- Cat. No.
- A21690
(R)-Sulforaphane
(R)-Sulforaphane is a highly potent inducer of the Keap1/Nrf2/ARE pathway. (R)-Sulforaphane is a far more potent inducer of the carcinogen-detoxifying enzyme systems in rat liver and lung than the S-isomer.
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Keap1-Nrf2 pathway activators and inhibitors act on the master regulator of the cellular antioxidant response. Kelch-like ECH-associated protein 1 (Keap1) binds nuclear factor erythroid 2-related factor 2 (Nrf2) and keeps it from accumulating in the nucleus. In 1997, Nrf2 and small Maf proteins were shown to induce detoxifying genes through antioxidant response elements (AREs). Electrophiles modify Keap1 cysteines, releasing Nrf2 to induce genes such as NAD(P)H quinone dehydrogenase 1 (NQO1). Activators include sulforaphane, an isothiocyanate isolated from broccoli in 1992, and dimethyl fumarate, oltipraz and the triterpenoid omaveloxolone. ML-385 inhibits Nrf2 itself, while dicoumarol blocks the downstream enzyme NQO1. Related oxidative stress tools are listed under Reactive Oxygen Species (ROS).
(R)-Sulforaphane is a highly potent inducer of the Keap1/Nrf2/ARE pathway. (R)-Sulforaphane is a far more potent inducer of the carcinogen-detoxifying enzyme systems in rat liver and lung than the S-isomer.
Synonyms: Ferulaldehyde
Coniferaldehyde (Ferulaldehyde), isolated from the ethanol extract of Vitex rotundifolia fruits, is an effective inducer of heme oxygenase-1 (HO-1).
ACA-28 (compound 2a) is a potent modulator of the ERK MAPK signaling pathway that exerts anticancer effects through a unique mechanism involving ERK hyperactivation. Rather than inhibiting ERK activity directly, ACA-28 induces sustained ERK activation, which paradoxically triggers apoptosis in cancer cells. It demonstrates selective cytotoxicity, inhibiting the growth of melanoma cells (SK-MEL-28) with an IC₅₀ of 5.3 μM, while showing lower toxicity toward normal human melanocytes (NHEM), with an IC₅₀ of 10.1 μM. ACA-28's ability to exploit ERK signaling dysregulation for selective induction of apoptosis makes it a promising candidate for further development in cancer therapy, particularly in ERK-dependent malignancies.
Nrf2 Activator-10 (Compound AI-1) acts as a PI3K-dependent inducer of the antioxidant response element (ARE), with an EC50 value of 2.7 μM, effectively activating Nrf2. By modifying Keap1 and inhibiting the Cul3-Keap1 ubiquitin ligase complex, Nrf2 Activator-10 enhances Nrf2 transcription and promotes cellular defense mechanisms. This compound is particularly valuable for research focused on oxidative stress and cytoprotection, demonstrating protective effects against H2O2-induced apoptosis.
Keap1-Nrf2-IN-10 is a potent inducer of NQO1, mediating the Keap1-Nrf2 signaling pathway. This compound effectively reduces oxidative stress by lowering levels of malondialdehyde (MDA), reactive oxygen species (ROS), and NQO1 in hepatic tissues. Research indicates that Keap1-Nrf2-IN-10 enhances the survival rates of gamma-irradiated mice, making it a valuable tool for studies focused on oxidative damage and cellular protection mechanisms.
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TBE 31 is a highly effective NQO1 inducer, exhibiting a dissociation constant (Kd) of 1.1 nM. It functions as a potent activator of the transcription factor Nrf2 by covalently modifying cysteine residues in Keap1, thereby inhibiting its role in the degradation of Nrf2. This mechanism leads to increased Nrf2 accumulation, promoting cytoprotective effects. TBE 31 is particularly valuable in research focused on oxidative stress response and protective signaling pathways.
AChE/Nrf2 Modulator 1 is an orally active compound that targets both acetylcholinesterase (AChE) and the nuclear factor erythroid 2-related factor 2 (Nrf2). It exhibits significant Nrf2 inductive activity along with potent AChE inhibitory effects, presenting IC50 values of 0.07 μM for eel AChE and 0.38 μM for human AChE. This compound is primarily utilized in research focused on Alzheimer's disease, providing insights into neuroprotective mechanisms and cholinergic system modulation.
VVD 065 is an allosteric modulator of the Keap1-Cul3 E3 ligase complex that functions as a molecular glue. By activating KEAP1, VVD 065 promotes the degradation of NRF2, an essential regulator of antioxidant defenses. This compound has demonstrated the ability to inhibit tumor growth in non-small cell lung cancer and esophageal squamous cell carcinoma xenograft models. VVD 065 serves as a valuable tool for research on cancer biology and therapeutic strategies targeting oxidative stress responses.
Tigloylgomisin H is a lignan that targets the induction of quinone reductase (QR) activity in Hepa1c1c7 mouse hepatocarcinoma cells. This compound functions as a monofunctional inducer, specifically enhancing the expression of the phase II detoxification enzyme NQO1 via the NF-E2-related factor 2 (Nrf2)-ARE pathway. As a result, Tigloylgomisin H demonstrates potential as a preventive agent against liver cancer, making it valuable for cancer research applications.