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Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!2025-02-06
603 Results for "
reduce stress
" in MedChemExpress (MCE) Product Catalog:
Products (603)
603 Results for "reduce stress" in MCE Product Catalog:
881
Research Areas:
Z-VAD-FMK is a pan-caspase inhibitor and also an ICE-like protease inhibitor, which inhibits apoptosis by preventing the processing of CPP32 to its active form. Z-VAD-FMK sensitivity varies primarily due to differential expression of receptor-interacting protein 1 (RIP1). Z-VAD-FMK limits the cryopreservation-induced apoptosis by reducing caspase-3 activity of in vitro produced bovine embryos. Z-VAD-FMK is immunosuppressive in vitro and inhibits T cell proliferation without blocking the processing of caspase-8 and caspase-3. Z-VAD-FMK leads to a decrease in intracellular glutathione (GSH) with a concomitant increase in reactive oxygen species (ROS) levels in activated T cells. Z-VAD-FMK is due to oxidative stress via the depletion of GSH. Z-VAD-FMK can be used for the study of acute pancreatitis .
114
114 Cited Publications
Cat. No.: HY-19696
CAS No.: 14605-22-2
Synonyms: Tauroursodeoxycholic acid; TUDCA; UR 906
Target:
114
114 Cited Publications
Cat. No.: HY-19696A
CAS No.: 35807-85-3
Synonyms: Tauroursodeoxycholic acid sodium; TUDCA sodium; UR 906 sodium
Target:
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Target:
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Exendin‑4 (Exenatide) is an orally active, blood-brain barrier-permeable glucagon-like peptide-1 receptor (GLP‑1 receptor) agonist that resists degradation mediated by dipeptidyl peptidase IV. Exendin‑4 mediates multiple glucose-regulating effects, including stimulation of glucose-dependent insulin secretion, inhibition of glucagon production, increase in β-cell mass, delay of gastric emptying, reduction of food intake, improvement of peripheral insulin sensitivity, and restoration of normal islet structure. Exendin‑4 inhibits oxidative stress, alleviates inflammatory responses, and reduces neuronal apoptosis. Exendin‑4 reduces the aggregation level of mutant huntingtin, improves motor function, prolongs survival time, and regulates the expression levels of leptin and ghrelin. Exendin‑4 can be used in research related to type 2 diabetes, acute ischemic stroke, and Huntington's disease .
72
72 Cited Publications
Synonyms: Exenatide acetate
Target:
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Exendin-4 acetate (Exenatide acetate) is an orally active, blood-brain barrier-permeable glucagon-like peptide-1 receptor (GLP‑1 receptor) agonist that resists degradation mediated by dipeptidyl peptidase IV. Exendin-4 acetate mediates multiple glucose-regulating effects, including stimulation of glucose-dependent insulin secretion, inhibition of glucagon production, increase in β-cell mass, delay of gastric emptying, reduction of food intake, improvement of peripheral insulin sensitivity, and restoration of normal islet structure. Exendin-4 acetate inhibits oxidative stress, alleviates inflammatory responses, and reduces neuronal apoptosis. Exendin-4 acetate reduces the aggregation level of mutant huntingtin, improves motor function, prolongs survival time, and regulates the expression levels of leptin and ghrelin. Exendin-4 acetate can be used in research related to type 2 diabetes, acute ischemic stroke, and Huntington's disease .
60
60 Cited Publications
Cat. No.: HY-B0356B
CAS No.: 86393-32-0
Synonyms: Bay-09867 hydrochloride monohydrate
Ciprofloxacin (Bay-09867) hydrochloride monohydrate is an orally active, blood-brain barrier permeable fluoroquinolone antibacterial agent. Ciprofloxacin hydrochloride monohydrate exerts bactericidal effects primarily by inhibiting topoisomerase II and IV. Ciprofloxacin hydrochloride monohydrate inhibits the proliferation of human dental pulp stem cells and chondrocytes from young rats, and also activates the Akt signaling pathway and upregulates markers such as β-catenin and Nanog to maintain the morphological characteristics of stem cells. Ciprofloxacin hydrochloride monohydrate induces significant neurotoxicity and tissue damage, including reducing serotonin and glutathione levels in the brain, inducing oxidative stress and depression-like behaviors, and causing articular cartilage damage. Ciprofloxacin hydrochloride monohydrate can be applied to research related to infections of necrotic young permanent teeth and neurotoxicity .
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Ciprofloxacin hydrochloride (Bay-09867 hydrochloride) is an orally active, blood-brain barrier permeable fluoroquinolone antibacterial agent. Ciprofloxacin hydrochloride exerts bactericidal effects primarily by inhibiting topoisomerase II and IV. Ciprofloxacin hydrochloride inhibits the proliferation of human dental pulp stem cells and chondrocytes from young rats, and also activates the Akt signaling pathway and upregulates markers such as β-catenin and Nanog to maintain the morphological characteristics of stem cells. Ciprofloxacin hydrochloride induces significant neurotoxicity and tissue damage, including reducing serotonin and glutathione levels in the brain, inducing oxidative stress and depression-like behaviors, and causing articular cartilage damage. Ciprofloxacin hydrochloride can be applied to research related to infections of necrotic young permanent teeth and neurotoxicity .
