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Results for "

c-Jun phosphorylation

" in MedChemExpress (MCE) Product Catalog:

35

Inhibitors & Agonists

4

Peptides

1

Natural
Products

1

Isotope-Labeled Compounds

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-13241
    Ralimetinib dimesylate
    Maximum Cited Publications
    15 Publications Verification

    LY2228820 dimesylate

    		 p38 MAPK Autophagy Apoptosis Inflammation/Immunology Cancer
    Ralimetinib dimesylate (LY2228820 dimesylate) is a selective, ATP-competitive inhibitor of p38 MAPK α/β with IC50s of 5.3 and 3.2 nM, respectively. Ralimetinib (LY2228820) selectively inhibits phosphorylation of MK2 (Thr334), with no effect on phosphorylation of p38a MAPK, JNK, ERK1/2, c-Jun, ATF2, or c-Myc.
    Ralimetinib dimesylate
  • HY-114332
    GNE-8505

    		MAP3K JNK Neurological Disease Metabolic Disease
    GNE-8505 is an orally active, blood-brain barrier-permeable selective dual leucine zipper kinase (DLK) inhibitor. GNE-8505 has an IC50 of 0.144 μM for pJNK, and EC50 of 0.457 μM for DRG. GNE-8505 inhibits the DLK/JNK pathway, reduces stress-induced c-Jun phosphorylation levels, decreases neuronal death and suppresses axonal degeneration. GNE-8505 reduces phosphorylated c-Jun levels in the retina, spinal cord and brain tissues of mice. GNE-8505 is applicable to research related to Alzheimer's disease and amyotrophic lateral sclerosis (ALS) .
    GNE-8505
  • HY-W050000
    OR-1855
    1 Publications Verification

    		 Drug Metabolite Reactive Oxygen Species (ROS) ERK p38 MAPK Cardiovascular Disease Inflammation/Immunology
    OR-1855, an active metabolite of Levosimendan (HY-14286), has effect on myometrial contractility. OR-1855 exerts anti-inflammatory effects by inhibiting IL-1β-induced ROS formation and NAD(P)H oxidase-dependent superoxide radical generation in HUVECs. OR-1855 inhibits IL-1β-induced phosphorylation p38 MAPK, ERK1/2, c-Jun and JNK in HUVECs. OR-1855 can be used for the study of inflammation .
    OR-1855
  • HY-B1451
    Imidapril hydrochloride

    TA-6366

    		 Angiotensin-converting Enzyme (ACE) MMP JNK Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    Imidapril hydrochloride (TA-6366) is an orally active dual inhibitor of angiotensin-converting enzyme (ACE) and MMP-9. Imidapril hydrochloride inhibits lipopolysaccharide-induced phosphorylation of c-Jun, MKK4 and JNK in monocytes, and downregulates the production of specific inflammatory factors such as TNF-α and IP-10, thereby exerting anti-inflammatory activity. Imidapril hydrochloride also effectively ameliorates mesangial expansion and reduces urinary albumin excretion by inhibiting angiotensin AngII production, lowering glomerular pressure and oxidative stress, thus delaying disease progression. Imidapril hydrochloride can also directly bind to the active site of MMP-9 to inhibit gelatinase activity, and suppress the enlargement of cerebral aneurysms without altering systemic blood pressure. Imidapril hydrochloride is widely applicable to related studies on autoimmune glomerulonephritis, diabetic nephropathy, cerebral aneurysms and other conditions .
    Imidapril hydrochloride
  • HY-14604
    Xaliproden hydrochloride
    1 Publications Verification

