time ( A ). Positive control for wound closure was M-199 with 10% serum (FBS). In panel ( B ), BEAS-2B cells were wounded in the presence of 5% cigarette smoke extract (CSE) and in the presence of 0–100 µM ADX-102, and % wound closure was measured. * p < 0.05 vs. 0 µM ADX-102. Bars represent SEM of n = 5, each with three replicates.

Techniques Used: Migration, Positive Control

ADX-102 and bronchial epithelial cell protein kinase C alpha (PKCα) activity. BEAS-2B cells were pretreated with or without 10 µM ADX-102 for 1 h prior to treatment with M-199 containing 10% serum (Media) or 5% cigarette smoke extract (CSE) for 1 h. In the absence of ADX-102, **** p < 0.0001 CSE vs. Media. In the presence of CSE, ** p < 0.01. No ADX vs. ADX. Bars represent SEM of n = 9, each with three replicates.

Figure Legend Snippet: ADX-102 and bronchial epithelial cell protein kinase C alpha (PKCα) activity. BEAS-2B cells were pretreated with or without 10 µM ADX-102 for 1 h prior to treatment with M-199 containing 10% serum (Media) or 5% cigarette smoke extract (CSE) for 1 h. In the absence of ADX-102, **** p < 0.0001 CSE vs. Media. In the presence of CSE, ** p < 0.01. No ADX vs. ADX. Bars represent SEM of n = 9, each with three replicates.

Techniques Used: Activity Assay

ADX-102 and tracheal epithelial ciliated cell protein kinase C epsilon mediated cilia beating. Ciliated MTECs were treated with or without the combination of 5% cigarette smoke extract (CSE) and 50 mM ethanol (EtOH) in the presence or absence of 10 µM ADX-102, and cilia beat frequency (CBF) was measured from 0–24 h ( A ). Baseline control consisted of DMEM with 10% serum (Media). * p < 0.05 ADX vs. no ADX in the presence of CSE + EtOH at 3, 6, and 24 h. Dose–response (0–100 µM) for ADX-102 on combined CSE and EtOH stimulated (3 h) and autodownregulated (24 h) protein kinase C epsilon (PKCε). * p < 0.01 vs. medium control. Bars represent SEM of n = 6, each with three replicates ( B ).

Figure Legend Snippet: ADX-102 and tracheal epithelial ciliated cell protein kinase C epsilon mediated cilia beating. Ciliated MTECs were treated with or without the combination of 5% cigarette smoke extract (CSE) and 50 mM ethanol (EtOH) in the presence or absence of 10 µM ADX-102, and cilia beat frequency (CBF) was measured from 0–24 h ( A ). Baseline control consisted of DMEM with 10% serum (Media). * p < 0.05 ADX vs. no ADX in the presence of CSE + EtOH at 3, 6, and 24 h. Dose–response (0–100 µM) for ADX-102 on combined CSE and EtOH stimulated (3 h) and autodownregulated (24 h) protein kinase C epsilon (PKCε). * p < 0.01 vs. medium control. Bars represent SEM of n = 6, each with three replicates ( B ).

Techniques Used:

ADX-102 and loss of tracheal epithelial cell cilia. Ciliated MTECs were treated with a combination of 5% cigarette smoke extract (CSE) and 50 mM ethanol (EtOH) in the presence or absence of 10 µM ADX-102, and the average number of motile cilia were measured at 3 ( A ) and 24 h ( B ). **** p < 0.01 vs. medium control or presence of ADX. Bars represent SEM of at least n = 9 individual experiments. ns = not significant.

Figure Legend Snippet: ADX-102 and loss of tracheal epithelial cell cilia. Ciliated MTECs were treated with a combination of 5% cigarette smoke extract (CSE) and 50 mM ethanol (EtOH) in the presence or absence of 10 µM ADX-102, and the average number of motile cilia were measured at 3 ( A ) and 24 h ( B ). **** p < 0.01 vs. medium control or presence of ADX. Bars represent SEM of at least n = 9 individual experiments. ns = not significant.

Techniques Used:

ADX-102 and bronchial epithelial cell permeability. 16HBE cells were grown to confluence until maximal barrier function (Resistance) achieved. Cells were treated with either DMEM and 10% serum (Media), 5% cigarette smoke extract (CSE), 50 mM alcohol (EtOH), or the combination of smoke and alcohol for up to 72 h in the absence ( A ) or presence ( B ) of 10 µM ADX-102. * p < 0.02 vs. media at 72 h. Bars represent SEM of n = 5, each with three replicates.

