bay k 8644  (Alomone Labs)


Bioz Verified Symbol Alomone Labs is a verified supplier
Bioz Manufacturer Symbol Alomone Labs manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 93
    Name:
    Bay K8644
    Description:
    Bay K 8644 is a dihydropyridine that acts as L type voltage gated Ca2 channel agonist The enantiomer has strong Ca2 channel agonist properties whereas the enantiomer has a weak Ca2 channel antagonist activity The net activity of the racemic mix is L type channels opening In the presence of this agonist channels tend to open for longer periods causing a large increase in the channel microscopic response Bay K8644 is also an inhibitor by increasing the inactivation of a Shaker Kv channel
    Catalog Number:
    B-350
    Price:
    63.0
    Category:
    Small Molecule
    Source:
    Synthetic
    Applications:
    0
    Purity:
    >99% (HPLC)
    Size:
    5 mg
    Format:
    Lyophilized/solid.
    Formula:
    C16H15F3N2O4
    Molecular Weight:
    356.3
    Molecule Name:
    1,4-Dihydro-2,6-dimethyl-5-nitro-4-[2-(trifluoromethyl) phenyl]-3-pyridinecarboxylic acid, methyl ester.
    Buy from Supplier


    Structured Review

    Alomone Labs bay k 8644
    Bay K8644
    Bay K 8644 is a dihydropyridine that acts as L type voltage gated Ca2 channel agonist The enantiomer has strong Ca2 channel agonist properties whereas the enantiomer has a weak Ca2 channel antagonist activity The net activity of the racemic mix is L type channels opening In the presence of this agonist channels tend to open for longer periods causing a large increase in the channel microscopic response Bay K8644 is also an inhibitor by increasing the inactivation of a Shaker Kv channel
    https://www.bioz.com/result/bay k 8644/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    bay k 8644 - by Bioz Stars, 2021-09
    93/100 stars

    Images

    1) Product Images from "Dynamics of Insulin Secretion from EndoC-βH1 β-Cell Pseudoislets in Response to Glucose and Other Nutrient and Nonnutrient Secretagogues"

    Article Title: Dynamics of Insulin Secretion from EndoC-βH1 β-Cell Pseudoislets in Response to Glucose and Other Nutrient and Nonnutrient Secretagogues

    Journal: Journal of Diabetes Research

    doi: 10.1155/2017/2309630

    Kinetic profiles of insulin secretion from perifused EndoC- β H1  β -cell pseudoislets in response to a 30 min stimulation with glibenclamide (10  μ M) (a) ( n  = 5) as well as with Bay K 8644 (1  μ M) (b) ( n  = 5) in the presence of glucose (10 mM) (a) ( n  = 7). After a 20 min preperifusion phase with basal glucose (3 mM), a 30 min stimulation period and thereafter a return of the perifusion to basal glucose medium for another 30 min are depicted. Shown are means ± SEM of insulin release rates expressed as ng/min and per 100 pseudoislets (PI).
    Figure Legend Snippet: Kinetic profiles of insulin secretion from perifused EndoC- β H1 β -cell pseudoislets in response to a 30 min stimulation with glibenclamide (10  μ M) (a) ( n = 5) as well as with Bay K 8644 (1  μ M) (b) ( n = 5) in the presence of glucose (10 mM) (a) ( n = 7). After a 20 min preperifusion phase with basal glucose (3 mM), a 30 min stimulation period and thereafter a return of the perifusion to basal glucose medium for another 30 min are depicted. Shown are means ± SEM of insulin release rates expressed as ng/min and per 100 pseudoislets (PI).