    SR57746A; SR57746 hydrochloride

    		 5-HT Receptor Dopamine Receptor Trk Receptor PKC ERK Akt JNK Neurological Disease Metabolic Disease
    Xaliproden (SR57746) hydrochloride (SR57746A) is an orally active, highly selective 5-HT1A receptor agonist. Xaliproden hydrochloride activates pertussis toxin-sensitive G protein-coupled signaling cascades, as well as the PKC, ERK1/ERK2, Akt and p21 Ras/MEK-1 pathways. Xaliproden hydrochloride also downregulates the JNK/p66/c-Jun signaling pathway, induces phosphorylation of the shc adaptor protein, regulates extracellular dopamine and 5-HT levels, and induces [ 35S]GTPγS labeling in rat brain structures rich in 5-HT1A receptors. Xaliproden hydrochloride exerts neurotrophic, neuroprotective, renoprotective, anti-inflammatory, anti-apoptotic, anti-fibrotic and analgesic effects. Xaliproden hydrochloride also enhances NGF-induced neurite outgrowth, promotes motor neuron survival, attenuates renal tubular injury and inhibits chemotherapy-induced mechanical allodynia, without activating or altering NGF-induced TrkA receptor activation. Xaliproden hydrochloride can be used in the research of motor neuron disease, diabetic nephropathy, chemotherapy-induced peripheral neuropathy, amyotrophic lateral sclerosis, Alzheimer's disease, acute tonic nociceptive pain, inflammatory pain, depression and anxiety .
    Xaliproden hydrochloride
  • HY-W010983
    SC-236
    2 Publications Verification

    		 COX PPAR Apoptosis Cardiovascular Disease Inflammation/Immunology Cancer
    SC-236 is an orally active COX-2 specific inhibitor (IC50 = 10 nM) and a PPARγ agonist. SC-236 suppresses activator protein-1 (AP-1) through c-Jun NH2-terminal kinase. SC-236 exerts anti-inflammatory effects by suppressing phosphorylation of ERK in a murine model .
    SC-236
  • HY-10851
    JNK-9L

    		JNK Reactive Oxygen Species (ROS) Neurological Disease
    JNK-9L (Compound 9l) is a BBB-penetrable and ATP-competitive JNK inhibitor with IC50s of 0.099 and 0.148  μM for JNK1 and JNK3, respectively. JNK-9L significantly inhibits c-jun phosphorylation and Streptozotocin (HY-13753)-induced ROS generation with an IC50 of 0.8  nM. JNK-9L can be used for neurodegenerative disorders like Parkinson’s disease research .
    JNK-9L
  • HY-B1451A
    Imidapril

    TA-6366 free base

    		 Angiotensin-converting Enzyme (ACE) MMP JNK Cardiovascular Disease Metabolic Disease
    Imidapril (TA-6366 free base) is an orally active dual inhibitor of angiotensin-converting enzyme (ACE) and MMP-9. Imidapril inhibits lipopolysaccharide-induced phosphorylation of c-Jun, MKK4 and JNK in monocytes, and downregulates the production of specific inflammatory factors such as TNF-α and IP-10, thereby exerting anti-inflammatory activity. Imidapril also effectively ameliorates mesangial expansion and reduces urinary albumin excretion by inhibiting angiotensin AngII production, lowering glomerular pressure and oxidative stress, thus delaying disease progression. Imidapril can also directly bind to the active site of MMP-9 to inhibit gelatinase activity, and suppress the enlargement of cerebral aneurysms without altering systemic blood pressure. Imidapril is widely applicable to related studies on autoimmune glomerulonephritis, diabetic nephropathy, cerebral aneurysms and other conditions .
    Imidapril
  • HY-P1190
    c-JUN peptide

    		JNK Apoptosis Inflammation/Immunology
    c-JUN peptide is a cell-permeable c-JUN-JNK interaction inhibitor. c-JUN peptide inhibits serum-induced c-Jun phosphorylation. c-JUN peptide induces apoptosis .
    c-JUN peptide
  • HY-P10506
    CMX-8933

    		JNK Neurological Disease
    CMX-8933 is an octapeptide fragment of the goldfish brain neurotrophic factor ependymin. CMX-8933 increases the enzymatic activity of c-Jun N-terminal kinase (JNK), increases the phosphorylation of JNK and c-Jun proteins, and increases the cellular levels of c-Jun and c-Fos mRNA. CMX-8933 can be used to study the role of ependymin in neuroplasticity, learning, memory formation, and neural regeneration .
    CMX-8933
  • HY-121683
    (E)-2-Hexadecenal

