Search Result
Results for "
ERK Activation Inhibitor Peptide
" in MedChemExpress (MCE) Product Catalog:
4
Isotope-Labeled Compounds
| Art. -Nr. |
Produktname |
Target |
Forschungsgebiete |
Chemical Structure |
-
- HY-13749
-
Sitagliptin
Maximum Cited Publications
30 Publications Verification
MK-0431
|
Dipeptidyl Peptidase
GLP Receptor
Endogenous Metabolite
PKA
ERK
|
Metabolic Disease
|
|
Sitagliptin (MK-0431) is an orally active and highly selective DPP4 inhibitor with an IC50 value of 19 nM. Sitagliptin blocks the degradation of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) by competing inhibition mechanism (Kᵢ = 1 nM), thereby increasing the level of active incretin. Sitagliptin can also directly stimulate the secretion of GLP-1 by intestinal L cells by activating the cAMP/PKA and ERK1/2 pathways, and this effect is independent of DPP-4. Sitagliptin shows protective effects on pancreatic islet grafts in 1-type diabetes models. Sitagliptin can be used for the study of 1-type and 2-type diabetes .
|
-
-
- HY-13749A
-
|
MK-0431 phosphate
|
Dipeptidyl Peptidase
GLP Receptor
Endogenous Metabolite
PKA
ERK
|
Metabolic Disease
|
|
Sitagliptin (MK-0431) phosphate is an orally active and highly selective DPP4 inhibitor with an IC50 value of 19 nM. Sitagliptin phosphate blocks the degradation of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) by competing inhibition mechanism (Kᵢ = 1 nM), thereby increasing the level of active incretin. Sitagliptin phosphate can also directly stimulate the secretion of GLP-1 by intestinal L cells by activating the cAMP/PKA and ERK1/2 pathways, and this effect is independent of DPP-4. Sitagliptin phosphate shows protective effects on pancreatic islet grafts in 1-type diabetes models. Sitagliptin phosphate can be used for the study of 1-type and 2-type diabetes .
|
-
-
- HY-13749B
-
|
MK-0431 phosphate monohydrate
|
Dipeptidyl Peptidase
GLP Receptor
Endogenous Metabolite
PKA
ERK
|
Metabolic Disease
|
|
Sitagliptin (MK-0431) phosphate monohydrate is an orally active and highly selective DPP4 inhibitor with an IC50 value of 19 nM. Sitagliptin phosphate monohydrate blocks the degradation of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) by competing inhibition mechanism (Kᵢ = 1 nM), thereby increasing the level of active incretin. Sitagliptin phosphate monohydrate can also directly stimulate the secretion of GLP-1 by intestinal L cells by activating the cAMP/PKA and ERK1/2 pathways, and this effect is independent of DPP-4. Sitagliptin phosphate monohydrate shows protective effects on pancreatic islet grafts in 1-type diabetes models. Sitagliptin phosphate monohydrate can be used for the study of 1-type and 2-type diabetes .
|
-
-
- HY-P3206
-
|
Thymulin; Thymic factor
|
ERK
|
Neurological Disease
Inflammation/Immunology
Endocrinology
|
|
Serum thymic factor (Thymulin) is a zinc-dependent immunomodulatory peptide hormone, which can be produced by the thymic epithelial cells. Serum thymic factor stimulates the release of hormones from the pituitary gland, exhibits hypophysiotropic activity. Serum thymic factor protects rats from Cephaloridine (HY-B2072)-induced nephrotoxicity by inhibiting ERK activation. Serum thymic factor exhibits anti-diabetic, anti-inflammatory and analgesic effects. Serum thymic factor can be used in research about endocrine, reproductive, neurodegenerative and inflammatory diseases .
|
-
-
- HY-P1633
-
|
PG1
|
Bacterial
ERK
COX
NF-κB
Apoptosis
NO Synthase
Dengue Virus
|
Infection
Inflammation/Immunology
|
|
Protegrin-1 is an orally active antibacterial peptide. Protegrin-1 activates ERK, COX2, NFκB, inhibits Apoptosis, and NO production. Protegrin-1 has antibacterial activity against S. aureus, E. faecium, E. coli, P. aeruginosa and K. Pneumoniae, with MBC values between 10 and 20 µM. Protegrin-1 has antiviral activity against dengue NS2B-NS3. Protegrin-1 has anti-inflammatory activity. Protegrin-1 is used in the study of inflammatory diseases and infections .
