Atg8/LC3 Activator

L-Azetidine-2-carboxylic acid is a proline analog. L-Azetidine-2-carboxylic acid upregulates the lipid autophagy marker LC3-II via activation of the PERK pathway. L-Azetidine-2-carboxylic acid increases pro-apoptotic BAX protein. L-Azetidine-2-carboxylic acid induces ATF6 cleavage and upregulates phosphorylated eIF2α levels. L-Azetidine-2-carboxylic acid induces ER stress, inducing protein misfolding and aggregation. L-Azetidine-2-carboxylic acid shows teratogenic, pro-inflammatory and pro-apoptotic effects.

Bifendate (DDB), extracted from Schisandrae chinensis, is an orally active anti-HBV agent against chronic hepatitis B. Bifendate inhibits ATG5-dependent autophagy and attenuates oleic acid-induced lipid accumulation with anti-oxidant properties in vitro. Bifendate can decrease alanine transaminase (ALT) level in mice. Bifendate attenuates hepatic steatosis in cholesterol/bile salt- and high-fat diet-induced hypercholesterolemia in mice. Bifendate potently increases the activity of cytochrome proteins (CYPs) and reverse P-gp-mediated multi-drug resistance (MDR).

Hyaluronic acid (Mw: 1000-2000 Da) is a long-chain unbranched polysaccharide with a molecular weight of 1000-2000 Da. Hyaluronic acid (Mw: 2000 Da) inhibits IL-1β expression and increases LC3-II. Hyaluronic acid (Mw: 1000-2000Da) can regulate tissue homeostasis and stress resistance, promote angiogenesis and tissue remodeling. Hyaluronic acid (Mw: 1000-2000 Da) has good biocompatibility and biodegradability, and can be used in drug delivery systems and tissue engineering. Hyaluronic acid (Mw: 2000 Da) can reduce facial skin blemishes and sagging.

Xylitol can be classified as a polyol and sugar alcohol, exhibiting inhibitory activity on cancer cell proliferation. It induces autophagy (Autophagy) and cell death in A549 cells by activating the autophagy signaling pathway, as evidenced by the increased expression of LC3-II and Atg5-Atg12 upon Xylitol treatment. Additionally, Xylitol inhibits acetaldehyde production by Candida species, thereby reducing their carcinogenic potential. In vivo, Xylitol induces alterations in the gut microbiota of mice, which may enhance cholesterol accumulation and upregulate hepatic ChREBP, while also slowing tumor growth in the B16F10 melanoma C57BL/6 mouse model.

Perfluoroundecanoic acid is a perfluoroalkyl substance (PFAS). Perfluoroundecanoic acid is an orally active oxidative stress inducer. Perfluoroundecanoic acid promotes macrophage M2 polarization, activates Wnt/β-catenin signaling and enhances β-catenin nuclear accumulation. Perfluoroundecanoic acid -induced M2 phenotype macrophage accelerates tumor progression in vitro and in vivo. Perfluoroundecanoic acid induces DNA damage, reproductive and pathophysiological dysfunctions via oxidative stress in male Swiss mice. Perfluoroundecanoic acid inhibits Leydig cell development in pubertal male rats via inducing oxidative stress and autophagy. Perfluoroundecanoic acid accelerates insulitis development in a mouse model of type 1 diabetes. Perfluoroundecanoic acid can be used for the study of ovarian cancer, type 1 diabetes and inflammation.

RNF5 inhibitor inh-02 is a potent inhibitor of E3 ubiquitin ligase RNF5/RMA1. RNF5 inhibitor inh-02 rescues F508del-CFTR function in F508del-CFTR-expressing immortalized cells (CFBE41o⁻, EC₅₀ = 2.6 μM; FRT, EC ₅₀ = 2.2 μM). RNF5 inhibitor inh-02 increases LC3IIB expression and autophagic vacuole number via reducing ATG4B ubiquitylation and promotes cell motility. RNF5 inhibitor inh-02 can be used for the study of cystic fibrosis.

N-Desmethyl clomipramine hydrochloride (Desmethylclomipramine hydrochloride; Norclomipramine hydrochloride) is the orally active major active metabolite of the tricyclic antidepressant Clomipramine (HY-B0457A), possessing multiple activities including anti-inflammatory, antioxidant, antibacterial, and antiparasitic effects. N-Desmethyl clomipramine hydrochloride blocks autophagosome-lysosome fusion, leading to the accumulation of LC3-II, p62, ATG7, WIPI2, and ATG5-12, reactivates the p53/p21 pathway, induces apoptosis through C-PARP and C-CAS3, and inhibits the proliferation, migration, and invasion of renal cancer cells. N-Desmethyl clomipramine hydrochloride inhibits LdTOPIA, inducing R-loop accumulation in the nucleus of Leishmania, ultimately causing parasite death. N-Desmethyl clomipramine hydrochloride can be used for research on depression, metastatic renal cell carcinoma, and leishmaniasis.