Figure Legend Snippet: ADX-102 and bronchial epithelial cell permeability. 16HBE cells were grown to confluence until maximal barrier function (Resistance) achieved. Cells were treated with either DMEM and 10% serum (Media), 5% cigarette smoke extract (CSE), 50 mM alcohol (EtOH), or the combination of smoke and alcohol for up to 72 h in the absence ( A ) or presence ( B ) of 10 µM ADX-102. * p < 0.02 vs. media at 72 h. Bars represent SEM of n = 5, each with three replicates.

Techniques Used: Permeability

ADX-102 and MAA adduct formation. 16HBE cells were grown to confluence in 60 mm culture dishes. Cells were treated with either M-199+10% serum (Media) or a combination of 5% cigarette smoke extract (CSE) and 50 mM alcohol (EtOH) for 72 h in the absence or presence of 10 µM ADX-102. * p <0.04 and ** p < 0.003 at 72 h. Bars represent SEM of n = 6.

Figure Legend Snippet: ADX-102 and MAA adduct formation. 16HBE cells were grown to confluence in 60 mm culture dishes. Cells were treated with either M-199+10% serum (Media) or a combination of 5% cigarette smoke extract (CSE) and 50 mM alcohol (EtOH) for 72 h in the absence or presence of 10 µM ADX-102. * p <0.04 and ** p < 0.003 at 72 h. Bars represent SEM of n = 6.

Techniques Used:

Model diagram for ADX-102 aldehyde-trapping action on cigarette smoke and alcohol mediated injury to airway epithelial cell function.

Figure Legend Snippet: Model diagram for ADX-102 aldehyde-trapping action on cigarette smoke and alcohol mediated injury to airway epithelial cell function.

Techniques Used: Cell Function Assay

Image Search Results

Journal: Biomolecules

Article Title: Aldehyde Trapping by ADX-102 Is Protective against Cigarette Smoke and Alcohol Mediated Lung Cell Injury

doi: 10.3390/biom12030393

Figure Lengend Snippet: ADX-102 and bronchial epithelial cell viability. Medium release of lactate dehydrogenase (LDH) was measured and expressed as % viability in BEAS-2B cells ( A ) or LDH activity in 16HBE cells ( B ) after 24 h treatment with 0.1 µM to 10 mM ADX-102 in M-199 with 10% serum (Media). An equal number of cells were sonicated for maximum LDH release (Lysed). Positive assay control (+) was provided by a manufacturer. * p < 0.05 and ** p < 0.01 vs. 10 µM ADX-102; **** p < 0.0001 vs. 0–100 µM ADX-102. Bars represent SEM of biological n of three with three technical replicates. ns = not significant.

Article Snippet: They were grown to confluency and treated with different doses of cigarette smoke or ethanol in the presence or absence of ADX-102 (TargetMol, Wellesley Hills, MA, USA) for a maximum of 72 h. Controls consisted of medium-only wells with and without cells.

Techniques: Activity Assay, Sonication

Journal: Biomolecules

Article Title: Aldehyde Trapping by ADX-102 Is Protective against Cigarette Smoke and Alcohol Mediated Lung Cell Injury

doi: 10.3390/biom12030393

Figure Lengend Snippet: ADX-102 and bronchial epithelial cell migration. Circular wounds in monolayers of BEAS-2B cells were measured for cell migration into the wound area in the presence of 0–100 µM ADX-102 over time ( A ). Positive control for wound closure was M-199 with 10% serum (FBS). In panel ( B ), BEAS-2B cells were wounded in the presence of 5% cigarette smoke extract (CSE) and in the presence of 0–100 µM ADX-102, and % wound closure was measured. * p < 0.05 vs. 0 µM ADX-102. Bars represent SEM of n = 5, each with three replicates.

Techniques: Migration, Positive Control

Journal: Biomolecules

Article Title: Aldehyde Trapping by ADX-102 Is Protective against Cigarette Smoke and Alcohol Mediated Lung Cell Injury

doi: 10.3390/biom12030393

Figure Lengend Snippet: ADX-102 and bronchial epithelial cell protein kinase C alpha (PKCα) activity. BEAS-2B cells were pretreated with or without 10 µM ADX-102 for 1 h prior to treatment with M-199 containing 10% serum (Media) or 5% cigarette smoke extract (CSE) for 1 h. In the absence of ADX-102, **** p < 0.0001 CSE vs. Media. In the presence of CSE, ** p < 0.01. No ADX vs. ADX. Bars represent SEM of n = 9, each with three replicates.

