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Results for "

LC3-II

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Akt (1) AMPK (1) Anaplastic lymphoma kinase (ALK) (1) Apoptosis (5) ATF6 (1) Atg7 (1) Atg8/LC3 (6) Autophagy (14) Bacterial (1) Bcl-2 Family (2) CaMK (1) Caspase (1) Cathepsin (2) Endogenous Metabolite (2) Eukaryotic Initiation Factor (eIF) (1) Ferroptosis (1) Filovirus (1) Hedgehog (1) JNK (1) MMP (1) mTOR (1) NAMPT (1) Necroptosis (1) p38 MAPK (1) p62 (2) Parasite (1) PERK (1) Phosphatase (1) Pim (1) Reactive Oxygen Species (2) RIP kinase (1) TGF-β Receptor (1) TrxR (1) ULK (1)
By Research Areas:	Cancer (16) Cardiovascular Disease (1) Endocrinology (1) Infection (1) Inflammation/Immunology (3) Metabolic Disease (3) Neurological Disease (3)
Oligonucleotides:	Fillers (1)

Inhibitors & Agonists

Biochemical Assay Reagents

Peptides

Natural
Products

Oligonucleotides

Targets Recommended: Photosystem II CD74

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-101535

ARP101 1 Publications Verification	Atg8/LC3 MMP	Cancer
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-163001

Microcolin H	Autophagy p62 Atg8/LC3	Cancer
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-W050044

L-Azetidine-2-carboxylic acid	Endogenous Metabolite PERK Atg8/LC3 Autophagy Bcl-2 Family Apoptosis Eukaryotic Initiation Factor (eIF) ATF6	Cardiovascular Disease Neurological Disease Metabolic Disease Endocrinology Cancer
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 ^[3] .

HY-P4532

Ac-Leu-Val-Lys-Aldehyde	Cathepsin	Neurological Disease
Ac-Leu-Val-Lys-Aldehyde is a potent cathepsin B inhibitor with IC₅₀s of 4 nM. Ac-Leu-Val-Lys-Aldehyde significantly reduces quinolinic acid (HY-100807)-induced striatal cell death and causes accumulation of LC3-II .

HY-111287

Autophagonizer DK-1-49	Autophagy	Cancer
Autophagonizer (DK-1-49) is a small molecule autophagy inducer that results in an accumulation of autophagy-associated LC3-II and enhances levels of autophagosomes and acidic vacuoles. Autophagonizer inhibits cell viability and induces cell death in not only cancer cells but also Bax/Bak double-knockout cells with EC₅₀ values of 3-4 μM .

HY-168206

Autophagy-IN-6	Autophagy	Cancer
Autophagy-IN-6 (compound 1u) is a lysosomotropic autophagy inhibitor and can induces LC3-II protein accumulation. Autophagy-IN-6 shows anti-proliferative activity .

HY-168640

RIP3 activator 1	Autophagy Necroptosis RIP kinase	Cancer
RIP3 activator 1 (compound C8) is a potent *RIP3* activator. RIP3 activator 1 inhibits cell growth. RIP3 activator 1 induces necroptosis through the RIP3/p62/Keap1 signaling pathway. RIP3 activator 1 increases the protein expression of p-MLKL. RIP3 activator 1 induces autophagy. RIP3 activator 1 increases accumulation of LC3-II and p62 protein expression .

HY-146307

TrxR-IN-3	TrxR	Cancer
TrxR-IN-3 (Compound 2c) is a potent inhibitor of TrxR. TrxR-IN-3 exhibits potent antiproliferative activities against five human cancer cell lines, especially against breast tumor cells. TrxR-IN-3 increases ROS levels and resulted in marked apoptosis by regulating apoptosis-related proteins expressed in the breast cancer cells. TrxR-IN-3 also triggers the formation of autophagosomes and autolysosomes by promoting the expression of LC3-II and Beclin-1 and diminishing the expression of LC3-I and p62 proteins .

HY-P3148

Astin B	p62 Atg8/LC3 Apoptosis Autophagy Reactive Oxygen Species JNK Bcl-2 Family Caspase	Metabolic Disease
Astin B is a orally active and potent cyclic pentapeptide, that can be isolated from Aster tataricus. Astin B has hepatotoxic effects in vitro and in vivo and that hepatic injury was primarily mediated by apoptosis in a mitochondria/caspase-dependent manner. Astin B induces autophagy in L-02 cells, increases LC3-II and decreases p62 expression .

HY-16121

CAA-0225	Cathepsin	Others
CAA-0225 is a tissue protease L inhibitor that inhibits rat liver tissue protease L with a IC₅₀ value of 1.9 nM. CAA-0225 can participate in the degradation of autophagosome membrane markers LC3-II and GABARAP (HY-P72639), improve cardiac function in mice with reperfusion injury, and kill and eliminate Trypanosoma brucei parasites ^[1][2][3].