Nrf2-IN-4 (Compound PhcY) hydrobromide is a Nrf2 inhibitor. Nrf2-IN-4 hydrobromide induces ferroptosis via NRF2 inhibition. Nrf2-IN-4 hydrobromide disrupts cellular iron homeostasis, facilitates ferritin degradation, and ultimately triggers ferroptosis. Nrf2-IN-4 hydrobromide induces lysosome activation by promoting iron-dependent ROS production and lysosomal acidification. Nrf2-IN-4 hydrobromide demonstrates significant antitumor efficacy. Nrf2-IN-4 hydrobromide can be used for the study of breast cancer.

N-Desmethyl clomipramine-d₃ hydrochloride (Desmethylclomipramine-d₃ hydrochloride; Norclomipramine-d₃ hydrochloride) is the deuterated-labeled N-Desmethyl clomipramine hydrochloride (HY-12388A). N-Desmethyl clomipramine hydrochloride is the orally active major active metabolite of the tricyclic antidepressant Clomipramine (HY-B0457A), possessing multiple activities including anti-inflammatory, antioxidant, antibacterial, and antiparasitic effects. N-Desmethyl clomipramine hydrochloride blocks autophagosome-lysosome fusion, leading to the accumulation of LC3-II, p62, ATG7, WIPI2, and ATG5-12, reactivates the p53/p21 pathway, induces apoptosis through C-PARP and C-CAS3, and inhibits the proliferation, migration, and invasion of renal cancer cells. N-Desmethyl clomipramine hydrochloride inhibits LdTOPIA, inducing R-loop accumulation in the nucleus of Leishmania, ultimately causing parasite death. N-Desmethyl clomipramine hydrochloride can be used for research on depression, metastatic renal cell carcinoma, and leishmaniasis.

Nrf2-IN-4 is a Nrf2 inhibitor. Nrf2-IN-4 induces ferroptosis via NRF2 inhibition. Nrf2-IN-4 disrupts cellular iron homeostasis, facilitates ferritin degradation, and ultimately triggers ferroptosis. Nrf2-IN-4 induces lysosome activation by promoting iron-dependent ROS production and lysosomal acidification. Nrf2-IN-4 demonstrates significant antitumor efficacy. Nrf2-IN-4 can be used for the study of breast cancer.

Atiprimod (Azaspirane) is a STAT3 inhibitor with antitumor, anti-inflammatory, and anti-angiogenic activities. Atiprimod blocks the signaling pathways of IL-6 and VEGF by inhibiting the phosphorylation of signal transducer and activator of STAT3. Atiprimod blocks the JAK-STAT signaling pathway by inhibiting the phosphorylation of JAK2 and JAK3. Atiprimod also inhibits cell proliferation, induces cell cycle arrest, and induces autophagy and apoptosis. Atiprimod triggers persistent ER stress-mediated apoptosis in breast cancer cells by activating the PERK/eIF2α/ATF4/CHOP axis and inhibiting the nuclear translocation of STAT3/NF-κB. Atiprimod shows great anti-tumor activities in tumor xenograft mouse models. Atiprimod can be used for the study of pituitary adenoma, breast cancer, multiple myeloma and acute myeloid leukemia (AML).

N-Desmethyl clomipramine hydrochloride (Standard) (Desmethylclomipramine hydrochloride (Standard); Norclomipramine hydrochloride (Standard)) is the analytical standard of N-Desmethyl clomipramine hydrochloride (HY-12388A). This product is intended for research and analytical applications. N-Desmethyl clomipramine hydrochloride is the orally active major active metabolite of the tricyclic antidepressant Clomipramine (HY-B0457A), possessing multiple activities including anti-inflammatory, antioxidant, antibacterial, and antiparasitic effects. N-Desmethyl clomipramine hydrochloride blocks autophagosome-lysosome fusion, leading to the accumulation of LC3-II, p62, ATG7, WIPI2, and ATG5-12, reactivates the p53/p21 pathway, induces apoptosis through C-PARP and C-CAS3, and inhibits the proliferation, migration, and invasion of renal cancer cells. N-Desmethyl clomipramine hydrochloride inhibits LdTOPIA, inducing R-loop accumulation in the nucleus of Leishmania, ultimately causing parasite death. N-Desmethyl clomipramine hydrochloride can be used for research on depression, metastatic renal cell carcinoma, and leishmaniasis.

Atiprimod (Azaspirane) (dimaleate) is a STAT3 inhibitor with antitumor, anti-inflammatory, and anti-angiogenic activities. Atiprimod blocks the signaling pathways of IL-6 and VEGF by inhibiting the phosphorylation of signal transducer and activator of STAT3. Atiprimod blocks the JAK-STAT signaling pathway by inhibiting the phosphorylation of JAK2 and JAK3. Atiprimod also inhibits cell proliferation, induces cell cycle arrest, and induces autophagy and apoptosis. Atiprimod triggers persistent ER stress-mediated apoptosis in breast cancer cells by activating the PERK/eIF2α/ATF4/CHOP axis and inhibiting the nuclear translocation of STAT3/NF-κB. Atiprimod shows great anti-tumor activities in tumor xenograft mouse models. Atiprimod can be used for the study of pituitary adenoma, breast cancer, multiple myeloma and acute myeloid leukemia (AML).