    Techniques Used:

    2) Product Images from "Role of age, Rho‐kinase 2 expression, and G protein‐mediated signaling in the myogenic response in mouse small mesenteric arteries. Role of age, Rho‐kinase 2 expression, and G protein‐mediated signaling in the myogenic response in mouse small mesenteric arteries"

    Article Title: Role of age, Rho‐kinase 2 expression, and G protein‐mediated signaling in the myogenic response in mouse small mesenteric arteries. Role of age, Rho‐kinase 2 expression, and G protein‐mediated signaling in the myogenic response in mouse small mesenteric arteries

    Journal: Physiological Reports

    doi: 10.14814/phy2.13863

    (A) Effect of the L‐type Ca 2+ channel agonist BayK 8644 (2 μ mol L −1 ) on MT . A total of five vessels from five young mice were tested. (B) In a parallel series of experiment the effect of the ROCK 2 inhibitor KD 025 (5 μ mol L −1 ) in the presence of BayK 8644 was investigated. A total of five vessels from four young mice were tested. (C) For comparison, the effect of ROCK 2 inhibition with KD 025 (5 μ mol L −1 ) was tested in a small pial arteries from three healthy Göttingen minipigs. This original trace showing a pial vessel that develops MT at 60, 90 and 120 mm Hg, and MT is strongly inhibited by direct bath application of KD 025. Note that the full effect of KD 025 takes 5–10 min to be established. (D) The same experiment but with results for all three minipigs depicted as myogenic tone. Also shown is the effect of washout (15–20 min) of the drug. (E) Active vasoconstriction to direct bath application of ET ‐1 (20 and 50 nmol L −1 ) in small pial arteries from three minipigs pressurized at 60 mm Hg. Potent inhibition of vascular tone is induced by KD 025, and the remainder of tone is abolished by direct bath application of the L‐type antagonist nifedipine (10 μ mol L −1 ).
    Figure Legend Snippet: (A) Effect of the L‐type Ca 2+ channel agonist BayK 8644 (2 μ mol L −1 ) on MT . A total of five vessels from five young mice were tested. (B) In a parallel series of experiment the effect of the ROCK 2 inhibitor KD 025 (5 μ mol L −1 ) in the presence of BayK 8644 was investigated. A total of five vessels from four young mice were tested. (C) For comparison, the effect of ROCK 2 inhibition with KD 025 (5 μ mol L −1 ) was tested in a small pial arteries from three healthy Göttingen minipigs. This original trace showing a pial vessel that develops MT at 60, 90 and 120 mm Hg, and MT is strongly inhibited by direct bath application of KD 025. Note that the full effect of KD 025 takes 5–10 min to be established. (D) The same experiment but with results for all three minipigs depicted as myogenic tone. Also shown is the effect of washout (15–20 min) of the drug. (E) Active vasoconstriction to direct bath application of ET ‐1 (20 and 50 nmol L −1 ) in small pial arteries from three minipigs pressurized at 60 mm Hg. Potent inhibition of vascular tone is induced by KD 025, and the remainder of tone is abolished by direct bath application of the L‐type antagonist nifedipine (10 μ mol L −1 ).

    Techniques Used: Mouse Assay, Inhibition

    3) Product Images from "Dynamics of Insulin Secretion from EndoC-βH1 β-Cell Pseudoislets in Response to Glucose and Other Nutrient and Nonnutrient Secretagogues"

    Article Title: Dynamics of Insulin Secretion from EndoC-βH1 β-Cell Pseudoislets in Response to Glucose and Other Nutrient and Nonnutrient Secretagogues

    Journal: Journal of Diabetes Research

    doi: 10.1155/2017/2309630

    Kinetic profiles of insulin secretion from perifused EndoC- β H1  β -cell pseudoislets in response to a 30 min stimulation with glibenclamide (10  μ M) (a) ( n  = 5) as well as with Bay K 8644 (1  μ M) (b) ( n  = 5) in the presence of glucose (10 mM) (a) ( n  = 7). After a 20 min preperifusion phase with basal glucose (3 mM), a 30 min stimulation period and thereafter a return of the perifusion to basal glucose medium for another 30 min are depicted. Shown are means ± SEM of insulin release rates expressed as ng/min and per 100 pseudoislets (PI).
    Figure Legend Snippet: Kinetic profiles of insulin secretion from perifused EndoC- β H1 β -cell pseudoislets in response to a 30 min stimulation with glibenclamide (10  μ M) (a) ( n = 5) as well as with Bay K 8644 (1  μ M) (b) ( n = 5) in the presence of glucose (10 mM) (a) ( n = 7). After a 20 min preperifusion phase with basal glucose (3 mM), a 30 min stimulation period and thereafter a return of the perifusion to basal glucose medium for another 30 min are depicted. Shown are means ± SEM of insulin release rates expressed as ng/min and per 100 pseudoislets (PI).