    16:1 Aldehyde; trans-2-Hexadecenal

    		 Mixed Lineage Kinase Apoptosis JNK Microtubule/Tubulin Cancer
    (E)-2-Hexadecenal (trans-2-Hexadecenal) is an MLK3 activator that induces cytoskeletal remodeling, leading to cell rounding, detachment, and ultimately apoptosis in human and mouse cells. (E)-2-Hexadecenal activates the MLK3 signaling pathway, phosphorylating MKK4/7 and JNK, subsequently activating downstream targets of JNK, such as c-Jun phosphorylation, cytochrome c release, Bax activation, Bid cleavage, and Bim translocation to mitochondria. (E)-2-Hexadecenal has potential applications in research related to sphingolipid signaling pathways .
    (E)-2-Hexadecenal
  • HY-N1326
    Santamarine

    Santamarin; Balchanin

    		 JNK p38 MAPK MMP NF-κB COX TNF Receptor Interleukin Related Reactive Oxygen Species (ROS) Apoptosis Mitochondrial Metabolism DNA/RNA Synthesis Keap1-Nrf2 Bcl-2 Family Caspase PARP TGF-beta/Smad Metabolic Disease Inflammation/Immunology Cancer
    Santamarine (Santamarin; Balchanin) is a sesquiterpene lactone found in Artemisia scoparia. Santamarine shows anti-inflammatory, antioxidant, anticancer and anti-photoaging activities. Santamarine suppresses UVA-induced phosphorylation of JNK and p38 MAPK, nuclear translocation of phosphorylated c-Fos and c-Jun, and AP-1-mediated MMP-1 transcription and secretion. Santamarine suppresses NF-κB signaling, iNOS, COX-2, TNF-α, and IL-1β production. Santamarine inhibits thioredoxin reductase activity, induces ROS production, mitochondrial apoptosis, G2/M cell cycle arrest, and DNA damage, and reduces cancer cell growth. Santamarine can be used for the photoaging, inflammatory diseases and cancer .
    Santamarine
  • HY-178692
    JNK-IN-25

    		JNK Neurological Disease Inflammation/Immunology Cancer
    JNK-IN-25 is a potent and selective JNK1/2/3 inhibitor with IC50 values of 1.54 (JNK1), 1.99 (JNK2), and 0.75 nM (JNK3), respectively. JNK-IN-25 inhibits phosphorylation of c-Jun in cells via covalently bonding with the conserved cysteine of JNK1/2/3. JNK-IN-25 can be used for research of  cancer, inflammatory and neurodegenerative diseases .
    JNK-IN-25
  • HY-168895
    c-Fos-IN-1

    		AP-1 ERK Apoptosis Cancer
    c-Fos-IN-1 (Compound P16) is a c-Jun inhibitor, and decreases mRNA levels and protein levels of c-Fos. c-Fos-IN-1 also inhibits the phosphorylation activity of ERK and the transcriptional activity of AP-1. c-Fos-IN-1 shows anticancer activity by inhibiting ERK/c-Fos/Jun pathway. c-Fos-IN-1 inhibits the proliferation and migration of gastric cancer cells (IC50: 2.31 μM for MGC-803 cell). c-Fos-IN-1 arrests cell cycle at G2/M phase and induces cancer cell apoptosis. c-Fos-IN-1 inhibits gastric cancer tumor growth .
    c-Fos-IN-1
  • HY-P10048
    TAT-JIP

    		JNK Inflammation/Immunology
    TAT-JIP inhibits the phosphorylation of endogenous c-jun activated by PHA–PMA .
    TAT-JIP
  • HY-171980
    OZO-H

    CAY10562

    		 Glutathione S-transferase JNK Cancer
    OZO-H is a GST inhibitor. OZO-H is an OZO derivative with potent anti-cancer effects. OZO-H releases JNK1 from GST-JNK1 complex. OZO-H induces JNK1 phosphorylation and activates c-Jun in cancer cells .
    OZO-H
  • HY-W010983R
    SC-236 (Standard)