HY-N0538

Xylitol Xylite	Autophagy Endogenous Metabolite Bacterial Atg7 Atg8/LC3	Metabolic Disease Cancer
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 ^[3] .

HY-111137

Puquitinib XC-302 free base	Akt	Cancer
Puquitinib (XC-302 free base) is a multi-target inhibitor with the activity of inducing autophagy in nasopharyngeal carcinoma cells by inhibiting the PI3K/AKT/mTOR signaling pathway. Puquitinib was able to inhibit the proliferation of CNE-2 cells, showing a dose-dependent antiproliferative effect. Puquitinib induced the formation of autophagosomes and autolysosomes in CNE-2 cells, which were observed by fluorescence microscopy and electron microscopy. Puquitinib promoted the formation of LC3-II and increased the expression of beclin 1, while reducing the level of p62. Puquitinib inhibited the PI3K/AKT/mTOR pathway by reducing the expression of p-AKT and p-mTOR. Puquitinib also induced apoptosis in CNE-2 cells, and when autophagy was inhibited, the apoptosis rate was reduced, which means that autophagy may interact with apoptosis to induce cell death .

HY-112624K

Dextran T5 (MW 5,000) Dextran 5; Dextran D5; Dextran T5(MW 4500-5500)	Apoptosis Autophagy	Others
Dextran T5 (MW 5,000) is a sulfated polysaccharide anti-apoptotic and autophagic agent. Dextran T5 (MW 5,000) has sulfated groups and interacts with cell membranes by mimicking endogenous glycosaminoglycans, inhibiting the mitochondrial apoptotic pathway and delaying DNA fragmentation to exert anti-apoptotic activity. Dextran T5 (MW 5,000) also promotes the conversion of LC3-I to LC3-II and the formation of autophagosomes to activate the autophagic pathway. Dextran T5 (MW 5,000) can prolong the survival cycle of CHO cells and increase the production of recombinant erythropoietin (EPO). The Dextran series of compounds are also natural polysaccharide drug carriers that can be connected to drugs through covalent bonding methods such as ester bonds, amide bonds or click chemistry, or self-assembled to form carriers such as nanoparticles and hydrogels. Dextran is biodegradable and biocompatible, and can achieve targeted delivery and controlled release of drugs. Dextran derivatives can prolong drug half-life, increase local concentration and reduce immune clearance activity. The Dextran series of compounds are also natural polysaccharide drug carriers that can be connected to drugs through covalent bonding methods such as ester bonds, amide bonds or click chemistry, or self-assembled to form carriers such as nanoparticles and hydrogels. Dextran is biodegradable and biocompatible, and can achieve targeted delivery and controlled release of drugs. Dextran derivatives can prolong the half-life of drugs, increase local concentrations, and reduce the activity of immune clearance ^[3].

HY-125535

OSU-53	AMPK mTOR Autophagy Atg8/LC3	Cancer
OSU-53 is an orally active AMPK activator (EC₅₀: 0.3 μM) and a direct mTOR inhibitor. OSU-53 induces autophagy and increases conversion of LC3 I to LC3 II. OSU-53 also modulates energy homeostasis by suppressing fatty acid biosynthesis and shifting the metabolism to oxidation by up-regulating the expression of PGC1α and NRF-1. OSU-53 has antitumor activity in various tumor models, such as breast cancer and thyroid cancer .

HY-N8678

Thonningianin B	Autophagy	Neurological Disease
Thonningianin B is an antioxidant and an autophagy enhancer .

HY-100515

Robotnikinin 3 Publications Verification	Hedgehog	Inflammation/Immunology
Robotnikinin is a small molecule capable of binding to and inhibiting the activity of Sonic Hedgehog (Shh) signaling up stream of Smo .

HY-14374

GPP78 1 Publications Verification CAY10618	NAMPT Autophagy	Inflammation/Immunology Cancer
GPP78 (CAY10618) is a potent Nampt inhibitor with an IC₅₀ of 3.0 nM for nicotinamide adenine dinucleotide (NAD) depletion. GPP78 is cytotoxic to neuroblastoma cell line SH-SY5Y cells with an IC₅₀ of 3.8 nM by inducing autophagy. GPP78 has anti-cancer and anti-inflammatory effects .

HY-122571

Retro-2 1 Publications Verification	Filovirus Parasite Autophagy	Infection Cancer
Retro-2 is a selective inhibitor of retrograde protein trafficking at the endosome-trans-Golgi network interface. Retro-2 is an ebolavirus (EBOV) infection inhibitor with an EC₅₀ of 12.2 µM in HeLa cells. Retro-2 induces cell autophagy ^[3].

HY-129163

HJ-PI01 1 Publications Verification 10-Acetylphenoxazine	Pim	Cancer
HJ-PI01 (10-Acetylphenoxazine) is an orally active Pim-2 inhibitor. HJ-PI01 induces apoptosis and autophagic cell death of cancer cells. HJ-PI01 inhibits tumor growth in MDA-MB-231 xenograft mice. HJ-PI01 can be used for cancer research .