|
-
-
- HY-P10102
-
Kp7-6
2 Publications Verification
|
Apoptosis
PERK
NF-κB
Caspase
JNK
|
Inflammation/Immunology
Cancer
|
|
Kp7-6 is a Fas mimetic peptide and also a Fas/FasL antagonist. Kp7-6 specifically binds to Fas and FasL, disrupts receptor complexes, and blocks downstream apoptosis signaling pathways. Kp7-6 inhibits the phosphorylation of ERK1-2, induces the phosphorylation of IκBα, and activates NF-κB. Kp7-6 inhibits the activation of caspase-8, caspase-3 and JNK, and suppresses human amylin-induced β-cell apoptosis. Kp7-6 inhibits FasL-induced lymphoid cytotoxicity and apoptosis. Kp7-6 reduces local tumor FasL expression, increases CD8 +Fas + T cell infiltration, and decreases tumor volume in pancreatic neuroendocrine tumor models. Kp7-6 prevents concanavalin A-induced liver injury in mice. Kp7-6 is applicable to research related to type 2 diabetes, concanavalin A-induced hepatitis and pancreatic neuroendocrine tumors .
|
-
-
- HY-P6442
-
|
|
Chemerin Receptor
Syk
ERK
Src
p38 MAPK
P-selectin
|
Cardiovascular Disease
Neurological Disease
Inflammation/Immunology
|
|
Chemerin15 is an anti-inflammatory peptide derived from Chemerin. Chemerin15 binds to ChemR23. Chemerin15 inhibits TNFα-induced activation of Syk, ERK and Src kinases. Chemerin15 increases the expression of p-p38 mRNA and protein. Chemerin15 mediates phagocytosis, resolution of inflammation, CD62L shedding and downregulation of PSGL-1 expression in macrophages and microglia. Chemerin15 inhibits neutrophil-mediated vascular inflammation and myocardial ischemia-reperfusion injury via ChemR23. Chemerin15 enhances microglial phagocytosis, thereby alleviating cerebral ischemia-reperfusion injury .
|
-
-
- HY-P0178
-
|
|
Integrin
|
Inflammation/Immunology
|
|
LXW7, a cyclic peptide containing Arg-Gly-Asp (RGD), is an integrin αvβ3 inhibitor. LXW7 has a high binding affinity to αvβ3 integrin with an IC50 of 0.68 μM. LXW7 increases phosphorylation of VEGFR-2 and activation of ERK1/2. Anti-inflammatory effect .
|
-
-
- HY-13749AS
-
|
MK-0431-d4 phosphate
|
Dipeptidyl Peptidase
GLP Receptor
Endogenous Metabolite
PKA
ERK
|
Metabolic Disease
|
|
Sitagliptin-d4 phosphate (MK-0431-d4) is the deuterium labeled Sitagliptin phosphate (HY-13749A). Sitagliptin phosphate is an orally active and highly selective DPP4 inhibitor with an IC50 value of 19 nM. Sitagliptin phosphate blocks the degradation of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) by competing inhibition mechanism (Kᵢ = 1 nM), thereby increasing the level of active incretin. Sitagliptin phosphate can also directly stimulate the secretion of GLP-1 by intestinal L cells by activating the cAMP/PKA and ERK1/2 pathways, and this effect is independent of DPP-4. Sitagliptin phosphate shows protective effects on pancreatic islet grafts in 1-type diabetes models. Sitagliptin phosphate can be used for the study of 1-type and 2-type diabetes.
|
-
-
- HY-P3206A
-
|
Thymulin acetate; Thymic factor acetate
|
ERK
|
Neurological Disease
Inflammation/Immunology
Endocrinology
|
|
Serum thymic factor acetate (Thymulin acetate) is the acetate salt form of Serum thymic factor (HY-P3206). Serum thymic factor acetate is a zinc-dependent immunomodulatory peptide hormone, which can be produced by the thymic epithelial cells. Serum thymic factor acetate stimulates the release of hormones from the pituitary gland, exhibits hypophysiotropic activity. Serum thymic factor acetate protects rats from Cephaloridine (HY-B2072)-induced nephrotoxicity by inhibiting ERK activation. Serum thymic factor acetate exhibits anti-diabetic, anti-inflammatory and analgesic effects. Serum thymic factor acetate can be used in research about endocrine, reproductive, neurodegenerative and inflammatory diseases .