    		Reference Standards COX PPAR Apoptosis Cardiovascular Disease Inflammation/Immunology Cancer
    SC-236 is an orally active COX-2 specific inhibitor (IC50 = 10 nM) and a PPARγ agonist. SC-236 suppresses activator protein-1 (AP-1) through c-Jun NH2-terminal kinase. SC-236 exerts anti-inflammatory effects by suppressing phosphorylation of ERK in a murine model .
    SC-236 (Standard)
  • HY-168859
    JNK3 inhibitor-9

    		JNK GSK-3 Amyloid-β Neurological Disease
    JNK3 inhibitor-9 (Compound 24a) is a potent, selective and BBB-permeable JNK3 inhibitor with an IC50 value of 12 nM. JNK3 inhibitor-9 also potently inhibits GSK3α/β (IC50s: 14 and 35 nM, respectively) involved in Tau phosphorylation. JNK3 inhibitor-9 reduces c-Jun and APP phosphorylation. JNK3 inhibitor-9 protects neurons from Aβ1-42 toxicity .
    JNK3 inhibitor-9
  • HY-P10401
    TAT-GluR6-9c

    		Apoptosis iGluR Cardiovascular Disease Neurological Disease
    TAT-GluR6-9c is a GluR6-PSD95 interaction blocker. By regulating the GluR6 mediated signaling pathway, TAT-GluR6-9c inhibits the activation of JNK and phosphorylation of c-Jun, reduces the expression of Fas L and thus reduces the occurrence of apoptosis. TAT-GluR6-9c can be used to study cerebral ischemia and neuroprotective strategies .
    TAT-GluR6-9c
  • HY-155593
    JNK-1-IN-2

    		JNK Inflammation/Immunology
    JNK-1-IN-2 (Compound c6) is a JNK-1 inhibitor (IC50: 33.5 nM). JNK-1-IN-2 also inhibits JNK-2 and JNK-3 with IC50s of 112.9 nM and 33.2 nM. JNK-1-IN-2 inhibits the phosphorylation of c-Jun. JNK-1-IN-2 reverses lung impairment. JNK-1-IN-2 can be used for research of pulmonary fibrosis .
    JNK-1-IN-2
  • HY-162922
    MAP4K4-IN-6

    		MAP4K JNK Neurological Disease
    MAP4K4-IN-6 (Compound 15f) is a MAP4K4 inhibitor (IC50: 80 nM). MAP4K4-IN-6 reduces the c-Jun phosphorylation. MAP4K4-IN-6 has neuroprotective effects. MAP4K4-IN-6 increases the viability of motor neurons. MAP4K4-IN-6 can be used for research of Amyotrophic lateral sclerosis (ALS) .
    MAP4K4-IN-6
  • HY-138844
    3-AP-Me

    		Eukaryotic Initiation Factor (eIF) p38 MAPK JNK Apoptosis Cancer
    3-AP-Me is a dimethyl derivative of the nucleotide reductase inhibitor 3-AP (SML0568). 3-AP-Me can activate the endoplasmic reticulum (ER) stress pathway by promoting the phosphorylation of eIF2α and increasing the gene expression of transcription factors ATF4 and ATF6, leading to cell apoptosis. Additionally, 3-AP-Me can activate the stress kinases c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinases. 3-AP-Me also leads to the upregulation of the spliced mRNA variant XBP1, can be used in cancer research .
    3-AP-Me
  • HY-169177
    JNK-1-IN-4

    		JNK Inflammation/Immunology
    JNK-1-IN-4 (Compound E1) is an inhibitor for JNK, that inhibits JNK-1, JNK-2 and JNK-3 with IC50s of 2.7, 19.0 and 9.0 nM, respectively. JNK-1-IN-4 inhibits the phosphorylation of c-Jun, and reduces the expression of TGF-β1-induced EMT marker proteins, such as fibronectin and α-SMA. JNK-1-IN-4 exhibits good pharmacokinetic characteristics with a bioavailability of 69%. JNK-1-IN-4 exhibits anti-fibrotic effect in Bleomycin (HY-17565)-induced mice idiopathic pulmonary fibrosis models .
    JNK-1-IN-4
  • HY-W050000R
    OR-1855 (Standard)