HY-158108

anti-TNBC agent-6	Autophagy Ferroptosis Reactive Oxygen Species	Cancer
anti-TNBC agent-6 (compound pt-3) is a potent anti-TNBC agent. anti-TNBC agent-6 shows cytotoxic activity. anti-TNBC agent-6 induces autophagy and ferroptosis. anti-TNBC agent-6 enhances intracellular ROS accumulatio. anti-TNBC agent-6 shows anti tumor activity and has the potential for the research of breast cancer .

HY-137506

XST-14 1 Publications Verification	ULK p38 MAPK TGF-β Receptor Anaplastic lymphoma kinase (ALK) CaMK Apoptosis	Cancer
XST-14 is a potent, competitive and highly selective ULK1 inhibitor with an IC₅₀ of 26.6 nM. XST-14 induces autophagy inhibition by reducing the phosphorylation of the ULK1 downstream substrate. XST-14 induces apoptosis in hepatocellular carcinoma (HCC) cells and has antitumor effects .

HY-124896

Bonannione A 6-Geranylnaringenin; Mimulone	Phosphatase Apoptosis Autophagy	Inflammation/Immunology Cancer
Bonannione A (6-Geranylnaringenin; Mimulone), a prenylflavonoid, is an orally active and potent protein tyrosine phosphatase 1B (PTP1B) inhibitor with an IC₅₀ of 14 µM. Bonannione A triggers caspase-dependent apoptosis. Bonannione A induces autophagy through p53-mediated AMPK/mTOR pathway. Bonannione A shows anti-inflammatory, antiradical and anti-cancer activity ^[3].

Cat. No.	Product Name	Type

HY-112624K

Dextran T5 (MW 5,000) Dextran 5; Dextran D5; Dextran T5(MW 4500-5500)	Thickeners
Dextran T5 (MW 5,000) is a sulfated polysaccharide anti-apoptotic and autophagic agent. Dextran T5 (MW 5,000) has sulfated groups and interacts with cell membranes by mimicking endogenous glycosaminoglycans, inhibiting the mitochondrial apoptotic pathway and delaying DNA fragmentation to exert anti-apoptotic activity. Dextran T5 (MW 5,000) also promotes the conversion of LC3-I to LC3-II and the formation of autophagosomes to activate the autophagic pathway. Dextran T5 (MW 5,000) can prolong the survival cycle of CHO cells and increase the production of recombinant erythropoietin (EPO). The Dextran series of compounds are also natural polysaccharide drug carriers that can be connected to drugs through covalent bonding methods such as ester bonds, amide bonds or click chemistry, or self-assembled to form carriers such as nanoparticles and hydrogels. Dextran is biodegradable and biocompatible, and can achieve targeted delivery and controlled release of drugs. Dextran derivatives can prolong drug half-life, increase local concentration and reduce immune clearance activity. The Dextran series of compounds are also natural polysaccharide drug carriers that can be connected to drugs through covalent bonding methods such as ester bonds, amide bonds or click chemistry, or self-assembled to form carriers such as nanoparticles and hydrogels. Dextran is biodegradable and biocompatible, and can achieve targeted delivery and controlled release of drugs. Dextran derivatives can prolong the half-life of drugs, increase local concentrations, and reduce the activity of immune clearance ^[3].

Dextran T5 (MW 5,000)

Dextran 5; Dextran D5; Dextran T5(MW 4500-5500)

Thickeners

Dextran T5 (MW 5,000) is a sulfated polysaccharide anti-apoptotic and autophagic agent. Dextran T5 (MW 5,000) has sulfated groups and interacts with cell membranes by mimicking endogenous glycosaminoglycans, inhibiting the mitochondrial apoptotic pathway and delaying DNA fragmentation to exert anti-apoptotic activity. Dextran T5 (MW 5,000) also promotes the conversion of LC3-I to LC3-II and the formation of autophagosomes to activate the autophagic pathway. Dextran T5 (MW 5,000) can prolong the survival cycle of CHO cells and increase the production of recombinant erythropoietin (EPO). The Dextran series of compounds are also natural polysaccharide drug carriers that can be connected to drugs through covalent bonding methods such as ester bonds, amide bonds or click chemistry, or self-assembled to form carriers such as nanoparticles and hydrogels. Dextran is biodegradable and biocompatible, and can achieve targeted delivery and controlled release of drugs. Dextran derivatives can prolong drug half-life, increase local concentration and reduce immune clearance activity. The Dextran series of compounds are also natural polysaccharide drug carriers that can be connected to drugs through covalent bonding methods such as ester bonds, amide bonds or click chemistry, or self-assembled to form carriers such as nanoparticles and hydrogels. Dextran is biodegradable and biocompatible, and can achieve targeted delivery and controlled release of drugs. Dextran derivatives can prolong the half-life of drugs, increase local concentrations, and reduce the activity of immune clearance ^[3].

Cat. No.	Product Name	Target	Research Area