Atg8/LC3

Autophagy-related 8;

Autophagy-related 8 proteins (Atg8s) are one of the 62 highly conserved eukaryote-specific protein families. Whereas yeast and other fungal species have a single Atg8 gene, multicellular animals, green plants and some protists have several. Animal Atg8 proteins comprise three subfamilies: microtubule-associated protein 1 light chain 3 (MAP1LC3, hereafter referred to as LC3), γ-aminobutyric acid receptor-associated protein (GABARAP) and Golgi-associated ATPase enhancer of 16 kDa (GATE-16).

Atg8 family members are expressed in various tissues, where they participate in multiple cellular processes, such as intracellular membrane trafficking and autophagy. Their role in autophagy has been intensively studied. Atg8 proteins undergo a unique ubiquitin-like conjugation to phosphatidylethanolamine on the autophagic membrane, a process essential for autophagosome formation.

Atg8/LC3 Related Products (71):

By Effects:	Inhibitors (7) Ligand (1) Activators (21) Modulators (2) Inducers (3)

Cat. No.	Product Name	Effect	Purity	Chemical Structure

HY-146131

ATG7-IN-3		99.26%
ATG7-IN-3 (Compound 18) is a potent ATG7 inhibitor with an IC₅₀ of 0.048 μM. ATG7-IN-3 inhibits Autophagy. ATG7-IN-3 inhibits the formation of LC3B puncta. ATG7-IN-3 can be used in the researches of glioma and colon cancer.

HY-N4180

Pennogenin 3-O-beta-chacotrioside		99.91%
Pennogenin 3-O-beta-chacotrioside is an autophagy (autophagy) inducer. Pennogenin 3-O-beta-chacotrioside exhibits strong binding affinity for the pro-apoptotic proteins CYTC, AIF1 and BAX. Pennogenin 3-O-beta-chacotrioside triggers reactive oxygen species-induced autophagy in cancer cells. Pennogenin 3-O-beta-chacotrioside can be used in studies related to colorectal cancer.

HY-123967

RNF5 inhibitor inh-02	Activator	99.91%
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.

HY-N1163

Tetrahydroalstonine	Inhibitor	99.88%
Tetrahydroalstonine ((-)-Tetrahydroalstonine) is an indole alkaloid and a selective α₂-adrenergic receptor antagonist. Tetrahydroalstonine exhibits certain neuroprotective effects. Tetrahydroalstonine can regulate autophagy-lysosomal function by activating the Akt/mTOR pathway, significantly reducing OGD/R-induced primary cortical neuronal injury.

HY-146052

Autophagy inducer 3		98.02%
Autophagy inducer 3 has autophagy induced activity. Autophagy inducer 3 possesses robust autophagic cell death in diverse cancer cells sparing normal counterpart. Autophagy inducer 3 induces lethal autophagy by formation of characteristic autophagic vacuoles, LC3 puncta formation, upregulation of signature autophagy markers like Beclin and Atg family proteins.

HY-W142432

Perfluoroundecanoic acid	Activator	99.85%
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.

HY-163001

Microcolin H		99.13%
Microcolin H is a marine lipopeptide and phosphatidylinositol transfer protein ligand that targets PITPα/β. Microcolin H increases the conversion of LC3I to LC3II and reduces p62 levels in cancer cells, leading to autophagy cell death (Autophagy). Microcolin H effectively inhibits tumor development and has anti-proliferative activity in nude mouse subcutaneous tumor models.

HY-B0113R

Omeprazole (Standard)
Omeprazole (Standard) is the analytical standard of Omeprazole. This product is intended for research and analytical applications. Omeprazole (H 16868) is an orally active H⁺,K⁺-ATPase inhibitor and a proton pump inhibitor. Omeprazole competitively inhibits CYP2C19, CYP3A4, and CYP2C9 activity. Omeprazole inhibits gastric acid secretion and can be used for acid-related gastrointestinal disorders. Omeprazole inhibits pancreatic cancer cell proliferation, induces apoptosis, autophagosome accumulation (elevated LC3-I and LC3-II levels), oxidative stress, and cytogenetic imbalance, modulates lysosomal transport, reduces inflammatory cytokines. Omeprazole alters small intestinal morphology and magnesium absorption, and induces gastric mucosa morphologic changes. Omeprazole aslo has neuroprotective and antibacterial effects.

HY-101535

ARP101		99.39%
ARP101 is a potent and selective inhibitor matrix metalloproteinase-2 (MMP-2). ARP101 induces autophagy-associated cell death in cancer cells. ARP101 is effective in inducing the formation of autophagosome and conversion of LC3I into LC3II.

HY-B0113S

Omeprazole-d₃		98.99%
Omeprazole-d₃ (H 16868-d₃) is deuterium labeled Omeprazole. Omeprazole (H 16868) is an orally active H⁺,K⁺-ATPase inhibitor and a proton pump inhibitor. Omeprazole competitively inhibits CYP2C19, CYP3A4, and CYP2C9 activity. Omeprazole inhibits gastric acid secretion and can be used for acid-related gastrointestinal disorders. Omeprazole inhibits pancreatic cancer cell proliferation, induces apoptosis, autophagosome accumulation (elevated LC3-I and LC3-II levels), oxidative stress, and cytogenetic imbalance, modulates lysosomal transport, reduces inflammatory cytokines. Omeprazole alters small intestinal morphology and magnesium absorption, and induces gastric mucosa morphologic changes. Omeprazole aslo has neuroprotective and antibacterial effects.

