629

Y-27632

629 Publications Verification

Cat. No.: HY-10071

CAS No.: 146986-50-7

Purity: 99.46%

Target:

ROCK NADPH Oxidase mTOR Reactive Oxygen Species (ROS) NF-κB Apoptosis Akt Autophagy PAK Ras

Research Areas:

Cancer

Y-27632 is a ROCK inhibitor with K_i values of 220 nM and 300 nM for ROCK1 and ROCK2, respectively. Y-27632 exerts anti-inflammatory and immunomodulatory effects in systemic lupus erythematosus models by inhibiting the ROCK/NF-κB pathway. Y-27632 enhances autophagy by inhibiting the AKT/mTOR pathway, thereby inducing apoptosis apoptosis in oral squamous cell carcinoma. Y-27632 induces the formation of tunneling nanotubes in ARPE-19 cells and significantly enhances mitochondrial transfer through these channels. Y-27632 promotes neurite outgrowth in PC12 cells by activating the Rac1/NOX1/ROS/AKT/PAK1 signaling cascade .

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629

Y-27632 hydrochloride hydrate

629 Publications Verification

Cat. No.: HY-10071A

CAS No.: 331752-47-7

Target:

ROCK NF-κB Apoptosis Autophagy Akt mTOR NADPH Oxidase Reactive Oxygen Species (ROS) PAK Ras

Research Areas:

Neurological Disease Inflammation/Immunology Cancer

Y-27632 hydrochloride hydrate is a ROCK inhibitor with K_i values of 220 nM and 300 nM for ROCK1 and ROCK2, respectively. Y-27632 hydrochloride hydrate exerts anti-inflammatory and immunomodulatory effects in systemic lupus erythematosus models by inhibiting the ROCK/NF-κB pathway. Y-27632 hydrochloride hydrate enhances autophagy by inhibiting the AKT/mTOR pathway, thereby inducing apoptosis apoptosis in oral squamous cell carcinoma. Y-27632 hydrochloride hydrate induces the formation of tunneling nanotubes in ARPE-19 cells and significantly enhances mitochondrial transfer through these channels. Y-27632 hydrochloride hydrate promotes neurite outgrowth in PC12 cells by activating the Rac1/NOX1/ROS/AKT/PAK1 signaling cascade .

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513

MK-2206 dihydrochloride

513 Cited Publications

Cat. No.: HY-10358

CAS No.: 1032350-13-2

Purity: 99.94%

Synonyms: MK-2206 (2HCl)

Target:

Bcl-2 Family Apoptosis mTOR Akt GSK-3

Research Areas:

Cardiovascular Disease Inflammation/Immunology Cancer

MK-2206 dihydrochloride (MK-2206 2HCl) is an orally active pan-AKT inhibitor, with IC₅₀ values of 8 nM, 12 nM and 65 nM against AKT1, AKT2 and AKT3, respectively. MK-2206 dihydrochloride inhibits the Akt/mTOR signaling pathway and reduces the levels of downstream GSK3β and Mcl-1 via proteasomal degradation. MK-2206 dihydrochloride induces G1-phase cell cycle arrest, apoptosis, epithelial-mesenchymal transition, fibroblast activation and extracellular matrix deposition. MK-2206 dihydrochloride causes transient hyperglycemia and hyperinsulinemia in animals. MK-2206 dihydrochloride can be used in research related to solid tumors, renal fibrosis and hypercholesterolemia .

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513

MK-2206

513 Cited Publications

Cat. No.: HY-108232

CAS No.: 1032349-77-1

Purity: 99.72%

Target:

Bcl-2 Family Apoptosis mTOR Akt GSK-3

Research Areas:

Metabolic Disease Inflammation/Immunology Cancer

MK-2206 is an orally active pan-AKT inhibitor, with IC₅₀ values of 8 nM, 12 nM and 65 nM against AKT1, AKT2 and AKT3, respectively. MK-2206 inhibits the Akt/mTOR signaling pathway and reduces the levels of downstream GSK3β and Mcl-1 via proteasomal degradation. MK-2206 induces G1-phase cell cycle arrest, apoptosis, epithelial-mesenchymal transition, fibroblast activation and extracellular matrix deposition. MK-2206 causes transient hyperglycemia and hyperinsulinemia in animals. MK-2206 can be used in research related to solid tumors, renal fibrosis and hypercholesterolemia .

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323

Sorafenib

323 Cited Publications

Cat. No.: HY-10201

CAS No.: 284461-73-0

Purity: 99.92%

Synonyms: Bay 43-9006

Target:

Raf VEGFR FLT3 Autophagy Apoptosis STAT Akt MMP Cadherin p38 MAPK ERK MEK PI3K PARP Bcl-2 Family Ephrin Receptor PDGFR

Research Areas:

Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer

Sorafenib (Bay 43-9006) is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib inhibits tumor growth and metastasis in mouse and rat models. Sorafenib can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma .

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323

Sorafenib tosylate

323 Cited Publications

Cat. No.: HY-10201A

CAS No.: 475207-59-1

Purity: 99.75%

Synonyms: Bay 43-9006 tosylate

Target:

Raf VEGFR FLT3 Autophagy Apoptosis STAT Akt MMP Cadherin p38 MAPK ERK MEK PI3K PARP Bcl-2 Family

Research Areas:

Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer

Sorafenib (Bay 43-9006) tosylate is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib tosylate induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib tosylate inhibits tumor growth and metastasis in mouse and rat models. Sorafenib tosylate can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma .

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202

Doxycycline monohydrate

202 Cited Publications

Cat. No.: HY-W008923

CAS No.: 17086-28-1

Target:

MMP Parasite Bacterial Antibiotic Apoptosis Akt PI3K

Research Areas:

Infection Neurological Disease Inflammation/Immunology Cancer

Doxycycline monohydrate is an orally active highly lipophilic, tissue-permeable MMP inhibitor with broad-spectrum antibacterial activity. Doxycycline monohydrate is also a semi-synthetic antibiotic with chelating properties, which blocks bacterial protein synthesis and inhibits extracellular matrix degradation through interactions with zinc and calcium atoms. Doxycycline monohydrate also inhibits mitochondrial biogenesis, translation, and the expression of respiratory chain proteins. Doxycycline monohydrate induces apoptosis, inhibits autophagy and EMT, downregulates stem cell markers, and activates the PI3K-AKT pathway, thereby effectively inhibiting the viability and proliferation of cancer cells such as breast cancer cells. Doxycycline monohydrate also promotes the survival and self-renewal of embryonic stem cells and neural stem cells, and reduces the frequency of medium changes in culture. Doxycycline monohydrate has been applied in studies related to breast cancer, prostate cancer, bladder cancer, and other cancers .

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138

Alpelisib

138 Cited Publications

Cat. No.: HY-15244

CAS No.: 1217486-61-7

Purity: 99.88%

Synonyms: BYL-719

Target:

PI3K Apoptosis

Research Areas:

Infection Neurological Disease Metabolic Disease Cancer

Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .

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138

Alpelisib hydrochloride

138 Cited Publications

Cat. No.: HY-15244A

CAS No.: 1584128-91-5

Synonyms: BYL-719 hydrochloride

Target:

PI3K Apoptosis

Research Areas:

Infection Neurological Disease Metabolic Disease Cancer

Alpelisib (BYL-719) hydrochloride is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib hydrochloride also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib hydrochloride not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib hydrochloride can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .

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82

Alisertib

82 Cited Publications

Cat. No.: HY-10971

CAS No.: 1028486-01-2

Purity: 99.36%

Synonyms: MLN 8237

Target:

Aurora Kinase Autophagy Apoptosis

Research Areas:

Cancer

Alisertib (MLN 8237) is an orally active and selective Aurora A kinase inhibitor (IC₅₀=1.2 nM), which binds to Aurora A kinase resulting in mitotic spindle abnormalities, mitotic accumulation. Alisertib (MLN 8237) induces apoptosis and autophagy through targeting the AKT/mTOR/AMPK/p38 pathway in leukemic cells. Antitumor activity .

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70

Leupeptin hemisulfate

70 Cited Publications

Cat. No.: HY-18234A

CAS No.: 103476-89-7

Category:

Natural Products Microorganisms Disease Research Fields Inflammation/Immunology

Target:

Ser/Thr Protease Cathepsin Autophagy SARS-CoV Atg8/LC3 NO Synthase COX p62 Arginase PTEN NF-κB PI3K Akt p38 MAPK ERK Reactive Oxygen Species (ROS)

Leupeptin hemisulfate is a broad-spectrum protease inhibitor . By inhibiting the activation of the PTEN/PI3K/Akt/NF-κB/ERK1/2/p38 signaling pathway, Leupeptin hemisulfate significantly reduces LPS-induced NO and ROS production, mitochondrial membrane potential hyperpolarization, phagocytic activity, pro-inflammatory cytokine release, and M1 polarization in mouse peritoneal macrophages, and reverses autophagic flux impairment. It also decreases Concanavalin A (HY-P2149)-induced proliferation index of mouse splenic lymphocytes and the Th1/IL-10 and Th2/IL-10 cytokine ratios, thereby modulating innate and adaptive immune responses. Leupeptin hemisulfate inhibits blood coagulation and tumorigenesis in mouse skin. Leupeptin hemisulfate can be used in research on chronic inflammatory diseases and skin tumorigenesis .

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60

Ciprofloxacin hydrochloride monohydrate

60 Cited Publications

Cat. No.: HY-B0356B

CAS No.: 86393-32-0

Synonyms: Bay-09867 hydrochloride monohydrate

Target:

Antibiotic Apoptosis Bacterial Reactive Oxygen Species (ROS) Topoisomerase Mitochondrial Metabolism Akt β-catenin

Research Areas:

Infection Cancer

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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60

Ciprofloxacin hydrochloride

60 Cited Publications

Cat. No.: HY-B0356C

CAS No.: 86483-48-9

Synonyms: Bay-09867 hydrochloride

Target:

Antibiotic Apoptosis Bacterial Reactive Oxygen Species (ROS) Topoisomerase Mitochondrial Metabolism Akt β-catenin

Research Areas:

Infection Cancer

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 .

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60

Ciprofloxacin monohydrochloride

60 Cited Publications

Cat. No.: HY-B0356A

CAS No.: 93107-08-5

Synonyms: Bay-09867 monohydrochloride

Target:

Antibiotic Apoptosis Bacterial Reactive Oxygen Species (ROS) Topoisomerase Mitochondrial Metabolism Akt β-catenin

Research Areas:

Infection Cancer

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 .

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