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

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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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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352

SC79

352 Cited Publications

Cat. No.: HY-18749

CAS No.: 305834-79-1

Target:

Akt

Research Areas:

Neurological Disease Inflammation/Immunology Cancer

SC79, a unique specific and BBB permeable Akt activator, activates Akt in the cytosol and inhibits Akt membrane translocation. SC79 specifically binds to the PH domain of Akt .

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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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114

Tauroursodeoxycholate dihydrate

114 Cited Publications

Cat. No.: HY-19696B

CAS No.: 117609-50-4

Synonyms: Tauroursodeoxycholic acid dihydrate; TUDCA dihydrate; UR 906 dihydrate

Category:

Endogenous metabolite Disease Research Fields Cancer Steroids

Target:

Caspase Apoptosis Endogenous Metabolite IRE1 NF-κB JNK Reactive Oxygen Species (ROS) Akt

Tauroursodeoxycholate dehydrate is an orally active taurine conjugate of Ursodeoxycholic acid (HY-13771). Tauroursodeoxycholate dehydrate inhibits caspase-3/7, Apoptosis, IRE1α/TRAF2/NF-κB, prevents JNK phosphorylation, inhibits ROS generation, and activates Akt signaling. Tauroursodeoxycholate dehydrate prevents cataract formation, reduces renal tubular damage in type 2 diabetic mice, reduces I/R injury in liver, and inhibits intestinal inflammation and barrier disruption in nonalcoholic fatty liver disease .

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99

Capivasertib

99 Cited Publications

Cat. No.: HY-15431

CAS No.: 1143532-39-1

Purity: 99.95%

Synonyms: AZD5363

Target:

Akt Autophagy

Research Areas:

Cancer

Capivasertib (AZD5363) is an orally active and potent pan-AKT kinase inhibitor with IC₅₀ of 3, 7 and 7 nM for Akt1,Akt2 and Akt3, respectively.

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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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78

Cilengitide

78 Cited Publications

Cat. No.: HY-16141

CAS No.: 188968-51-6

Synonyms: EMD 121974

Target:

Integrin TGF-β Receptor Apoptosis PD-1/PD-L1 STAT Akt mTOR

Cilengitide (EMD 121974) is an integrin (integrin) inhibitor with blood-brain barrier permeability, with IC₅₀ values against human targets as follows: 0.61 nM for αvβ3, 8.4 nM for αvβ5, 14.9 nM for α5β1, 5400 nM for αIIbβ3, 2050 nM for αvβ6, 2350 nM for αvβ8. Cilengitide inhibits the binding of integrins to vitronectin, fibronectin, fibrinogen and LAP (TGF-β), and serves as an internal standard for solid-phase integrin binding assays. Cilengitide inhibits tumor cell viability, induces apoptosis, reduces the phosphorylation levels of STAT3, AKT and mTOR, downregulates the expression of PD-L1, inhibits cell viability and angiogenesis, regulates anti-tumor immune responses and slows tumor growth. Cilengitide can be used in research related to glioblastoma, melanoma, advanced solid tumors and refractory brain tumors .

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78

Cilengitide TFA

78 Cited Publications

Cat. No.: HY-16143

CAS No.: 199807-35-7

Synonyms: EMD 121974 TFA

Target:

Integrin TGF-β Receptor Apoptosis PD-1/PD-L1 STAT Akt mTOR

Cilengitide TFA (EMD 121974 TFA) is an integrin (integrin) inhibitor with blood-brain barrier permeability, with IC₅₀ values against human targets as follows: 0.61 nM for αvβ3, 8.4 nM for αvβ5, 14.9 nM for α5β1, 5400 nM for αIIbβ3, 2050 nM for αvβ6, 2350 nM for αvβ8. Cilengitide TFA inhibits the binding of integrins to vitronectin, fibronectin, fibrinogen and LAP (TGF-β), and serves as an internal standard for solid-phase integrin binding assays. Cilengitide TFA inhibits tumor cell viability, induces apoptosis, reduces the phosphorylation levels of STAT3, AKT and mTOR, downregulates the expression of PD-L1, inhibits cell viability and angiogenesis, regulates anti-tumor immune responses and slows tumor growth. Cilengitide TFA can be used in research related to glioblastoma, melanoma, advanced solid tumors and refractory brain tumors .

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74

CX-5461

74 Cited Publications

Cat. No.: HY-13323

CAS No.: 1138549-36-6

Purity: 99.49%

Target:

DNA/RNA Synthesis MDM-2/p53 AMPK Akt Autophagy Apoptosis Checkpoint Kinase (Chk)

Research Areas:

Cancer

CX-5461 is a selective, orally active RNA polymerase I inhibitor. CX-5461 disrupts the formation of the SL1-rDNA complex, thereby blocking the transcription initiation of ribosomal RNA without altering the activity of RNA polymerase II, DNA replication, or protein translation processes. CX-5461 upregulates the expression of p21, MDM2, Sestrin1/2, and phosphorylated AMPKα, and reduces the level of phosphorylated Akt. CX-5461 induces G2/G2/M cell cycle arrest, Autophagy, Apoptosis, and cellular senescence, and activates CHK1, CHK2, and RPA. CX-5461 can be used in research related to osteosarcoma, cervical cancer, hematologic malignancies, high-grade serous ovarian cancer, and solid tumors .

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74

CX-5461 dihydrochloride

74 Cited Publications

Cat. No.: HY-13323A

Purity: 99.41%

Target:

DNA/RNA Synthesis MDM-2/p53 AMPK Akt Autophagy Apoptosis Checkpoint Kinase (Chk)

Research Areas:

Cancer

CX-5461 dihydrochloride is a selective, orally active RNA polymerase I inhibitor. CX-5461 dihydrochloride disrupts the formation of the SL1-rDNA complex, thereby blocking the transcription initiation of ribosomal RNA without altering the activity of RNA polymerase II, DNA replication, or protein translation processes. CX-5461 dihydrochloride upregulates the expression of p21, MDM2, Sestrin1/2, and phosphorylated AMPKα, and reduces the level of phosphorylated Akt. CX-5461 dihydrochloride induces G2/G2/M cell cycle arrest, Autophagy, Apoptosis, and cellular senescence, and activates CHK1, CHK2, and RPA. CX-5461 dihydrochloride can be used in research related to osteosarcoma, cervical cancer, hematologic malignancies, high-grade serous ovarian cancer, and solid tumors .

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71

Ipatasertib dihydrochloride

71 Cited Publications

Cat. No.: HY-15186A

CAS No.: 1396257-94-5

Purity: 99.09%

Synonyms: GDC-0068 dihydrochloride; RG-7440 dihydrochloride

Target:

Organoid Akt

Research Areas:

Cancer

Ipatasertib dihydrochloride (GDC-0068 dihydrochloride) is a highly selective and ATP-competitive pan-Akt inhibitor with IC₅₀s of 5, 18 and 8 nM for Akt1, Akt2 and Akt3, respectively.

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71

Ipatasertib

71 Cited Publications

Cat. No.: HY-15186

CAS No.: 1001264-89-6

Purity: 99.79%

Synonyms: GDC-0068; RG7440

Target:

Organoid Akt Apoptosis

Research Areas:

Cancer

Ipatasertib (GDC-0068) is an orally active, highly selective and ATP-competitive pan-Akt inhibitor with IC₅₀ values of 5, 18, 8 nM for Akt1/2/3, respectively. Ipatasertib synchronously activates FoxO3a and NF-κB through inhibition of Akt leading to p53-independent activation of PUMA. Ipatasertib also induces apoptosis in cancer cells and inhibits tumor growth in xenograft mouse models .

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