    		Drug Metabolite Reference Standards Reactive Oxygen Species (ROS) ERK p38 MAPK Cardiovascular Disease Inflammation/Immunology
    OR-1855 (Standard) is an analytical standard of OR-1855 (HY-W050000). This product is intended for research and analytical applications. OR-1855, an active metabolite of Levosimendan (HY-14286), has effect on myometrial contractility. OR-1855 exerts anti-inflammatory effects by inhibiting IL-1β-induced ROS formation and NAD(P)H oxidase-dependent superoxide radical generation in HUVECs. OR-1855 inhibits IL-1β-induced phosphorylation p38 MAPK, ERK1/2, c-Jun and JNK in HUVECs. OR-1855 can be used for the study of inflammation .
    OR-1855 (Standard)
  • HY-B1451S
    Imidapril-d3 hydrochloride

    		Isotope-Labeled Compounds Angiotensin-converting Enzyme (ACE) MMP JNK Cardiovascular Disease
    Imidapril-d3 hydrochloride (TA-6366-d3) is the deuterium labeled Imidapril hydrochloride. Imidapril hydrochloride (TA-6366) is an orally active dual inhibitor of angiotensin-converting enzyme (ACE) and MMP-9. Imidapril hydrochloride inhibits lipopolysaccharide-induced phosphorylation of c-Jun, MKK4 and JNK in monocytes, and downregulates the production of specific inflammatory factors such as TNF-α and IP-10, thereby exerting anti-inflammatory activity. Imidapril hydrochloride also effectively ameliorates mesangial expansion and reduces urinary albumin excretion by inhibiting angiotensin AngII production, lowering glomerular pressure and oxidative stress, thus delaying disease progression. Imidapril hydrochloride can also directly bind to the active site of MMP-9 to inhibit gelatinase activity, and suppress the enlargement of cerebral aneurysms without altering systemic blood pressure. Imidapril hydrochloride is widely applicable to related studies on autoimmune glomerulonephritis, diabetic nephropathy, cerebral aneurysms and other conditions .
    Imidapril-d3 hydrochloride
  • HY-B1451R
    Imidapril hydrochloride (Standard)

    TA-6366 (Standard)

    		 Reference Standards Angiotensin-converting Enzyme (ACE) MMP JNK Cardiovascular Disease Metabolic Disease
    Imidapril (hydrochloride) (Standard) is the analytical standard of Imidapril (hydrochloride). This product is intended for research and analytical applications. Imidapril hydrochloride (TA-6366) is an orally active dual inhibitor of angiotensin-converting enzyme (ACE) and MMP-9. Imidapril hydrochloride inhibits lipopolysaccharide-induced phosphorylation of c-Jun, MKK4 and JNK in monocytes, and downregulates the production of specific inflammatory factors such as TNF-α and IP-10, thereby exerting anti-inflammatory activity. Imidapril hydrochloride also effectively ameliorates mesangial expansion and reduces urinary albumin excretion by inhibiting angiotensin AngII production, lowering glomerular pressure and oxidative stress, thus delaying disease progression. Imidapril hydrochloride can also directly bind to the active site of MMP-9 to inhibit gelatinase activity, and suppress the enlargement of cerebral aneurysms without altering systemic blood pressure. Imidapril hydrochloride is widely applicable to related studies on autoimmune glomerulonephritis, diabetic nephropathy, cerebral aneurysms and other conditions .
    Imidapril hydrochloride (Standard)
  • HY-170484
    KAI-11101

    		MAP3K p38 MAPK Neurological Disease
    KAI-11101 is the inhibitor for dual leucine zipper kinase (DLK, MAP3K12) with a Ki of 0.7 nM. KAI-11101 inhibits Paclitaxel (HY-B0015)-induced cJun phosphorylation (IC50=95 nM) and thus inhibits the activation of MAPK pathway. KAI-11101 is blood brain barrier penetrable and can be further investigated for its neuroprotective property .
    KAI-11101
  • HY-119820
    Xaliproden free base