|
-
-
- HY-13749S1
-
|
MK-0431-d4 hydrochloride
|
Isotope-Labeled Compounds
Dipeptidyl Peptidase
GLP Receptor
Endogenous Metabolite
PKA
ERK
|
Metabolic Disease
|
|
Sitagliptin-d4 hydrochloride is the deuterium labeled Sitagliptin hydrochloride (HY-13749E). Sitagliptin hydrochloride is an orally active and highly selective DPP4 inhibitor with an IC50 value of 19 nM. Sitagliptin hydrochloride blocks the degradation of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) by competing inhibition mechanism (Kᵢ = 1 nM), thereby increasing the level of active incretin. Sitagliptin hydrochloride can also directly stimulate the secretion of GLP-1 by intestinal L cells by activating the cAMP/PKA and ERK1/2 pathways, and this effect is independent of DPP-4. Sitagliptin hydrochloride shows protective effects on pancreatic islet grafts in 1-type diabetes models. Sitagliptin hydrochloride can be used for the study of 1-type and 2-type diabetes.
|
-
-
- HY-P0178A
-
|
|
Integrin
|
Inflammation/Immunology
|
|
LXW7 TFA, a cyclic peptide containing Arg-Gly-Asp (RGD), is an integrin αvβ3 inhibitor. LXW7 has a high binding affinity to αvβ3 integrin with an IC50 of 0.68 μM. LXW7 TFA increases phosphorylation of VEGFR-2 and activation of ERK1/2. Anti-inflammatory effect .
|
-
-
- HY-P4133
-
|
|
ERK
MEK
|
Cancer
|
|
MEK1 Derived Peptide Inhibitor 1 is a peptide inhibitor. MEK1 Derived Peptide Inhibitor 1 can inhibit the in vitro activation of ERK2 by MEK1 with an IC50 value of 30 μM. MEK1 Derived Peptide Inhibitor 1 can be used for the research of cell-permeable .
|
-
-
- HY-P4866
-
|
|
Integrin
Transglutaminase
Akt
p38 MAPK
ERK
Caspase
Apoptosis
|
Cardiovascular Disease
Metabolic Disease
Inflammation/Immunology
|
|
Q-Peptide is an angiopoietin-1 derived peptide (QHREDGS). Q-Peptide interacts with β1-integrin, binds to integrins on the surface of osteoblasts, and serves as an acyl donor substrate for Streptomyces mobaraensis transglutaminase. Q-Peptide activates Akt, MAPKp42/44, ILK, ERK1/2, and downregulates caspase-3/7. Q-Peptide inhibits cell apoptosis, enhances cell adhesion and migration, and promotes osteoblast differentiation, bone matrix deposition and mineralization. Q-Peptide can be used in studies related to myocardial infarction, bone regeneration, diabetic wound repair and human induced pluripotent stem cells .
|
-
-
- HY-13749E
-
|
MK-0431 hydrochloride
|
Dipeptidyl Peptidase
GLP Receptor
Endogenous Metabolite
PKA
ERK
|
Metabolic Disease
|
|
Sitagliptin (MK-0431) hydrochloride is an orally active and highly selective DPP4 inhibitor with an IC50 value of 19 nM. Sitagliptin hydrochloride blocks the degradation of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) by competing inhibition mechanism (Kᵢ = 1 nM), thereby increasing the level of active incretin. Sitagliptin hydrochloride can also directly stimulate the secretion of GLP-1 by intestinal L cells by activating the cAMP/PKA and ERK1/2 pathways, and this effect is independent of DPP-4. Sitagliptin hydrochloride shows protective effects on pancreatic islet grafts in 1-type diabetes models. Sitagliptin hydrochloride can be used for the study of 1-type and 2-type diabetes .
|
-
-
- HY-P5977
-
|
Ste-MPKKKPTPIQLNP-NH₂; ERK Activation Inhibitor Peptide
|
ERK
|
Cancer
|
|
STE-MEK1(13) (Ste-MPKKKPTPIQLNP-NH ) is a cell permeable ERK1/2 inhibitor (IC50: 13-30 μM). STE-MEK1(13) inhibits ERK1/2 phosphorylation .
