β funaltrexamine hydrochloride β fna  (Millipore)

 
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    Name:
    beta Funaltrexamine hydrochloride
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    Catalog Number:
    O003
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    Millipore β funaltrexamine hydrochloride β fna
    beta Funaltrexamine hydrochloride

    https://www.bioz.com/result/β funaltrexamine hydrochloride β fna/product/Millipore
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    β funaltrexamine hydrochloride β fna - by Bioz Stars, 2021-07
    93/100 stars

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    Incubation:

    Article Title: Naloxonazine, an Amastigote-Specific Compound, Affects Leishmania Parasites through Modulation of Host-Encoded Functions
    Article Snippet: Cells were washed and incubated with complete RPMI medium containing stationary phase L . donovani promastigotes at a macrophage/promastigote ratio of 1/10. .. After 4 h incubation at 37°C, non-internalized promastigotes were removed by 3 successive washes with PBS and incubated with naloxonazine, naloxone, β-funaltrexamine, CTOP, endomorphine, DAMGO, sinomenine, concanamycin A (all purchased from Sigma) or imatinib (Cell Signaling Technology) for 24 to 72 h. Half maximal inhibitory concentrations (GI50 ) were determined using a high-content imaging assay as described previously [ ]. .. Briefly, compounds were serially diluted 3-fold in DMSO, with final assay concentrations ranging from 50 μM to 0.02 μM (1% final concentration of DMSO), 2 μM amphotericin B and 1% DMSO were used as positive and negative controls respectively.

    Imaging:

    Article Title: Naloxonazine, an Amastigote-Specific Compound, Affects Leishmania Parasites through Modulation of Host-Encoded Functions
    Article Snippet: Cells were washed and incubated with complete RPMI medium containing stationary phase L . donovani promastigotes at a macrophage/promastigote ratio of 1/10. .. After 4 h incubation at 37°C, non-internalized promastigotes were removed by 3 successive washes with PBS and incubated with naloxonazine, naloxone, β-funaltrexamine, CTOP, endomorphine, DAMGO, sinomenine, concanamycin A (all purchased from Sigma) or imatinib (Cell Signaling Technology) for 24 to 72 h. Half maximal inhibitory concentrations (GI50 ) were determined using a high-content imaging assay as described previously [ ]. .. Briefly, compounds were serially diluted 3-fold in DMSO, with final assay concentrations ranging from 50 μM to 0.02 μM (1% final concentration of DMSO), 2 μM amphotericin B and 1% DMSO were used as positive and negative controls respectively.

    other:

    Article Title: Co-Expression of GRK2 Reveals a Novel Conformational State of the u-Opioid Receptor
    Article Snippet: Drugs and Chemicals used [3 H]-diprenorphine, [3 H]-DAMGO and [35 S]GTPγS were obtained from PerkinElmer Life Sciences (Cambridge, UK), β-funaltrexamine, oxycodone, [D-Ala2 , MePhe4 , gly5 –ol]-enkephalin (DAMGO), endomorphin 1 and 2, morphine and pertussis toxin were obtained from Sigma-Aldrich.

    Article Title: Tolerance to Repeated Morphine Administration Is Associated with Increased Potency of Opioid Agonists
    Article Snippet: ME, baclofen, deltorphin II, NO-711, BaCl, and β -funaltrexamine ( β -FNA) were obtained from Sigma (St Louis, MO).

    Article Title: Novel κ-opioid receptor agonist MB-1C-OH produces potent analgesia with less depression and sedation
    Article Snippet: Drugs [3 H]diprenorphine (1.85 TBq/mmol) and guanosine 5-O-(3-[35 S]thio)triphosphate ([35 S]GTPγS) (38.11 TBq/mmol) were purchased from Amersham Biosciences (Piscataway, NJ, USA). (−)U50,488H; naloxone; naltrindole; nor-binaltorphimine; β-funaltrexamine; GTPγS and GDP were obtained from Sigma-Aldrich (St Louis, MO, USA).

    Article Title: Role of phosphodiesterase inhibitor Ibudilast in morphine-induced hippocampal injury
    Article Snippet: Group D (n=6): Rats were made dependent by chronic administration of morphine sulfate and co-administrated with β-Funaltrexamine (sigma).

    Article Title: Zerumbone-Induced Analgesia Modulated via Potassium Channels and Opioid Receptors in Chronic Constriction Injury-Induced Neuropathic Pain
    Article Snippet: Naloxone hydrochloride, β-funaltrexamine, naltrindole, nor-binaltorphimine, DMSO, and Tween 20 were bought from Sigma-Aldrich (St. Louis, MO, USA).