Techniques: Activity Assay

Journal: Biomolecules

Article Title: Aldehyde Trapping by ADX-102 Is Protective against Cigarette Smoke and Alcohol Mediated Lung Cell Injury

doi: 10.3390/biom12030393

Figure Lengend Snippet: ADX-102 and tracheal epithelial ciliated cell protein kinase C epsilon mediated cilia beating. Ciliated MTECs were treated with or without the combination of 5% cigarette smoke extract (CSE) and 50 mM ethanol (EtOH) in the presence or absence of 10 µM ADX-102, and cilia beat frequency (CBF) was measured from 0–24 h ( A ). Baseline control consisted of DMEM with 10% serum (Media). * p < 0.05 ADX vs. no ADX in the presence of CSE + EtOH at 3, 6, and 24 h. Dose–response (0–100 µM) for ADX-102 on combined CSE and EtOH stimulated (3 h) and autodownregulated (24 h) protein kinase C epsilon (PKCε). * p < 0.01 vs. medium control. Bars represent SEM of n = 6, each with three replicates ( B ).

Techniques:

Journal: Biomolecules

Article Title: Aldehyde Trapping by ADX-102 Is Protective against Cigarette Smoke and Alcohol Mediated Lung Cell Injury

doi: 10.3390/biom12030393

Figure Lengend Snippet: ADX-102 and loss of tracheal epithelial cell cilia. Ciliated MTECs were treated with a combination of 5% cigarette smoke extract (CSE) and 50 mM ethanol (EtOH) in the presence or absence of 10 µM ADX-102, and the average number of motile cilia were measured at 3 ( A ) and 24 h ( B ). **** p < 0.01 vs. medium control or presence of ADX. Bars represent SEM of at least n = 9 individual experiments. ns = not significant.

Techniques:

Journal: Biomolecules

Article Title: Aldehyde Trapping by ADX-102 Is Protective against Cigarette Smoke and Alcohol Mediated Lung Cell Injury

doi: 10.3390/biom12030393

Figure Lengend Snippet: ADX-102 and bronchial epithelial cell permeability. 16HBE cells were grown to confluence until maximal barrier function (Resistance) achieved. Cells were treated with either DMEM and 10% serum (Media), 5% cigarette smoke extract (CSE), 50 mM alcohol (EtOH), or the combination of smoke and alcohol for up to 72 h in the absence ( A ) or presence ( B ) of 10 µM ADX-102. * p < 0.02 vs. media at 72 h. Bars represent SEM of n = 5, each with three replicates.

Techniques: Permeability

Journal: Biomolecules

Article Title: Aldehyde Trapping by ADX-102 Is Protective against Cigarette Smoke and Alcohol Mediated Lung Cell Injury

doi: 10.3390/biom12030393

Figure Lengend Snippet: ADX-102 and MAA adduct formation. 16HBE cells were grown to confluence in 60 mm culture dishes. Cells were treated with either M-199+10% serum (Media) or a combination of 5% cigarette smoke extract (CSE) and 50 mM alcohol (EtOH) for 72 h in the absence or presence of 10 µM ADX-102. * p <0.04 and ** p < 0.003 at 72 h. Bars represent SEM of n = 6.

Techniques:

Journal: Biomolecules

Article Title: Aldehyde Trapping by ADX-102 Is Protective against Cigarette Smoke and Alcohol Mediated Lung Cell Injury

doi: 10.3390/biom12030393

Figure Lengend Snippet: Model diagram for ADX-102 aldehyde-trapping action on cigarette smoke and alcohol mediated injury to airway epithelial cell function.

Techniques: Cell Function Assay

Current and recently completed registered clinical trials, awaiting for results to be published

Journal: Orphanet Journal of Rare Diseases

Article Title: New developments in the molecular treatment of ichthyosis: review of the literature

doi: 10.1186/s13023-022-02430-6

Figure Lengend Snippet: Current and recently completed registered clinical trials, awaiting for results to be published

Article Snippet: In 2018, Aldeyra Therapeutics Inc [ ]. announced their phase III randomized double-blind vehicle-controlled trial with topical application of ADX-102 1% (Reproxalap) in SLS patients (NCT03445650), which has now been completed.

Techniques: Clinical Proteomics, Binding Assay, Cream, Protease Inhibitor, Plasmid Preparation, Expressing, Genetically Modified

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