|
-
-
- HY-13749R
-
|
MK-0431 (Standard)
|
Reference Standards
Dipeptidyl Peptidase
GLP Receptor
Endogenous Metabolite
PKA
ERK
|
Metabolic Disease
|
|
Sitagliptin (Standard) is the analytical standard of Sitagliptin (HY-13749). This product is intended for research and analytical applications. Sitagliptin is an orally active and highly selective DPP4 inhibitor with an IC50 value of 19 nM. Sitagliptin blocks the degradation of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) by competing inhibition mechanism (Kᵢ = 1 nM), thereby increasing the level of active incretin. Sitagliptin can also directly stimulate the secretion of GLP-1 by intestinal L cells by activating the cAMP/PKA and ERK1/2 pathways, and this effect is independent of DPP-4. Sitagliptin shows protective effects on pancreatic islet grafts in 1-type diabetes models. Sitagliptin can be used for the study of 1-type and 2-type diabetes.
|
-
-
- HY-P10074
-
|
|
ERK
|
Inflammation/Immunology
|
|
TAT-MEK1 is an inhibitor ofERK2, consisting of TAT and MEK1 (N-terminal), TAT (YGRKKRRQRRR) derived from human immunodeficiency (HIV-1) transcriptional trans activator (TAT), is a cell-penetrating peptide. TAT-MEK1 IC50 in vitro for ERK2 is 29 μM .
|
-
-
- HY-13749AR
-
|
MK-0431 phosphate (Standard)
|
Reference Standards
Dipeptidyl Peptidase
GLP Receptor
Endogenous Metabolite
PKA
ERK
|
Metabolic Disease
|
|
Sitagliptin (MK-0431) phosphate (Standard) is the analytical standard of Sitagliptin phosphate (HY-13749A). This product is intended for research and analytical applications. Sitagliptin phosphate is an orally active and highly selective DPP4 inhibitor with an IC50 value of 19 nM. Sitagliptin phosphate blocks the degradation of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) by competing inhibition mechanism (Kᵢ = 1 nM), thereby increasing the level of active incretin. Sitagliptin phosphate can also directly stimulate the secretion of GLP-1 by intestinal L cells by activating the cAMP/PKA and ERK1/2 pathways, and this effect is independent of DPP-4. Sitagliptin phosphate shows protective effects on pancreatic islet grafts in 1-type diabetes models. Sitagliptin phosphate can be used for the study of 1-type and 2-type diabetes.
|
-
-
- HY-13749S3
-
|
MK-0431-d6
|
Isotope-Labeled Compounds
Dipeptidyl Peptidase
GLP Receptor
Endogenous Metabolite
PKA
ERK
|
Metabolic Disease
|
|
Sitagliptin-d6 (MK-0431-d6) is deuterium labeled Sitagliptin (HY-13749). Sitagliptin is an orally active and highly selective DPP4 inhibitor with an IC50 value of 19 nM. Sitagliptin blocks the degradation of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) by competing inhibition mechanism (Kᵢ = 1 nM), thereby increasing the level of active incretin. Sitagliptin can also directly stimulate the secretion of GLP-1 by intestinal L cells by activating the cAMP/PKA and ERK1/2 pathways, and this effect is independent of DPP-4. Sitagliptin shows protective effects on pancreatic islet grafts in 1-type diabetes models. Sitagliptin can be used for the study of 1-type and 2-type diabetes.
|
-
-
- HY-13749S2
-
|
MK-0431-d4
|
Isotope-Labeled Compounds
Dipeptidyl Peptidase
GLP Receptor
Endogenous Metabolite
PKA
ERK
|
Metabolic Disease
|
|
Sitagliptin-d4 (MK-0431-d4) is deuterium labeled Sitagliptin (HY-13749). Sitagliptin is an orally active and highly selective DPP4 inhibitor with an IC50 value of 19 nM. Sitagliptin blocks the degradation of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) by competing inhibition mechanism (Kᵢ = 1 nM), thereby increasing the level of active incretin. Sitagliptin can also directly stimulate the secretion of GLP-1 by intestinal L cells by activating the cAMP/PKA and ERK1/2 pathways, and this effect is independent of DPP-4. Sitagliptin shows protective effects on pancreatic islet grafts in 1-type diabetes models. Sitagliptin can be used for the study of 1-type and 2-type diabetes.