60
Ciprofloxacin (Bay-09867) monohydrochloride is an orally active, blood-brain barrier permeable fluoroquinolone antibacterial agent. Ciprofloxacin monohydrochloride exerts bactericidal effects primarily by inhibiting topoisomerase II and IV. Ciprofloxacin monohydrochloride inhibits the proliferation of human dental pulp stem cells and chondrocytes from young rats, and also activates the Akt signaling pathway and upregulates markers such as β-catenin and Nanog to maintain the morphological characteristics of stem cells. Ciprofloxacin monohydrochloride induces significant neurotoxicity and tissue damage, including reducing serotonin and glutathione levels in the brain, inducing oxidative stress and depression-like behaviors, and causing articular cartilage damage. Ciprofloxacin monohydrochloride can be applied to research related to infections of necrotic young permanent teeth and neurotoxicity .
53
53 Cited Publications
Research Areas:
53
53 Cited Publications
Research Areas:
53
53 Cited Publications
Cat. No.: HY-114118A
Purity: 99.92%
Research Areas:
44
Target:
40
40 Cited Publications
Rhosin hydrochloride is a potent, specific RhoA subfamily Rho GTPases inhibitor. Rhosin hydrochloride specifically binds to RhoA to inhibit RhoA-GEF interaction with a Kd of ~ 0.4 uM, and does not interact with Cdc42 or Rac1, nor the GEF, LARG. Rhosin hydrochloride induces cell apoptosis . Rhosin hydrochloride promotes stress resiliency through enhancing D1-MSN plasticity and reducing hyperexcitability .
40
40 Cited Publications
Rhosin is a potent, specific RhoA subfamily Rho GTPases inhibitor, which specifically binds to RhoA to inhibit RhoA-GEF interaction with a Kd of ~ 0.4 uM, and does not interact with Cdc42 or Rac1, nor the GEF, LARG. Rhosin induces cell apoptosis . Rhosin promotes stress resiliency through enhancing D1-MSN plasticity and reducing hyperexcitability .
38
38 Cited Publications
Cat. No.: HY-N0148A
CAS No.: 207671-50-9
Synonyms: Rutoside hydrate; Quercetin 3-O-rutinoside hydrate
38
38 Cited Publications
Synonyms: Rutoside; Quercetin 3-O-rutinoside
33
Research Areas:
FX-11 is a potent, selective, reversible and competitive lactate dehydrogenase A (LDHA) inhibitor, with a Ki of 8 μM. FX-11 reduces ATP levels and induces oxidative stress, ROS production and cell death. FX-11 shows antitumor activity in lymphoma and pancreatic cancer xenografts .
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1400W is a slow, tight binding, and highly selective inducible nitric-oxide synthase (iNOS) inhibitor, with a Kd value ≤ 7 nM. 1400W inhibits iNOS induction in microglial cells, and reduces generation of NO, thereby mitigating oxidative stress and neuronal cell apoptosis in the rat cerebral cortex, and improving the spatial memory dysfunction caused by acute hypobaric hypoxia-reoxygenation .
33
33 Cited Publications
Cat. No.: HY-18731
CAS No.: 214358-33-5
Target:
Research Areas:
1400W dihydrochloride is the dihydrochloride form of 1400W (HY-18730). 1400W is a slow, tight binding, and highly selective inducible nitric-oxide synthase (iNOS) inhibitor, with a Kd value ≤ 7 nM. 1400W inhibits iNOS induction in microglial cells, and reduces generation of NO, thereby mitigating oxidative stress and neuronal cell apoptosis in the rat cerebral cortex, and improving the spatial memory dysfunction caused by acute hypobaric hypoxia-reoxygenation .
26
26 Cited Publications
Target:
Research Areas:
Cardiovascular Disease Neurological Disease Endocrinology Cancer
IU1 is a selective, reversible USP14 inhibitor with an IC50 of 4-5 μM. IU1 binds USP14’s catalytic cleft to block deubiquitinase activity. IU1 induces calpain-dependent Tau cleavage, causes ATP deficits, reduces E1~Ub thioester levels and 26S proteasome assembly. IU1 enhances 26S proteasome chymotrypsin-like activity, modulates LC3B-dependent autophagy flux, reduces cancer cell proliferation and migration, and blocks G0/G1 to S phase cell cycle transition in follicular thyroid cancer cells. IU1 activates autophagy-lysosomal and ubiquitin-proteasome pathways, triggers apoptosis, and reduces cervical cancer cell growth. IU1 enhances degradation of proteasome substrates linked to neurodegenerative disease, accelerates oxidized protein degradation, and increases oxidative stress resistance. IU1 can be used for the research of Alzheimer’s disease, follicular thyroid cancer, ischemic stroke, cervical cancer, and neurodegenerative disease .
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Protocols
Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!A suitable model is crucial in drug screening experiments. Organs can mimic the three-dimensional functional structure of internal organs, have similar spatial organization to corresponding organs, maintain some key characteristics, and reproduce some physiological functions. They are widely used for modeling and personalized drug screening physiological functions.2025-02-06