    Techniques Used:

    4) Product Images from "Differential outgrowth of axons and their branches is regulated by localized calcium transients"

    Article Title: Differential outgrowth of axons and their branches is regulated by localized calcium transients

    Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience

    doi: 10.1523/JNEUROSCI.4548-07.2008

    Bath application of BayK 8644 increases differential process outgrowth. A, Timelapse images of a cortical neuron exposed to BayK for 8 hours, showing extension of the primary axon extends and retraction of the branch. B, C, Phase images showing the effect
    Figure Legend Snippet: Bath application of BayK 8644 increases differential process outgrowth. A, Timelapse images of a cortical neuron exposed to BayK for 8 hours, showing extension of the primary axon extends and retraction of the branch. B, C, Phase images showing the effect

    Techniques Used:

    Bath application of BayK 8644 induces localized calcium transients. A, DIC (left) and fluorescence images (right) of a cortical neuron exposed to BayK 8644. Bath application of BayK at 0:00 induced high frequency localized calcium transients primarily
    Figure Legend Snippet: Bath application of BayK 8644 induces localized calcium transients. A, DIC (left) and fluorescence images (right) of a cortical neuron exposed to BayK 8644. Bath application of BayK at 0:00 induced high frequency localized calcium transients primarily

    Techniques Used: Fluorescence

    Related Articles

    other:

    Article Title: Dynamics of Insulin Secretion from EndoC-βH1 β-Cell Pseudoislets in Response to Glucose and Other Nutrient and Nonnutrient Secretagogues
    Article Snippet: The following chemicals were used in the experiments: d -glucose, l -leucine, l -glutamine, pyruvate, l-lactate, IBMX, and forskolin (Sigma-Aldrich, Taufkirchen, Germany), mannoheptulose (Bujno Synthesis, Warsaw, Poland), glibenclamide (Santa Cruz Biotechnology, Dallas, USA), and Bay K 8644 (Alomone Labs, Jerusalem, Israel).

    Article Title: Dynamics of Insulin Secretion from EndoC-βH1 β-Cell Pseudoislets in Response to Glucose and Other Nutrient and Nonnutrient Secretagogues
    Article Snippet: A strong potentiation of insulin secretion was also observed by the sulfonylurea drug glibenclamide, a Kir 6.2 potassium channel blocker that exerts its effect via interaction with the sulfonylurea receptor SUR1 and by Bay K 8644, a voltage-sensitive Ca2+ channel activator, which mediates its potentiating effect on insulin secretion through opening of this channel.

    Article Title: Upregulation of voltage-gated Na+ channels by long-term activation of the ghrelin-growth hormone secretagogue receptor in clonal GC somatotropes.
    Article Snippet: A central question in adenohypophyseal cell physiology concerns the role of transmembrane ionic fluxes in the initiation of the hormone secretion process.. In the current report, we investigated the effects of the growth hormone (GH) secretagogues ghrelin and GH-releasing peptide-6 (GHRP-6) on the regulation of the functional expression of voltage-gated Na(+) channels using the tumoral somatotrope GC cell line as a model.

