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MPP+ iodide, a toxic metabolite of the neurotoxin MPTP, causes symptom of Parkinson's disease in animal models by selectively destroying dopaminergic neurons in substantia nigra. MPP+ iodide is taken up by the dopamine transporter into dopaminergic neurons where it exerts its neurotoxic action on mitochondria by affecting complexI of the respiratory chain. MPP+ iodide is also a high affinity substrate for the serotonin transporter (SERT) .
Phenformin (Phenethylbiguanide) hydrochloride is an orally active biguanide hypoglycemic agent. Phenformin hydrochloride inhibits mitochondrial respiratory chain complexI, leading to an increased AMP/ATP ratio, activation of AMPK, and subsequent inhibition of the mTOR pathway, thereby suppressing cell proliferation, inducing apoptosis and autophagy. Phenformin hydrochloride inhibits cancer stem cells (CSCs) and possesses potent antitumor potential .
Phenformin (Phenethylbiguanide) is an orally active biguanide hypoglycemic agent. Phenformin inhibits mitochondrial respiratory chain complexI, leading to an increased AMP/ATP ratio, activation of AMPK, and subsequent inhibition of the mTOR pathway, thereby suppressing cell proliferation, inducing apoptosis and autophagy. Phenformin inhibits cancer stem cells (CSCs) and possesses potent antitumor potential .
CMIT/MIT is a CMIT and MIT mixture. CMIT and MIT are powerful synthetic biocidal substances. CMIT and MIT are used as preservatives in various cosmetics and industrial products. CMIT and MIT are present in many water-soluble consumer products, such as shampoos, toothpastes. CMIT/MIT (3:1 mixture of CMIT and MIT) produces mitochondrial ROS via inhibiting mitochondrial complexI and II. CMIT/MIT (in 3:1 ratio) induces neurotoxicity through the upregulation of the MAPKs signaling pathways. CMIT/MIT can be used in the research of respiratory diseases and neuroblastoma .
NADH is an orally active dehydrogenase coenzyme that acts as a crucial electron carrier in cellular respiration and participates in ATP production. NADH promotes metabolism, supports brain function, and counteracts oxidative stress by transferring electrons to the electron transport chain. As a signaling molecule, NADH regulates multiple biological processes, including anti-apoptosis, synaptic plasticity, gene expression, and calcium homeostasis. Redox imbalance of NADH/NAD⁺ is one of the key pathological mechanisms of various diseases, such as diabetic nephropathy, neurodegenerative diseases, and ischemia-reperfusion injury.
Ureidopropionic acid is a mitochondrial respiratory chain complex V inhibitor that selectively inhibits the activity of mitochondrial respiratory chain complex V, with no effect on respiratory chain complexesI-IV or mitochondrial fatty acid β-oxidation. Ureidopropionic acid induces the production of reactive oxygen species, delayed elevation of intracellular calcium concentration, secondary energy-dependent excitotoxicity and neurodegeneration in neurons. Ureidopropionic acid promotes neuropathological changes by impairing mitochondrial energy metabolism, oxidative stress and excitotoxicity pathways. Ureidopropionic acid can be used in studies related to 3-ureidopropionase deficiency and severe propionic aciduria .
S1QEL1.1 is a small molecule inhibitor that specifically inhibits the generation of superoxide and hydrogen peroxide at the IQ site during reverse electron transfer in mitochondrial respiratory chain complexI (ComplexI), with an IC50 of 0.07 μM. S1QEL1.1 can significantly reduce the activation of cysteine-aspartic protease (caspase) triggered by endoplasmic reticulum stress. S1QEL1.1 helps to decrease excessive proliferation of stem cells by inhibiting the Reactive Oxygen Species signaling pathway initiated by endoplasmic reticulum stress .
ND-011992 is a reversible, selective quinazoline-type inhibitor targeting quinone reductases and quinol oxidases. ND-011992 inhibits respiratorycomplexI and bo3 oxidase in addition to bd-I and bd-II oxidases in E. coli strain BL21*Δcyo with the IC50 of 0.12, 2.47, 0.63 and 1.3 μM, respectively. ND-011992 can be used for tuberculosis study .
Difluoromethyl 2,2,2-trifluoroethyl ether is an intermediate of Isoflurane (HY-A0134). Isoflurane is a volatile general anaesthetic used for induction and maintenance of general anesthesia. Isoflurane binds to and enhances GABAA receptor. Isoflurane inhibits electron transfer in respiratorycomplexI.
Lilial is a widely used synthetic fragrance and ester in consumer products. Lilial possesses estrogenic activity in vitro. Lilial can induce a toxic effect on mitochondria that causes a decrease in the viability of HaCaT cells. Lilial can increase NRF2 protein level in vitro. Lilial is able to target respiratory chain complexes, inhibit complexesI and II of the electron transport chain, increase the generation of reactive oxygen species, and decrease the level of intracellular ATP. Lilial can induce systemic toxicity in vivo. Lilial induces significant DNA strand breaks .