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  • 93
    Millipore β funaltrexamine
    Antinociceptive effects of SK-9709 alone and in combination with <t>β-funaltrexamine</t> (β-FNA) (A) or nor-binaltorphimine (nor-BNI) (B) in the acetic acid-induced writhing test. Mice were treated with SK-9709 (1.93 μmol kg −1 , s.c.) 120 min before testing. (A) β-FNA (5.1 nmol per mouse, i.c.v.) and nor-BNI (4.9 nmol per mouse, i.t.) were injected 24 h and 25 min before testing, respectively. Acetic acid (0.7 %) was injected 10 min before writhing test, and then writhing responses were counted for 10 min. Each value is the mean±s.e.mean. The numbers of mice used are shown in parentheses. Significance levels; ** P
    β Funaltrexamine, supplied by Millipore, 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/β funaltrexamine/product/Millipore
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    β funaltrexamine - by Bioz Stars, 2021-07
    93/100 stars
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    Antinociceptive effects of SK-9709 alone and in combination with β-funaltrexamine (β-FNA) (A) or nor-binaltorphimine (nor-BNI) (B) in the acetic acid-induced writhing test. Mice were treated with SK-9709 (1.93 μmol kg −1 , s.c.) 120 min before testing. (A) β-FNA (5.1 nmol per mouse, i.c.v.) and nor-BNI (4.9 nmol per mouse, i.t.) were injected 24 h and 25 min before testing, respectively. Acetic acid (0.7 %) was injected 10 min before writhing test, and then writhing responses were counted for 10 min. Each value is the mean±s.e.mean. The numbers of mice used are shown in parentheses. Significance levels; ** P

    Journal: British Journal of Pharmacology

    Article Title: Long-lasting antinociceptive effects of a novel dynorphin analogue, Tyr-D-Ala-Phe-Leu-Arg ? (CH2NH) Arg-NH2, in mice

    doi: 10.1038/sj.bjp.0703982

    Figure Lengend Snippet: Antinociceptive effects of SK-9709 alone and in combination with β-funaltrexamine (β-FNA) (A) or nor-binaltorphimine (nor-BNI) (B) in the acetic acid-induced writhing test. Mice were treated with SK-9709 (1.93 μmol kg −1 , s.c.) 120 min before testing. (A) β-FNA (5.1 nmol per mouse, i.c.v.) and nor-BNI (4.9 nmol per mouse, i.t.) were injected 24 h and 25 min before testing, respectively. Acetic acid (0.7 %) was injected 10 min before writhing test, and then writhing responses were counted for 10 min. Each value is the mean±s.e.mean. The numbers of mice used are shown in parentheses. Significance levels; ** P

    Article Snippet: Morphine hydrochloride (Shionogi, Osaka, Japan), U-50,488H (trans-(±)3,4-dichloro-N-methyl-N-(2-[1-pyrrolidinyl]-cyclohexyl) benzeneacetamide methanesulphonate salt (Sigma, St. Louis, MO, U.S.A.), naloxone hydrochloride (Endo Lab., U.S.A.), β-funaltrexamine (β-FNA, Research Biochemicals International, MA, U.S.A.), nor-binaltorphimine (nor-BNI, Research Biochemicals International), DAMGO ([ D -Ala2 , (Me)Phe4 ,Gly(ol)5 ] enkephalin) and DPDPE ([D-Pen2 ,D-Pen5 ] enkephalin) were used.

    Techniques: Mouse Assay, Injection

    Repeated intermittent administration of morphine increases desensitization of met-enkephalin (ME)-induced responses from morphine tolerant rats. (a) Top left panel: representative current–voltage relationships for a saline pretreated rat voltage-clamped at −70 mV at the peak ME (20 µM) response and after 10 min of superfusion. The inset shows currents elicited in steps to −120mV and at the baseline (−70 mV) by ME (20 µM) at the peak response (medium traces) and after 10 min superfusion (dark traces). The remaining current was blocked by the selective μ -opioid receptor inhibitor β -funaltrexamine ( β -FNA) (10 µM; light traces). Scale bar (100pA per 250 ms). Middle left panel: averaged current–voltage relationships for saline pretreated rats voltage-clamped at −70 mV at the peak ME (20 µM) response and after 10 min of superfusion ( n = 3). (b) Top right panel: representative current–voltage relationships for a morphine pretreated rat voltage-clamped at −70 mV at the peak ME (20 µM) response and after 10 min of superfusion. The inset shows currents elicited in steps to −120 mV and at the baseline (−70 mV) by ME (20 µM) at the peak response (medium traces) and after 10 min superfusion (dark traces). The remaining current was blocked by the selective GIRK blocker r-teriaptinQ (10nM; light traces). Scale bar (100pA per 250ms). Middle right panel: averaged current–voltage relationships for morphine pretreated rats voltage-clamped at −70 mV at peak ME (20 µM) and after 10 min of superfusion ( n = 7). (c) Bar graph showing amount of desensitization of peak outward ME-induced currents after 10min in saline ( n = 11) and morphine ( n = 14) pretreated rats. The higher n in bar graph is the addition of experiments where current–voltage relationships were not run during the experiment. ME-induced currents significantly desensitize within 10 min (* p