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 92
    Alomone Labs k252a
    In vivo efficacy of <t>K252a</t> in a DLBCL xenograft model. For the GCB-DLBCL xenograft model, SCID mice were injected with 1 × 10 7 SUDHL4 cells subcutaneously. ( A ) The human SUDHL4 cell origin of tumours was confirmed by immunohistochemistry (with anti-human CD20) and representative stainings for NGF, BDNF, Trk, and p75 NTR receptor are done (× 400). ( B ) After the tumours had become established (∼6 weeks after tumour inoculation), mice were treated with vehicle (Controls, n =10), K252a (0.5 mg kg −1 , n =10) or rituximab (25 mg kg −1 , n =5) or both agents ( n =8) for 3 weeks. Results are expressed as mean tumour volumes (cm 3 )±s.d. *, ** P
    K252a, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/k252a/product/Alomone Labs
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    k252a - by Bioz Stars, 2021-09
    92/100 stars
      Buy from Supplier

    93
    Alomone Labs bay k 8644
    Kinetic profiles of insulin secretion from perifused EndoC- β H1  β -cell pseudoislets in response to a 30 min stimulation with glibenclamide (10  μ M) (a) ( n  = 5) as well as with Bay K 8644 (1  μ M) (b) ( n  = 5) in the presence of glucose (10 mM) (a) ( n  = 7). After a 20 min preperifusion phase with basal glucose (3 mM), a 30 min stimulation period and thereafter a return of the perifusion to basal glucose medium for another 30 min are depicted. Shown are means ± SEM of insulin release rates expressed as ng/min and per 100 pseudoislets (PI).
    Bay K 8644, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bay k 8644/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    bay k 8644 - by Bioz Stars, 2021-09
    93/100 stars
      Buy from Supplier

    Image Search Results


    In vivo efficacy of K252a in a DLBCL xenograft model. For the GCB-DLBCL xenograft model, SCID mice were injected with 1 × 10 7 SUDHL4 cells subcutaneously. ( A ) The human SUDHL4 cell origin of tumours was confirmed by immunohistochemistry (with anti-human CD20) and representative stainings for NGF, BDNF, Trk, and p75 NTR receptor are done (× 400). ( B ) After the tumours had become established (∼6 weeks after tumour inoculation), mice were treated with vehicle (Controls, n =10), K252a (0.5 mg kg −1 , n =10) or rituximab (25 mg kg −1 , n =5) or both agents ( n =8) for 3 weeks. Results are expressed as mean tumour volumes (cm 3 )±s.d. *, ** P

    Journal: British Journal of Cancer

    Article Title: Anti-apoptotic role and clinical relevance of neurotrophins in diffuse large B-cell lymphomas

    doi: 10.1038/bjc.2015.274

    Figure Lengend Snippet: In vivo efficacy of K252a in a DLBCL xenograft model. For the GCB-DLBCL xenograft model, SCID mice were injected with 1 × 10 7 SUDHL4 cells subcutaneously. ( A ) The human SUDHL4 cell origin of tumours was confirmed by immunohistochemistry (with anti-human CD20) and representative stainings for NGF, BDNF, Trk, and p75 NTR receptor are done (× 400). ( B ) After the tumours had become established (∼6 weeks after tumour inoculation), mice were treated with vehicle (Controls, n =10), K252a (0.5 mg kg −1 , n =10) or rituximab (25 mg kg −1 , n =5) or both agents ( n =8) for 3 weeks. Results are expressed as mean tumour volumes (cm 3 )±s.d. *, ** P

    Article Snippet: For the viability tests, cells were incubated with: various concentrations of rituximab (1–20 μ g ml−1 , MabThera, stock 10 mg ml−1 , a generous gift from CHRU Dupuytren of Limoges, Pharmacie centrale), K252a (350 nM ; Alomone Labs, Jerusalem, Israel), pro-BDNF (1–10 ng ml−1 , Alomone Labs), neutralising anti-BDNF (15 μ g ml−1 , Promega, Madison, WI, USA), exogenous BDNF (100 ng ml−1 , Promega), anti-p75NTR neutralising antibody (1–10–100 ng ml−1 , clone ME20.4, Merck KGaA, Darmstadt, Germany) alone or in combination.