HY-B0113S3

Omeprazole-¹³C,d₃		98.00%
Omeprazole-¹³C,d₃ is a ¹³C-labeled and deuterium labeled Omeprazole. Omeprazole (H 16868) is an orally active H⁺,K⁺-ATPase inhibitor and a proton pump inhibitor. Omeprazole competitively inhibits CYP2C19, CYP3A4, and CYP2C9 activity. Omeprazole inhibits gastric acid secretion and can be used for acid-related gastrointestinal disorders. Omeprazole inhibits pancreatic cancer cell proliferation, induces apoptosis, autophagosome accumulation (elevated LC3-I and LC3-II levels), oxidative stress, and cytogenetic imbalance, modulates lysosomal transport, reduces inflammatory cytokines. Omeprazole alters small intestinal morphology and magnesium absorption, and induces gastric mucosa morphologic changes. Omeprazole aslo has neuroprotective and antibacterial effects.

HY-P991570

Zaptuzumab	Inhibitor	99.0%
Zaptuzumab (AD5-10) is a DR5-specific humanized monoclonal antibody that selectively binds to DR5 with high affinity. Zaptuzumab specifically induces cancer cell death by both caspase-apoptosis and autophagic cell death (ACD). Zaptuzumab activates both ADCC and CDC. Zaptuzumab induces ROS generation and GSH level reduction. Zaptuzumab shows a significant suppression of the tumor growth and good safety in various xenografts mice tumor models.

HY-N6651

Isocryptotanshinone		≥98.0%
Isocryptotanshinone is a dual STAT3 and PTP1B (IC₅₀ = 56.1 μM) inhibitor. Isocryptotanshinone inhibits STAT3 by binding to the STAT3 SH2 domain to block phosphorylation and nuclear translocation^[1][2]. Isocryptotanshinone exerts its anti-proliferative effect via the induction of cell cycle arrest, apoptosis, and pro-death autophagy, through the regulation of STAT3, AKT/mTOR and MAPK signaling pathways. Isocryptotanshinone suppresses the xenograft gastric cancer (GC) tumor growth in BALB/c nude mice. Isocryptotanshinone can be used for cancer research, such as lung cancer, breast cancer and GC.

HY-W010201R

Citronellol (Standard)	Inhibitor
Citronellol (Standard) is the analytical standard of Citronellol. Citronellol (Standard) is an orally active inducer of apoptosis. Citronellol (Standard) can prevent oxidative stress, mitochondrial dysfunction, and apoptosis in the SH-SY5Y cell Parkinson's disease model induced by 6-OHDA by regulating the ROS-NO, MAPK/ERK, and PI3K/Akt signaling pathways. Citronellol (Standard) can induce necroptosis in human lung cancer cells through the TNF-α pathway and accumulation of ROS. Citronellol (Standard) can reduce the levels of LC-3 and p62 to regulate the autophagy pathway, inhibit oxidative stress and neuroinflammation, and thus have neuroprotective effects on Parkinson's rats. Citronellol (Standard) exhibits anti-fungal activity against Trichophyton rubrum by inhibiting ergosterol synthesis.

HY-175209

Nrf2-IN-4	Activator
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.

HY-I0501R

2'-Aminoacetophenone (Standard)	Inhibitor
2'-Aminoacetophenone (Standard) is the analytical standard of 2'-Aminoacetophenone. This product is intended for research and analytical applications. 2'-Aminoacetophenone is an orally active inducer of apoptosis and respiratory biomarker. 2'-Aminoacetophenone can be used to detect Pseudomonas aeruginosa infections in the lungs of cystic fibrosis patients. 2'-Aminoacetophenone can inhibit the protein levels of LC3BII and p62 in macrophages infected with pqsA or mvfR and regulate autophagy. 2'-Aminoacetophenone can disrupt mitochondrial function by inducing oxidative stress and apoptosis signaling, leading to dysfunction in mouse skeletal muscle.

HY-13559

Atiprimod	Activator
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).

HY-10542A

(Z)-GW 5074
(Z)-GW 5074 is a compound which interacts with both mHTT (mutant huntingtin protein) and LC3, but not but not with the wild-type HTT protein. (Z)-GW 5074 inhibits c-Raf, shows no effect on autophagy, and is effective for neurodegenerative disorder.

HY-109546

Omeprazole magnesium
Omeprazole (H 16868) magnesium is an orally active H⁺,K⁺-ATPase inhibitor and a proton pump inhibitor. Omeprazole magnesium competitively inhibits CYP2C19, CYP3A4, and CYP2C9 activity. Omeprazole magnesium inhibits gastric acid secretion and can be used for acid-related gastrointestinal disorders. Omeprazole magnesium inhibits pancreatic cancer cell proliferation, induces apoptosis, autophagosome accumulation (elevated LC3-I and LC3-II levels), oxidative stress, and cytogenetic imbalance, modulates lysosomal transport, reduces inflammatory cytokines. Omeprazole magnesium alters small intestinal morphology and magnesium absorption, and induces gastric mucosa morphologic changes. Omeprazole magnesium aslo has neuroprotective and antibacterial effects.

HY-13559A

Atiprimod dimaleate	Activator
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).

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