    Journal: Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

    Article Title: Tolerance to Repeated Morphine Administration Is Associated with Increased Potency of Opioid Agonists

    doi: 10.1038/sj.npp.1301634

    Figure Lengend Snippet: Repeated intermittent administration of morphine increases desensitization of met-enkephalin (ME)-induced responses from morphine tolerant rats. (a) Top left panel: representative current–voltage relationships for a saline pretreated rat voltage-clamped at −70 mV at the peak ME (20 µM) response and after 10 min of superfusion. The inset shows currents elicited in steps to −120mV and at the baseline (−70 mV) by ME (20 µM) at the peak response (medium traces) and after 10 min superfusion (dark traces). The remaining current was blocked by the selective μ -opioid receptor inhibitor β -funaltrexamine ( β -FNA) (10 µM; light traces). Scale bar (100pA per 250 ms). Middle left panel: averaged current–voltage relationships for saline pretreated rats voltage-clamped at −70 mV at the peak ME (20 µM) response and after 10 min of superfusion ( n = 3). (b) Top right panel: representative current–voltage relationships for a morphine pretreated rat voltage-clamped at −70 mV at the peak ME (20 µM) response and after 10 min of superfusion. The inset shows currents elicited in steps to −120 mV and at the baseline (−70 mV) by ME (20 µM) at the peak response (medium traces) and after 10 min superfusion (dark traces). The remaining current was blocked by the selective GIRK blocker r-teriaptinQ (10nM; light traces). Scale bar (100pA per 250ms). Middle right panel: averaged current–voltage relationships for morphine pretreated rats voltage-clamped at −70 mV at peak ME (20 µM) and after 10 min of superfusion ( n = 7). (c) Bar graph showing amount of desensitization of peak outward ME-induced currents after 10min in saline ( n = 11) and morphine ( n = 14) pretreated rats. The higher n in bar graph is the addition of experiments where current–voltage relationships were not run during the experiment. ME-induced currents significantly desensitize within 10 min (* p

    Article Snippet: ME, baclofen, deltorphin II, NO-711, BaCl, and β -funaltrexamine ( β -FNA) were obtained from Sigma (St Louis, MO).

    Techniques: Mass Spectrometry

    Repeated intermittent administration of morphine induces larger met-enkephalin (ME)-induced currents. (a) Representative current–voltage relationships to different concentrations of ME (1 and 10 µM) in a slice from a saline pretreated rat. The neuron was voltage-clamped to −70 mV. The inset shows currents elicited in steps to −120mV and at the baseline (−70 mV) in control/wash (light traces) and ME (10µM; dark traces). Scale bar is the same for both sets of traces (50 pA per 250 ms). (b) Representative current–voltage relationships from a morphine pretreated rat. The neuron was voltage-clamped to −70mV. ME induced outward currents were inhibited by the GIRK blocker, r-teriaptinQ (10nM). The inset shows currents elicited in steps to −120mV and at the baseline (−70 mV) in control/r-teriaptinQ (light traces) and ME (10µM; dark traces). (c) Averaged current–voltage relationships for ME (5 µM)—control for saline ( n = 10) and morphine ( n = 7) pretreated rats. Naloxone (1–10 µM; n = 5) and β -funaltrexamine ( β -FNA) (10 µM; n = 4) reversed the effects of ME. (d) Concentration–response relationship for ME-induced outward currents in saline and morphine pretreated slices. Morphine pretreatment induces an increase in potency of ME. Number of cells for saline/morphine pretreated groups were 50 nM (4/4); 100 nM (5/6); 300 nM (3/6); 1 µM (4/4); 5 µM (7/9); 10 µM (4/10); 20 µM (13/14).

    Journal: Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

    Article Title: Tolerance to Repeated Morphine Administration Is Associated with Increased Potency of Opioid Agonists

    doi: 10.1038/sj.npp.1301634

    Figure Lengend Snippet: Repeated intermittent administration of morphine induces larger met-enkephalin (ME)-induced currents. (a) Representative current–voltage relationships to different concentrations of ME (1 and 10 µM) in a slice from a saline pretreated rat. The neuron was voltage-clamped to −70 mV. The inset shows currents elicited in steps to −120mV and at the baseline (−70 mV) in control/wash (light traces) and ME (10µM; dark traces). Scale bar is the same for both sets of traces (50 pA per 250 ms). (b) Representative current–voltage relationships from a morphine pretreated rat. The neuron was voltage-clamped to −70mV. ME induced outward currents were inhibited by the GIRK blocker, r-teriaptinQ (10nM). The inset shows currents elicited in steps to −120mV and at the baseline (−70 mV) in control/r-teriaptinQ (light traces) and ME (10µM; dark traces). (c) Averaged current–voltage relationships for ME (5 µM)—control for saline ( n = 10) and morphine ( n = 7) pretreated rats. Naloxone (1–10 µM; n = 5) and β -funaltrexamine ( β -FNA) (10 µM; n = 4) reversed the effects of ME. (d) Concentration–response relationship for ME-induced outward currents in saline and morphine pretreated slices. Morphine pretreatment induces an increase in potency of ME. Number of cells for saline/morphine pretreated groups were 50 nM (4/4); 100 nM (5/6); 300 nM (3/6); 1 µM (4/4); 5 µM (7/9); 10 µM (4/10); 20 µM (13/14).

    Article Snippet: ME, baclofen, deltorphin II, NO-711, BaCl, and β -funaltrexamine ( β -FNA) were obtained from Sigma (St Louis, MO).

    Techniques: Mass Spectrometry, Concentration Assay