    Techniques: In Vivo, Mouse Assay, Injection, Immunohistochemistry

    Pharmacological inhibition of Trk receptors sensitises the effect of rituximab in ABC and GCB cell lines. GCB- (SUDHL4) and ABC (OCI-LY10)-like DLBCL cells were exposed to rituximab (RTX, 1 and 20 μ g ml −1 ) with or without (C, controls) pharmacological inhibitor of Trk receptors, K252a (350 n M ). ( A ) Inhibition of Trk signalling by K252a was confirmed in both cell lines by western blot analysis of TrkA, TrkB and TrkC receptor phosphorylation. ( B ) Viability of cells was evaluated during 48 h and 72 h using the XTT test and data are expressed as means±s.d. of relative cell viability (ratio) related to control obtained from four independent experiments. ** P

    Journal: British Journal of Cancer

    Article Title: Anti-apoptotic role and clinical relevance of neurotrophins in diffuse large B-cell lymphomas

    doi: 10.1038/bjc.2015.274

    Figure Lengend Snippet: Pharmacological inhibition of Trk receptors sensitises the effect of rituximab in ABC and GCB cell lines. GCB- (SUDHL4) and ABC (OCI-LY10)-like DLBCL cells were exposed to rituximab (RTX, 1 and 20 μ g ml −1 ) with or without (C, controls) pharmacological inhibitor of Trk receptors, K252a (350 n M ). ( A ) Inhibition of Trk signalling by K252a was confirmed in both cell lines by western blot analysis of TrkA, TrkB and TrkC receptor phosphorylation. ( B ) Viability of cells was evaluated during 48 h and 72 h using the XTT test and data are expressed as means±s.d. of relative cell viability (ratio) related to control obtained from four independent experiments. ** P

    Article Snippet: For the viability tests, cells were incubated with: various concentrations of rituximab (1–20 μ g ml−1 , MabThera, stock 10 mg ml−1 , a generous gift from CHRU Dupuytren of Limoges, Pharmacie centrale), K252a (350 nM ; Alomone Labs, Jerusalem, Israel), pro-BDNF (1–10 ng ml−1 , Alomone Labs), neutralising anti-BDNF (15 μ g ml−1 , Promega, Madison, WI, USA), exogenous BDNF (100 ng ml−1 , Promega), anti-p75NTR neutralising antibody (1–10–100 ng ml−1 , clone ME20.4, Merck KGaA, Darmstadt, Germany) alone or in combination.

    Techniques: Inhibition, Western Blot

    Kinetic profiles of insulin secretion from perifused EndoC- β H1  β -cell pseudoislets in response to a 30 min stimulation with glibenclamide (10  μ M) (a) ( n  = 5) as well as with Bay K 8644 (1  μ M) (b) ( n  = 5) in the presence of glucose (10 mM) (a) ( n  = 7). After a 20 min preperifusion phase with basal glucose (3 mM), a 30 min stimulation period and thereafter a return of the perifusion to basal glucose medium for another 30 min are depicted. Shown are means ± SEM of insulin release rates expressed as ng/min and per 100 pseudoislets (PI).

    Journal: Journal of Diabetes Research

    Article Title: Dynamics of Insulin Secretion from EndoC-βH1 β-Cell Pseudoislets in Response to Glucose and Other Nutrient and Nonnutrient Secretagogues

    doi: 10.1155/2017/2309630

    Figure Lengend Snippet: Kinetic profiles of insulin secretion from perifused EndoC- β H1 β -cell pseudoislets in response to a 30 min stimulation with glibenclamide (10  μ M) (a) ( n = 5) as well as with Bay K 8644 (1  μ M) (b) ( n = 5) in the presence of glucose (10 mM) (a) ( n = 7). After a 20 min preperifusion phase with basal glucose (3 mM), a 30 min stimulation period and thereafter a return of the perifusion to basal glucose medium for another 30 min are depicted. Shown are means ± SEM of insulin release rates expressed as ng/min and per 100 pseudoislets (PI).

    Article Snippet: The following chemicals were used in the experiments: d -glucose, l -leucine, l -glutamine, pyruvate, l-lactate, IBMX, and forskolin (Sigma-Aldrich, Taufkirchen, Germany), mannoheptulose (Bujno Synthesis, Warsaw, Poland), glibenclamide (Santa Cruz Biotechnology, Dallas, USA), and Bay K 8644 (Alomone Labs, Jerusalem, Israel).