|
-
-
- HY-13749BR
-
|
MK-0431 phosphate monohydrate (Standard)
|
Reference Standards
Dipeptidyl Peptidase
GLP Receptor
Endogenous Metabolite
PKA
ERK
|
Metabolic Disease
|
|
Sitagliptin (MK-0431) phosphate monohydrate (Standard) is the analytical standard of Sitagliptin phosphate monohydrate (HY-13749B). This product is intended for research and analytical applications. Sitagliptin phosphate monohydrate is an orally active and highly selective DPP4 inhibitor with an IC50 value of 19 nM. Sitagliptin phosphate monohydrate blocks the degradation of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) by competing inhibition mechanism (Kᵢ = 1 nM), thereby increasing the level of active incretin. Sitagliptin phosphate monohydrate can also directly stimulate the secretion of GLP-1 by intestinal L cells by activating the cAMP/PKA and ERK1/2 pathways, and this effect is independent of DPP-4. Sitagliptin phosphate monohydrate shows protective effects on pancreatic islet grafts in 1-type diabetes models. Sitagliptin phosphate monohydrate can be used for the study of 1-type and 2-type diabetes.
|
-
-
- HY-P11242
-
|
|
Bacterial
NF-κB
p38 MAPK
JNK
ERK
TNF Receptor
Interleukin Related
|
Infection
|
Cm-CATH2 is an antimicrobial peptide discovered from Chelonia mydas. Cm-CATH2 has a potent, broad-spectrum and rapid bactericidal ability by rapidly destroying the integrity of bacterial cell membranes. It shows strong activity against Gram-positive bacteria (such as VREF, Staphylococcus aureus), Gram-negative bacteria (such as Escherichia coli, Klebsiella pneumoniae), and fungi (such as Candida albicans) with MICs ranges from 1.17 to 18.75 μg/mL. Cm-CATH2 is also effective against various aquatic pathogenic bacteria. Cm-CATH2 not only inhibits biofilm formation but can also remove the formed biofilms. Cm-CATH2 has immunomodulatory functions and chemotactic effects on immune cells, and can inhibit the production of pro-inflammatory cytokines by macrophages stimulated by LPS (HY-D1056). Cm-CATH2 prevents the activation of NF-κB by inhibiting the degradation of IκBα, and also inhibits the phosphorylation of MAPK signaling pathways (p38, JNK, ERK). Cm-CATH2 demonstrates strong anti-infective ability in mouse peritonitis models and pneumonia models .
|
-
-
- HY-P4136
-
|
|
ERK
|
Cancer
|
|
Myristoyl-MEK1 Derived Peptide Inhibitor 1 is the myristoylated form of the MEK1 Derived Peptide Inhibitor 1 (HY-P4133). Myristoyl-MEK1 Derived Peptide Inhibitor 1 inhibits ERK activation with an IC50 of 10 μM .
|
-
-
- HY-P11467
-
|
|
Bacterial
p38 MAPK
NF-κB
PERK
JNK
|
Cardiovascular Disease
Infection
|
|
Gy-CATH is an anionic antimicrobial peptide. Gy-CATH activates MAPK and NF-κB signaling pathways (elevated levels of phospho-ERK, -p38, -JNK, -p65, and -IκBα). Gy-CATH upregulates the expression levels of three physiological anticoagulant pathways. Gy-CATH inhibits ADP-, Collagen-, and PMA-induced platelet aggregation. Gy-CATH has no direct antimicrobial activity, but shows significant preventive abilities against mice infected with Staphylococcus aureus, Escherichia coli, and Methicillin (HY-121544)-resistant Staphylococcus aureus. Gy-CATH exhibits potent immunomodulatory activity, enhancing macrophage-and neutrophil-mediated bactericidal functions. Gy-CATH significantly reduces the extent of pulmonary fibrin deposition and prevents thrombosis in mice .