Dehydromonocrotaline is a mitochondrial respiratory chain complexI NADH oxidase inhibitor, with a IC50 of 62.06 μM and a Ki of 8.1 μM in rats. Dehydromonocrotaline exerts non-competitive inhibitory effects by modifying cysteine thiol groups on complexI, and does not bind to the NADH-binding site. Dehydromonocrotaline dissipates mitochondrial membrane potential and reduces ATP levels. Dehydromonocrotaline can be used in studies related to hepatotoxicity, pulmonary hypertension and liver tumors .
9-Methyl-β-carboline is a monoamine oxidase inhibitor and dopaminergic modulator, with an IC50 of 1 μM against human MAO-A and an IC50 of 15.5 μM against human MAO-B. 9-Methyl-β-carboline possesses cognitive enhancement potential and can cross the blood-brain barrier. 9-Methyl-β-carboline increases dopamine levels by inhibiting monoamine oxidase activity and microglial proliferation. 9-Methyl-β-carboline activates PKA/PKC and mitochondrial respiratory chain complexI, promotes neurotrophic factor expression and reduces α-synuclein (α-synuclein) levels, thereby reversing neurotoxin-induced dopaminergic neuron damage. 9-Methyl-β-carboline also regulates the PI3K pathway and exerts an anti-proliferative effect on astrocytes. 9-Methyl-β-carboline is widely used in Parkinson's disease-related studies .
Influenza HA (518-526) is an H-2d-restricted CTL epitope derived from influenza virus hemagglutinin. Influenza HA (518-526) is highly conserved across various H5N1, some H9N2, and H1N1 strains. Influenza HA (518-526) binds to the mouse MHC class I allele K d to form a complex, which is then recognized by specific CD8 + T cells. Influenza HA (518-526) is an immunodominant epitope in influenza-infected BALB/c mice, and it stimulates CD8 + T cells to secrete IFN-γ to induce a robust immune response. Currently, Influenza HA (518-526) is widely used in research related to respiratory syncytial virus (RSV), influenza virus, and H5N1 influenza .
MPP+-d3 (iodide) is deuterium labeled MPP+ (iodide). MPP+ iodide, a toxic metabolite of the neurotoxin MPTP, causes symptom of Parkinson's disease in animal models by selectively destroying dopaminergic neurons in substantia nigra. MPP+ iodide is taken up by the dopamine transporter into dopaminergic neurons where it exerts its neurotoxic action on mitochondria by affecting complexI of the respiratory chain. MPP+ iodide is also a high affinity substrate for the serotonin transporter (SERT) .
BMT-297376 is an optimized derivative of Linrodostat (HY-101560). BMT-297376 inhibits IDO1 and the ubiquinone (Q) site of mitochondrial respiratory chain complexI. BMT-297376 is suitable for tumor immunology-related research .
Lilial (Standard) is the analytical standard of Lilial. This product is intended for research and analytical applications. Lilial is a widely used synthetic fragrance and ester in consumer products. Lilial possesses estrogenic activity in vitro. Lilial can induce a toxic effect on mitochondria that causes a decrease in the viability of HaCaT cells. Lilial can increase NRF2 protein level in vitro. Lilial is able to target respiratory chain complexes, inhibit complexesI and II of the electron transport chain, increase the generation of reactive oxygen species, and decrease the level of intracellular ATP. Lilial can induce systemic toxicity in vivo. Lilial induces significant DNA strand breaks .
NPD8790 is a species selective mitochondrial respiratorycomplexI inhibitor with an IC50 of 2.4 µM for C. eleganscomplexI. NPD8790 is more selective for nematode species mitochondria than human, bovine, and mouse mitochondria. NPD8790 is an anthelmintic that kills adult soil-transmitted helminths .
Phenformin-d5 (Phenethylbiguanide-d5) hydrochloride is the deuterium labeled Phenformin hydrochloride. Phenformin hydrochloride is an orally active biguanide hypoglycemic agent. Phenformin hydrochloride inhibits mitochondrial respiratory chain complexI, leading to an increased AMP/ATP ratio, activation of AMPK, and subsequent inhibition of the mTOR pathway, thereby suppressing cell proliferation, inducing apoptosis and autophagy. Phenformin hydrochloride inhibits cancer stem cells (CSCs) and possesses potent antitumor potential.
Phenformin (Phenethylbiguanide) (Standard) is the analytical standard of Phenformin (HY-16397). This product is intended for research and analytical applications. Phenformin (Phenethylbiguanide) is an orally active biguanide hypoglycemic agent. Phenformin inhibits mitochondrial respiratory chain complexI, leading to an increased AMP/ATP ratio, activation of AMPK, and subsequent inhibition of the mTOR pathway, thereby suppressing cell proliferation, inducing apoptosis and autophagy. Phenformin inhibits cancer stem cells (CSCs) and possesses potent antitumor potential.