SHP2 protein degrader-3 is a SHP2 AUTAC degrader. SHP2 protein degrader-3 shows dose-dependent SHP2 degradation ability (DC₅₀ = 3.22 μM) and anti-tumor activity (IC₅₀ = 5.59 μM) in HeLa cells. SHP2 protein degrader-3 induces degradation through the LC3-mediated autophagy pathway, which can be inhibited by lysosome inhibitors. SHP2 protein degrader-3 induces apoptosis in various cancer cells (HeLa cells, HepG2 cells, LoVo cells, Huh-7 cells) (SHP2 Ligand : (HY-100388); LC3 Ligand: (HY-10542); Linker : (HY-128834)).

TrxR-IN-2 is a thioredoxin reductase (TrxR) inhibitor. TrxR-IN-2 increases reactive oxidative species (ROS) levels and decreases mitochondrial transmembrane potential levels. TrxR-IN-2 triggers DNA damage via H2AX regulation, and induces autophagy via LC3, beclin-1, and p62 regulation. TrxR-IN-2 can be used for the research of drug-resistant hepatocellular carcinoma^[1].

EGFR/tubulin-IN-1 (Compound 26) is a dual-target inhibitor of EGFR and tubulin. EGFR/tubulin-IN-1 significantly reduces the levels of p-EGFR, p-AKT, and p-ERK in cells, disrupting the microtubule structure of the cells. EGFR/tubulin-IN-1 significantly inhibits the proliferation of H1975 cells and significantly blocks the cells in the G2/M phase. EGFR/tubulin-IN-1 induces the expression of autophagy markers LC3B-II and Beclin-1, while down-regulating the expression of p62. EGFR/tubulin-IN-1 induces ferroptosis, with increased ROS content and depletion of glutathione (GSH). EGFR/tubulin-IN-1 inhibits epithelial-mesenchymal transition (EMT) and tumor metastasis. EGFR/tubulin-IN-1 has a significant tumor-suppressing effect in the H1975 transplanted tumor nude mouse model. EGFR/tubulin-IN-1 can be used for the study of non-small cell lung cancer.

N-Desmethyl clomipramine (Desmethylclomipramine; Norclomipramine) is the orally active major active metabolite of the tricyclic antidepressant Clomipramine (HY-B0457A), possessing multiple activities including anti-inflammatory, antioxidant, antibacterial, and antiparasitic effects. N-Desmethyl clomipramine blocks autophagosome-lysosome fusion, leading to the accumulation of LC3-II, p62, ATG7, WIPI2, and ATG5-12, reactivates the p53/p21 pathway, induces apoptosis through C-PARP and C-CAS3, and inhibits the proliferation, migration, and invasion of renal cancer cells. N-Desmethyl clomipramine inhibits LdTOPIA, inducing R-loop accumulation in the nucleus of Leishmania, ultimately causing parasite death. N-Desmethyl clomipramine can be used for research on depression, metastatic renal cell carcinoma, and leishmaniasis.

NCO-90 is a selective SIRT2 inhibitor with an IC₅₀ of 1.0 μM. NCO-90 induces Apoptosis via Caspase activation and mitochondrial superoxide anion production, and also induces Autophagic cell death by increasing LC3-II levels and autophagosome accumulation. NCO-90 exhibits anticancer activity against leukemia. NCO-90 can be used in research related to acute lymphoblastic leukemia and acute myeloid leukemia.

PY-Alo is a DNA intercalator with a K_a of 3.46 × 10⁵ M⁻¹. PY-Alo induces DNA damage through backbone intercalation and non-covalent hydrogen bonding, downregulates the transcription of key genes in mitochondrial oxidative phosphorylation, and disrupts mitochondrial homeostasis, thereby synergistically inducing apoptosis (apoptosis) and autophagy (autophagy) in cells. PY-Alo exhibits cytotoxicity against both wild-type and Cisplatin (HY-17394)-resistant ovarian cancer cells. PY-Alo can be used for research on ovarian cancer.

ICSN3250 hydrochloride is a halitulin analogue and a mTORC1 inhibitor. ICSN3250 hydrochloride directly binds to mTOR's FRB domain and displaces phosphatidic acid (PA), reversing mTORC1 activation. ICSN3250 hydrochloride shows high cytotoxicity in cancer cells (nanomolar concentration) through a caspase-independent cell death mechanism. ICSN3250 hydrochloride specifically inhibits the mTORC1 pathway, inducing autophagy and G0-G1 cell-cycle arrest in cancer cells. ICSN3250 hydrochloride can be used for the study of cancer .