|
-
| Art. -Nr. |
Produktname |
Target |
Research Area |
-
- HY-P3206
-
|
Thymulin; Thymic factor
|
ERK
|
Neurological Disease
Inflammation/Immunology
Endocrinology
|
|
Serum thymic factor (Thymulin) is a zinc-dependent immunomodulatory peptide hormone, which can be produced by the thymic epithelial cells. Serum thymic factor stimulates the release of hormones from the pituitary gland, exhibits hypophysiotropic activity. Serum thymic factor protects rats from Cephaloridine (HY-B2072)-induced nephrotoxicity by inhibiting ERK activation. Serum thymic factor exhibits anti-diabetic, anti-inflammatory and analgesic effects. Serum thymic factor can be used in research about endocrine, reproductive, neurodegenerative and inflammatory diseases .
|
-
- HY-P1633
-
|
PG1
|
Bacterial
ERK
COX
NF-κB
Apoptosis
NO Synthase
Dengue Virus
|
Infection
Inflammation/Immunology
|
|
Protegrin-1 is an orally active antibacterial peptide. Protegrin-1 activates ERK, COX2, NFκB, inhibits Apoptosis, and NO production. Protegrin-1 has antibacterial activity against S. aureus, E. faecium, E. coli, P. aeruginosa and K. Pneumoniae, with MBC values between 10 and 20 µM. Protegrin-1 has antiviral activity against dengue NS2B-NS3. Protegrin-1 has anti-inflammatory activity. Protegrin-1 is used in the study of inflammatory diseases and infections .
|
-
- HY-P10102
-
Kp7-6
2 Publications Verification
|
Apoptosis
PERK
NF-κB
Caspase
JNK
|
Inflammation/Immunology
Cancer
|
|
Kp7-6 is a Fas mimetic peptide and also a Fas/FasL antagonist. Kp7-6 specifically binds to Fas and FasL, disrupts receptor complexes, and blocks downstream apoptosis signaling pathways. Kp7-6 inhibits the phosphorylation of ERK1-2, induces the phosphorylation of IκBα, and activates NF-κB. Kp7-6 inhibits the activation of caspase-8, caspase-3 and JNK, and suppresses human amylin-induced β-cell apoptosis. Kp7-6 inhibits FasL-induced lymphoid cytotoxicity and apoptosis. Kp7-6 reduces local tumor FasL expression, increases CD8 +Fas + T cell infiltration, and decreases tumor volume in pancreatic neuroendocrine tumor models. Kp7-6 prevents concanavalin A-induced liver injury in mice. Kp7-6 is applicable to research related to type 2 diabetes, concanavalin A-induced hepatitis and pancreatic neuroendocrine tumors .
|
-
- HY-P6442
-
|
|
Chemerin Receptor
Syk
ERK
Src
p38 MAPK
P-selectin
|
Cardiovascular Disease
Neurological Disease
Inflammation/Immunology
|
|
Chemerin15 is an anti-inflammatory peptide derived from Chemerin. Chemerin15 binds to ChemR23. Chemerin15 inhibits TNFα-induced activation of Syk, ERK and Src kinases. Chemerin15 increases the expression of p-p38 mRNA and protein. Chemerin15 mediates phagocytosis, resolution of inflammation, CD62L shedding and downregulation of PSGL-1 expression in macrophages and microglia. Chemerin15 inhibits neutrophil-mediated vascular inflammation and myocardial ischemia-reperfusion injury via ChemR23. Chemerin15 enhances microglial phagocytosis, thereby alleviating cerebral ischemia-reperfusion injury .
|
-
- HY-P0178
-
|
|
Integrin
|
Inflammation/Immunology
|
|
LXW7, a cyclic peptide containing Arg-Gly-Asp (RGD), is an integrin αvβ3 inhibitor. LXW7 has a high binding affinity to αvβ3 integrin with an IC50 of 0.68 μM. LXW7 increases phosphorylation of VEGFR-2 and activation of ERK1/2. Anti-inflammatory effect .
|
-
- HY-P3206A
-
|
Thymulin acetate; Thymic factor acetate
|
ERK
|
Neurological Disease
Inflammation/Immunology
Endocrinology
|
|
Serum thymic factor acetate (Thymulin acetate) is the acetate salt form of Serum thymic factor (HY-P3206). Serum thymic factor acetate is a zinc-dependent immunomodulatory peptide hormone, which can be produced by the thymic epithelial cells. Serum thymic factor acetate stimulates the release of hormones from the pituitary gland, exhibits hypophysiotropic activity. Serum thymic factor acetate protects rats from Cephaloridine (HY-B2072)-induced nephrotoxicity by inhibiting ERK activation. Serum thymic factor acetate exhibits anti-diabetic, anti-inflammatory and analgesic effects. Serum thymic factor acetate can be used in research about endocrine, reproductive, neurodegenerative and inflammatory diseases .