Phenformin (Phenethylbiguanide) hydrochloride (Standard) is the analytical standard of Phenformin hydrochloride (HY-16397). This product is intended for research and analytical applications. Phenformin hydrochloride (Phenethylbiguanide) is an orally active biguanide hypoglycemic agent. Phenformin hydrochloride inhibits mitochondrial respiratory chain complexI, leading to an increased AMP/ATP ratio, activation of AMPK, and subsequent inhibition of the mTOR pathway, thereby suppressing cell proliferation, inducing apoptosis and autophagy. Phenformin hydrochloride inhibits cancer stem cells (CSCs) and possesses potent antitumor potential.
Tolfenpyrad (Standard) is the analytical standard of Tolfenpyrad (HY-17516). This product is intended for research and analytical applications. Tolfenpyrad is an orally active insecticide, acaricide and antibacterial agent. Tolfenpyrad inhibits ComplexI in the mitochondrial respiratory electron transport chain, interfering with the cell respiration process. Tolfenpyrad has significant insecticidal activity against a variety of insect pests such as H. contortus, Coccinella septempunctata. Tolfenpyrad has antibacterial activity against Francisella novicida, with an IC50 of 1.2 µM or 1.5 µM .
Mandestrobin is a mitochondrial respiratory chain complex III inhibitor with bactericidal activity. The enantiomers of Mandestrobin exhibit differential bactericidal activity, with the R-enantiomer showing higher activity than the S-enantiomer .
Influenza HA (518-526) is an H-2d-restricted CTL epitope derived from influenza virus hemagglutinin. Influenza HA (518-526) is highly conserved across various H5N1, some H9N2, and H1N1 strains. Influenza HA (518-526) binds to the mouse MHC class I allele K d to form a complex, which is then recognized by specific CD8 + T cells. Influenza HA (518-526) is an immunodominant epitope in influenza-infected BALB/c mice, and it stimulates CD8 + T cells to secrete IFN-γ to induce a robust immune response. Currently, Influenza HA (518-526) is widely used in research related to respiratory syncytial virus (RSV), influenza virus, and H5N1 influenza .
NADH is an orally active dehydrogenase coenzyme that acts as a crucial electron carrier in cellular respiration and participates in ATP production. NADH promotes metabolism, supports brain function, and counteracts oxidative stress by transferring electrons to the electron transport chain. As a signaling molecule, NADH regulates multiple biological processes, including anti-apoptosis, synaptic plasticity, gene expression, and calcium homeostasis. Redox imbalance of NADH/NAD⁺ is one of the key pathological mechanisms of various diseases, such as diabetic nephropathy, neurodegenerative diseases, and ischemia-reperfusion injury.
Ureidopropionic acid is a mitochondrial respiratory chain complex V inhibitor that selectively inhibits the activity of mitochondrial respiratory chain complex V, with no effect on respiratory chain complexesI-IV or mitochondrial fatty acid β-oxidation. Ureidopropionic acid induces the production of reactive oxygen species, delayed elevation of intracellular calcium concentration, secondary energy-dependent excitotoxicity and neurodegeneration in neurons. Ureidopropionic acid promotes neuropathological changes by impairing mitochondrial energy metabolism, oxidative stress and excitotoxicity pathways. Ureidopropionic acid can be used in studies related to 3-ureidopropionase deficiency and severe propionic aciduria .
Dehydromonocrotaline is a mitochondrial respiratory chain complexI NADH oxidase inhibitor, with a IC50 of 62.06 μM and a Ki of 8.1 μM in rats. Dehydromonocrotaline exerts non-competitive inhibitory effects by modifying cysteine thiol groups on complexI, and does not bind to the NADH-binding site. Dehydromonocrotaline dissipates mitochondrial membrane potential and reduces ATP levels. Dehydromonocrotaline can be used in studies related to hepatotoxicity, pulmonary hypertension and liver tumors .
MPP+-d3 (iodide) is deuterium labeled MPP+ (iodide). MPP+ iodide, a toxic metabolite of the neurotoxin MPTP, causes symptom of Parkinson's disease in animal models by selectively destroying dopaminergic neurons in substantia nigra. MPP+ iodide is taken up by the dopamine transporter into dopaminergic neurons where it exerts its neurotoxic action on mitochondria by affecting complexI of the respiratory chain. MPP+ iodide is also a high affinity substrate for the serotonin transporter (SERT) .
Phenformin-d5 (Phenethylbiguanide-d5) hydrochloride is the deuterium labeled Phenformin hydrochloride. Phenformin hydrochloride is an orally active biguanide hypoglycemic agent. Phenformin hydrochloride inhibits mitochondrial respiratory chain complexI, leading to an increased AMP/ATP ratio, activation of AMPK, and subsequent inhibition of the mTOR pathway, thereby suppressing cell proliferation, inducing apoptosis and autophagy. Phenformin hydrochloride inhibits cancer stem cells (CSCs) and possesses potent antitumor potential.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
MedchemExpress Validation 03
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
MedchemExpress Validation 04
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
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