    Techniques:

    (A) Effect of the L‐type Ca 2+ channel agonist BayK 8644 (2 μ mol L −1 ) on MT . A total of five vessels from five young mice were tested. (B) In a parallel series of experiment the effect of the ROCK 2 inhibitor KD 025 (5 μ mol L −1 ) in the presence of BayK 8644 was investigated. A total of five vessels from four young mice were tested. (C) For comparison, the effect of ROCK 2 inhibition with KD 025 (5 μ mol L −1 ) was tested in a small pial arteries from three healthy Göttingen minipigs. This original trace showing a pial vessel that develops MT at 60, 90 and 120 mm Hg, and MT is strongly inhibited by direct bath application of KD 025. Note that the full effect of KD 025 takes 5–10 min to be established. (D) The same experiment but with results for all three minipigs depicted as myogenic tone. Also shown is the effect of washout (15–20 min) of the drug. (E) Active vasoconstriction to direct bath application of ET ‐1 (20 and 50 nmol L −1 ) in small pial arteries from three minipigs pressurized at 60 mm Hg. Potent inhibition of vascular tone is induced by KD 025, and the remainder of tone is abolished by direct bath application of the L‐type antagonist nifedipine (10 μ mol L −1 ).

    Journal: Physiological Reports

    Article Title: Role of age, Rho‐kinase 2 expression, and G protein‐mediated signaling in the myogenic response in mouse small mesenteric arteries. Role of age, Rho‐kinase 2 expression, and G protein‐mediated signaling in the myogenic response in mouse small mesenteric arteries

    doi: 10.14814/phy2.13863

    Figure Lengend Snippet: (A) Effect of the L‐type Ca 2+ channel agonist BayK 8644 (2 μ mol L −1 ) on MT . A total of five vessels from five young mice were tested. (B) In a parallel series of experiment the effect of the ROCK 2 inhibitor KD 025 (5 μ mol L −1 ) in the presence of BayK 8644 was investigated. A total of five vessels from four young mice were tested. (C) For comparison, the effect of ROCK 2 inhibition with KD 025 (5 μ mol L −1 ) was tested in a small pial arteries from three healthy Göttingen minipigs. This original trace showing a pial vessel that develops MT at 60, 90 and 120 mm Hg, and MT is strongly inhibited by direct bath application of KD 025. Note that the full effect of KD 025 takes 5–10 min to be established. (D) The same experiment but with results for all three minipigs depicted as myogenic tone. Also shown is the effect of washout (15–20 min) of the drug. (E) Active vasoconstriction to direct bath application of ET ‐1 (20 and 50 nmol L −1 ) in small pial arteries from three minipigs pressurized at 60 mm Hg. Potent inhibition of vascular tone is induced by KD 025, and the remainder of tone is abolished by direct bath application of the L‐type antagonist nifedipine (10 μ mol L −1 ).

    Article Snippet: The following drugs and final concentrations were used: AACOCF3 (5 μ mol L−1 ); BayK 8644 (2 μ mol L−1 ; Alomone Labs, Jerusalem, Israel); Bisindolylmaleimide X (BIM‐X) (1 μ mol L−1 ); ET‐18‐OCH3 (edelfosine) (10 μ mol L−1 ); HET0016 (10 μ mol L−1 , Cayman Chemical, Ann Arbor, USA); KD025 (SLx 2119) (5 μ mol L−1 ; Cayman Chemical, Ann Arbor, USA); RHC 80267 (20 μ mol L−1 ); U‐73122 (0.5 μ mol L−1 ); Wortmannin (0.03 μ mol L−1 ); YM‐254890 (0.1 μ mol L−1 ; Adipogen AG, Liestal, Switzerland; and generous gift from Astellas Pharma, Tokyo, Japan).

    Techniques: Mouse Assay, Inhibition