|
-
- HY-P0178A
-
|
|
Integrin
|
Inflammation/Immunology
|
|
LXW7 TFA, a cyclic peptide containing Arg-Gly-Asp (RGD), is an integrin αvβ3 inhibitor. LXW7 has a high binding affinity to αvβ3 integrin with an IC50 of 0.68 μM. LXW7 TFA increases phosphorylation of VEGFR-2 and activation of ERK1/2. Anti-inflammatory effect .
|
-
- HY-P4133
-
|
|
ERK
MEK
|
Cancer
|
|
MEK1 Derived Peptide Inhibitor 1 is a peptide inhibitor. MEK1 Derived Peptide Inhibitor 1 can inhibit the in vitro activation of ERK2 by MEK1 with an IC50 value of 30 μM. MEK1 Derived Peptide Inhibitor 1 can be used for the research of cell-permeable .
|
-
- HY-P4866
-
|
|
Integrin
Transglutaminase
Akt
p38 MAPK
ERK
Caspase
Apoptosis
|
Cardiovascular Disease
Metabolic Disease
Inflammation/Immunology
|
|
Q-Peptide is an angiopoietin-1 derived peptide (QHREDGS). Q-Peptide interacts with β1-integrin, binds to integrins on the surface of osteoblasts, and serves as an acyl donor substrate for Streptomyces mobaraensis transglutaminase. Q-Peptide activates Akt, MAPKp42/44, ILK, ERK1/2, and downregulates caspase-3/7. Q-Peptide inhibits cell apoptosis, enhances cell adhesion and migration, and promotes osteoblast differentiation, bone matrix deposition and mineralization. Q-Peptide can be used in studies related to myocardial infarction, bone regeneration, diabetic wound repair and human induced pluripotent stem cells .
|
-
- HY-P5977
-
|
Ste-MPKKKPTPIQLNP-NH₂; ERK Activation Inhibitor Peptide
|
ERK
|
Cancer
|
|
STE-MEK1(13) (Ste-MPKKKPTPIQLNP-NH ) is a cell permeable ERK1/2 inhibitor (IC50: 13-30 μM). STE-MEK1(13) inhibits ERK1/2 phosphorylation .
|
-
- HY-P10074
-
|
|
ERK
|
Inflammation/Immunology
|
|
TAT-MEK1 is an inhibitor ofERK2, consisting of TAT and MEK1 (N-terminal), TAT (YGRKKRRQRRR) derived from human immunodeficiency (HIV-1) transcriptional trans activator (TAT), is a cell-penetrating peptide. TAT-MEK1 IC50 in vitro for ERK2 is 29 μM .
|
-
- HY-P11242
-
|
|
Bacterial
NF-κB
p38 MAPK
JNK
ERK
TNF Receptor
Interleukin Related
|
Infection
|
Cm-CATH2 is an antimicrobial peptide discovered from Chelonia mydas. Cm-CATH2 has a potent, broad-spectrum and rapid bactericidal ability by rapidly destroying the integrity of bacterial cell membranes. It shows strong activity against Gram-positive bacteria (such as VREF, Staphylococcus aureus), Gram-negative bacteria (such as Escherichia coli, Klebsiella pneumoniae), and fungi (such as Candida albicans) with MICs ranges from 1.17 to 18.75 μg/mL. Cm-CATH2 is also effective against various aquatic pathogenic bacteria. Cm-CATH2 not only inhibits biofilm formation but can also remove the formed biofilms. Cm-CATH2 has immunomodulatory functions and chemotactic effects on immune cells, and can inhibit the production of pro-inflammatory cytokines by macrophages stimulated by LPS (HY-D1056). Cm-CATH2 prevents the activation of NF-κB by inhibiting the degradation of IκBα, and also inhibits the phosphorylation of MAPK signaling pathways (p38, JNK, ERK). Cm-CATH2 demonstrates strong anti-infective ability in mouse peritonitis models and pneumonia models .
