Autophagy Activator

Semaglutide is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer.

Chlorpromazine is an orally active, blood-brain barrier-transparent antipsychotic agent that effectively antagonises D2 dopamine receptors and 5-HT_2A, which is widely used in schizophrenia and other psychiatric disorders. Chlorpromazine exerts anti-cancer activity through a variety of pathways, including anti-proliferation, induction of autophagy and cycle arrest (G2-M phase), inhibition of cytochrome c oxidase (CcO), inhibition of tumour growth and metastasis, and inhibition of tumour immune escape. Chlorpromazine also blocks hNa_v1.7 channels (IC₅₀=25.9 μM; concentration-dependent) and HERG potassium channels (IC₅₀=21.6 μM), which has potential for analgesic and cardiac arrhythmic studies. Chlorpromazine also can inhibit clathrin-mediated endocytosis.

EIPA (L593754) is an orally active TRPP3 channel inhibitor with an IC₅₀ of 10.5 μM. EIPA also enhances autophagy by inhibiting Na⁺/H⁺-exchanger 3 (NHE3). EIPA inhibits macropinocytosis as well. EIPA can be used in the research of inflammation and cancers, such as gastric cancer, colon carcinoma, pancreatic carcinoma.

PX-478 is a multifunctional HIF-1α inhibitor with properties including radiosensitization, autophagy activation, and lipid accumulation inhibition. PX-478 also blocks hypoxia-induced VEGF production and regulates β-cell phenotypes under hypoxic conditions. PX-478 induces cell cycle arrest and DNA damage, restores autophagic function, reduces foam cell formation, and maintains glucose homeostasis. PX-478 is widely used in research on related diseases such as human tumors (e.g., prostate cancer), type 2 diabetes, and atherosclerosis.

Sodium propionate is an orally active short-chain fatty acid. Sodium propionate can be produced by intestinal bacteria from the metabolism of dietary fiber. Sodium propionate increases PPAR-γ, inhibits NF-κB activation, and reduces COX-2 expression and NO production. Sodium propionate also induces Apoptosis and Autophagy. Sodium propionate reduces HSV-1-induced keratitis. Sodium propionate has anticancer effects against glioblastoma. Sodium propionate exhibits neuroprotective, antioxidant, and anti-inflammatory activities. Sodium propionate can be used in the research of spinal cord injury and Alzheimer's disease.

Isoginkgetin is a pre-mRNA splicing inhibitor inhibitor. Isoginkgetin also inhibits activities of both Akt, NF-κB and MMP-9. Isoginkgetin inhibits the activity of the 20S proteasome, induces apoptosis and activates autophagy.

EN6 is a small-molecule in vivo autophagy activator that covalently targets cysteine 277 in the ATP6V1A subunit of the lysosomal v-ATPase. EN6-mediated modification of ATP6V1A uncouples v-ATPase from Rag, leading to inhibition of mTORC1 signalling, increased lysosomal acidification, and activation of autophagy. EN6 also scavenges TDP-43 aggregates (causative agents of frontotemporal dementia) in a lysosome-dependent manner.

Semaglutide TFA is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide TFA promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide TFA also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide TFA has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide TFA can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer.

EIPA (L593754) hydrochloride is an orally active TRPP3 channel inhibitor with an IC₅₀ of 10.5 μM. EIPA hydrochloride also enhances autophagy by inhibiting Na⁺/H⁺-exchanger 3 (NHE3). EIPA hydrochloride inhibits macropinocytosis as well. EIPA hydrochloride can be used in the research of inflammation and cancers, such as gastric cancer, colon carcinoma, pancreatic carcinoma.

Tubeimoside I is an orally active HSPD1 inhibitor. Tubeimoside I inhibits NF-κB, MAPK, as well as regulates eNOS-VEGF. Tubeimoside I induces cytoprotective Autophagy via an Akt-mediated pathway. Tubeimoside I inhibits proinflammatory cytokine (IL-6 and IL-1β) production. Tubeimoside I exhibits anti-inflammatory activities. Tubeimoside I promotes angiogenesis and improves sepsis symptoms. Tubeimoside I is used in the research of inflammatory diseases, various cancers, sepsis and ischemic diseases.

Semaglutide acetate is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide acetate promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide acetate also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide acetate has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide acetate can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer.

Ketanserin is a selective 5-HT2 receptor antagonist. Ketanserin also blocks hERG current (I_hERG) in a concentration-dependent manner (IC₅₀=0.11 μM).

Phytic acid (myo-Inositol; hexakis dihydrogen phosphate; Inositol hexaphosphate) sodium salt is an orally active compound. Phytic acid sodium salt can be derived from the seeds of legumes. Phytic acid sodium salt is a [PO4]³- storage depot and precursor for other inositol phosphates and pyrophosphates. Phytic acid sodium salt attenuates Aβ oligomers and upregulates autophagy protein. Phytic acid sodium salt can be used in cardiovascular disease, metabolic disease, nervous system disease and cancer research.

9''-Methyl salvianolate B (MSB) is a blood-brain barrier-permeable inhibitor with high affinity for g5Rp, with a K_d value of 117 nM against African swine fever virus (ASFV) g5Rp. 9''-Methyl salvianolate B also acts as a ZBP1 inhibitor. It exhibits strong binding affinity to key proteins in the PPARγ/NF-κB pathway. 9''-Methyl salvianolate B blocks the interaction between ASFV g5Rp and host proteins eIF5A or RPS15. It restores hypusination modification of eIF5A, promotes autophagy (Autophagy), and inhibits ASFV replication. 9''-Methyl salvianolate B effectively disrupts ZBP1-mediated PANoptosome assembly. It effectively alleviates myocardial ischemia/reperfusion injury. 9''-Methyl salvianolate B can be used in studies related to African swine fever.

Cephalin form bovine brain is an orally active phospholipid widely present in organisms.Cephalin form bovine brain participates in the formation of autophagosome membrane as a lipid anchor of autophagy-related protein Atg8/LC3. Cephalin form bovine brain enhances Autophagic flux, promotes cell differentiation, regulates lipid droplet fusion, delays aging, and also affects lipid metabolism and membrane integrity.

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.

Plantamajoside is an orally active phenylpropanoid glycoside. Plantamajoside can be isolated from Plantago asiatica L.(Plantaginaceae). Plantamajoside inactivates NF-κB, PI3K/akt, induces Apoptosis, and improves Autophagy. Plantamajoside regulates MAPK, integrin-linked kinase/c-Src. Plantamajoside inhibits multiple cancers, improves lung and kidney damage. Plantamajoside has neuroprotective and anti-inflammatory effects.

Cilengitide is a potent and selective integrin inhibitor for α_vβ₃ and α_vβ₅ receptor, with IC₅₀ values of 4 nM and 79 nM, respectively.

BV02 is a 14-3-3 inhibitor and an antibacterial agent. BV02 enhances the cleavage of PARP and caspase-3. BV02 induces Apoptosis, Autophagy, and enhances Akt activation. BV02 has anti-B. melitensis infection and epilepsy-promoting effects. BV02 can also be used in colitis research.

Samotolisib (LY3023414) potently and selectively inhibits class I PI3K isoforms, DNA-PK, and mTORC1/2 with IC₅₀s of 6.07 nM, 77.6 nM, 38 nM, 23.8 nM, 4.24 nM and 165 nM for PI3Kα, PI3Kβ, PI3Kδ, PI3Kγ, DNA-PK and mTOR, respectively. Samotolisib potently inhibits mTORC1/2 at low nanomolar concentrations.