    SR57746A free base

    		 Akt Dopamine Receptor Trk Receptor 5-HT Receptor PKC JNK ERK Neurological Disease
    Xaliproden (SR57746) free base is an orally active, highly selective 5-HT1A receptor agonist. Xaliproden free base activates pertussis toxin-sensitive G protein-coupled signaling cascades, as well as the PKC, ERK1/ERK2, Akt and p21 Ras/MEK-1 pathways. Xaliproden free base also downregulates the JNK/p66/c-Jun signaling pathway, induces phosphorylation of the shc adaptor protein, regulates extracellular dopamine and 5-HT levels, and induces [ 35S]GTPγS labeling in rat brain structures rich in 5-HT1A receptors. Xaliproden free base exerts neurotrophic, neuroprotective, renoprotective, anti-inflammatory, anti-apoptotic, anti-fibrotic and analgesic effects. Xaliproden free base also enhances NGF-induced neurite outgrowth, promotes motor neuron survival, attenuates renal tubular injury and inhibits chemotherapy-induced mechanical allodynia, without activating or altering NGF-induced TrkA receptor activation. Xaliproden free base can be used in the research of motor neuron disease, diabetic nephropathy, chemotherapy-induced peripheral neuropathy, amyotrophic lateral sclerosis, Alzheimer's disease, acute tonic nociceptive pain, inflammatory pain, depression and anxiety .
    Xaliproden free base
  • HY-181662
    DLK-IN-2

    		MAP3K Neurological Disease
    DLK-IN-2 is a selective inhibitor of DLK and neuroprotective agent. DLK-IN-2 shows no significant inhibition against CYPs 3A4, 2D6 and 2C9. DLK-IN-2 inhibits acute axonal palmitoylation of DLK, blocks DLK-dependent pro-degenerative axon-to-soma retrograde signaling and suppresses c-Jun phosphorylation. DLK-IN-2 can be used for the mechanistic study of neurodegenerative diseases .
    DLK-IN-2
  • HY-181993
    JNK3-IN-11

    		JNK Cadherin Collagen PAI-1 Endocrinology
    JNK3-IN-11 is a selective JNK3 inhibitor with an IC50 of 2.08 nM. JNK3-IN-11 binds to the JNK3 ATP-binding pocket, forming conserved hydrogen bonds with Met149 and a water-mediated hydrogen bond with Lys93. JNK3-IN-11 suppresses TGF-β1-induced c-Jun phosphorylation, reduces profibrotic markers COL1A1 and PAI-1, restores E-cadherin expression, and has protection against podocyte injure. JNK3-IN-11 can be used for the research of chronic kidney disease .
    JNK3-IN-11
  • HY-181812
    JNK2/MKK7 PPI-IN-1

    		JNK p38 MAPK Interleukin Related TNF Receptor Inflammation/Immunology
    JNK2/MKK7 PPI-IN-1 is an orally active JNK2 inhibitor with an IC50 of 0.99 μM and a Kd of 81.6 μM. JNK2/MKK7 PPI-IN-1 inhibits JNK2 kinase activity, disrupts JNK2-MKK7 protein-protein interaction, and reduces c-Jun phosphorylation. JNK2/MKK7 PPI-IN-1 inhibits LPS-induced overexpression of inflammatory cytokines IL-6 and TNF-α. JNK2/MKK7 PPI-IN-1 can be used for the research of acute lung injury .
    JNK2/MKK7 PPI-IN-1
  • HY-164111
    JNK-IN-17

    		JAK Neurological Disease
    JNK-IN-17 (Compound 9J) is a selective and potent JNK inhibitor with IC50 values of 0.039, 0.079 μM for JNK1 and JNK3. JNK-IN-17 can inhibit c-Jun phosphorylation with an IC50 of 0.082 μM in Streptozotocin (HY-13753)-infuced INS-1 pancreatic islet β cells. JNK-IN-17 shows inhibition rate ≤ 33% on the four main P450 subtypes (2C9, 2D6, 3A4, 1A2) in human liver microsomes, indicating a relatively low risk of drug interactions. JNK-IN-17 can be used for researches of neurological and metabolic disease, such as Parkinson's disease .
    JNK-IN-17
  • HY-107091R
    Aspartyl-alanyl-diketopiperazine (Standard)