|
-
- HY-P4136
-
|
|
ERK
|
Cancer
|
|
Myristoyl-MEK1 Derived Peptide Inhibitor 1 is the myristoylated form of the MEK1 Derived Peptide Inhibitor 1 (HY-P4133). Myristoyl-MEK1 Derived Peptide Inhibitor 1 inhibits ERK activation with an IC50 of 10 μM .
|
-
- HY-P11467
-
|
|
Bacterial
p38 MAPK
NF-κB
PERK
JNK
|
Cardiovascular Disease
Infection
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Gy-CATH is an anionic antimicrobial peptide. Gy-CATH activates MAPK and NF-κB signaling pathways (elevated levels of phospho-ERK, -p38, -JNK, -p65, and -IκBα). Gy-CATH upregulates the expression levels of three physiological anticoagulant pathways. Gy-CATH inhibits ADP-, Collagen-, and PMA-induced platelet aggregation. Gy-CATH has no direct antimicrobial activity, but shows significant preventive abilities against mice infected with Staphylococcus aureus, Escherichia coli, and Methicillin (HY-121544)-resistant Staphylococcus aureus. Gy-CATH exhibits potent immunomodulatory activity, enhancing macrophage-and neutrophil-mediated bactericidal functions. Gy-CATH significantly reduces the extent of pulmonary fibrin deposition and prevents thrombosis in mice .
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Chemical Structure |
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- HY-13749AS
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Sitagliptin-d4 phosphate (MK-0431-d4) is the deuterium labeled Sitagliptin phosphate (HY-13749A). Sitagliptin phosphate is an orally active and highly selective DPP4 inhibitor with an IC50 value of 19 nM. Sitagliptin phosphate blocks the degradation of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) by competing inhibition mechanism (Kᵢ = 1 nM), thereby increasing the level of active incretin. Sitagliptin phosphate can also directly stimulate the secretion of GLP-1 by intestinal L cells by activating the cAMP/PKA and ERK1/2 pathways, and this effect is independent of DPP-4. Sitagliptin phosphate shows protective effects on pancreatic islet grafts in 1-type diabetes models. Sitagliptin phosphate can be used for the study of 1-type and 2-type diabetes.
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- HY-13749S1
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Sitagliptin-d4 hydrochloride is the deuterium labeled Sitagliptin hydrochloride (HY-13749E). Sitagliptin hydrochloride is an orally active and highly selective DPP4 inhibitor with an IC50 value of 19 nM. Sitagliptin hydrochloride blocks the degradation of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) by competing inhibition mechanism (Kᵢ = 1 nM), thereby increasing the level of active incretin. Sitagliptin hydrochloride can also directly stimulate the secretion of GLP-1 by intestinal L cells by activating the cAMP/PKA and ERK1/2 pathways, and this effect is independent of DPP-4. Sitagliptin hydrochloride shows protective effects on pancreatic islet grafts in 1-type diabetes models. Sitagliptin hydrochloride can be used for the study of 1-type and 2-type diabetes.
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- HY-13749S3
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Sitagliptin-d6 (MK-0431-d6) is deuterium labeled Sitagliptin (HY-13749). Sitagliptin is an orally active and highly selective DPP4 inhibitor with an IC50 value of 19 nM. Sitagliptin blocks the degradation of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) by competing inhibition mechanism (Kᵢ = 1 nM), thereby increasing the level of active incretin. Sitagliptin can also directly stimulate the secretion of GLP-1 by intestinal L cells by activating the cAMP/PKA and ERK1/2 pathways, and this effect is independent of DPP-4. Sitagliptin shows protective effects on pancreatic islet grafts in 1-type diabetes models. Sitagliptin can be used for the study of 1-type and 2-type diabetes.
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- HY-13749S2
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Sitagliptin-d4 (MK-0431-d4) is deuterium labeled Sitagliptin (HY-13749). Sitagliptin is an orally active and highly selective DPP4 inhibitor with an IC50 value of 19 nM. Sitagliptin blocks the degradation of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) by competing inhibition mechanism (Kᵢ = 1 nM), thereby increasing the level of active incretin. Sitagliptin can also directly stimulate the secretion of GLP-1 by intestinal L cells by activating the cAMP/PKA and ERK1/2 pathways, and this effect is independent of DPP-4. Sitagliptin shows protective effects on pancreatic islet grafts in 1-type diabetes models. Sitagliptin can be used for the study of 1-type and 2-type diabetes.
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