    DA-DKP (Standard)

    		 Reference Standards MEK p38 MAPK IFNAR TNF Receptor Ras JNK Inflammation/Immunology
    Aspartyl-alanyl-diketopiperazine (DA-DKP) (Standard) is the analytical standard of Aspartyl-alanyl-diketopiperazine (HY-107091). This product is intended for research and analytical applications. Aspartyl-alanyl-diketopiperazine is an immunomodulatory molecule and anti-inflammatory agent. Aspartyl-alanyl-diketopiperazine increases the level of active Rap1 in activated human T lymphocytes and reduces the phosphorylation levels of Ras, ATF-2, c-jun, MEK1, MEKK1, ERK1, JNK1,2,3, p38MAPK and MEF-2. Aspartyl-alanyl-diketopiperazine inhibits the production of pro-inflammatory cytokines, including the levels of IFN-γ and TNF-α. Aspartyl-alanyl-diketopiperazine can be used in studies of inflammatory immune responses .
    Aspartyl-alanyl-diketopiperazine (Standard)
  • HY-181556
    JNK3-IN-10

    		JNK TGF-beta/Smad Cadherin Inflammation/Immunology
    JNK3-IN-10 is a blood-brain barrier-impermeable JNK3 inhibitor (IC50=0.257 nM) with over 400-fold selectivity over JNK1. JNK3-IN-10 blocks the JNK3-mediated signaling pathway downstream of TGF-β1, inhibits TGF-β1-induced phosphorylation of c-Jun, reduces the expression of pro-fibrotic markers, and restores the expression of the epithelial protein E-cadherin. JNK3-IN-10 exhibits low cytotoxicity, anti-fibrotic, cytoprotective and renoprotective effects, and alleviates albuminuria, glomerulosclerosis and podocyte foot process fusion. JNK3-IN-10 can be used for the research of chronic kidney disease, glomerulosclerosis and adriamycin-induced nephropathy .
    JNK3-IN-10
  • HY-14604R
    Xaliproden hydrochloride (Standard)

    SR57746A (Standard); SR57746 hydrochloride (Standard)

    		 Reference Standards Akt Dopamine Receptor Trk Receptor 5-HT Receptor PKC JNK ERK Neurological Disease Cancer
    Xaliproden (hydrochloride) (Standard) is the analytical standard of Xaliproden (hydrochloride). This product is intended for research and analytical applications. Xaliproden (SR57746) hydrochloride (SR57746A) is an orally active, highly selective 5-HT1A receptor agonist. Xaliproden hydrochloride activates pertussis toxin-sensitive G protein-coupled signaling cascades, as well as the PKC, ERK1/ERK2, Akt and p21 Ras/MEK-1 pathways. Xaliproden hydrochloride also downregulates the JNK/p66/c-Jun signaling pathway, induces phosphorylation of the shc adaptor protein, regulates extracellular dopamine and 5-HT levels, and induces [ 35S]GTPγS labeling in rat brain structures rich in 5-HT1A receptors. Xaliproden hydrochloride exerts neurotrophic, neuroprotective, renoprotective, anti-inflammatory, anti-apoptotic, anti-fibrotic and analgesic effects. Xaliproden hydrochloride also enhances NGF-induced neurite outgrowth, promotes motor neuron survival, attenuates renal tubular injury and inhibits chemotherapy-induced mechanical allodynia, without activating or altering NGF-induced TrkA receptor activation. Xaliproden hydrochloride can be used in the research of motor neuron disease, diabetic nephropathy, chemotherapy-induced peripheral neuropathy, amyotrophic lateral sclerosis, Alzheimer's disease, acute tonic nociceptive pain, inflammatory pain, depression and anxiety .
    Xaliproden hydrochloride (Standard)

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