az-23 Search Results


az23  (TargetMol)
94
TargetMol az23
Az23, supplied by TargetMol, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/az-23/AZ-23/pm41539418-79-0-4
Average 94 stars, based on 1 article reviews
az23 - by Bioz Stars, 2026-11
94/100 stars
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az-23  (MedChemExpress)
N/A
AZ-23 is an ATP-competitive and orally bioavailable Trk kinase A/B/C inhibitor with IC50s of 2 nM (TrkA), 8 nM (TrkB), 24 nM (FGFR1), 52 nM (Flt3), 55 nM (Ret), 84 nM (MuSk), 99 nM (Lck),
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azd 1332  (Alomone Labs)
92
Alomone Labs azd 1332
The specificity of TrkB agonistic antibody AS86. (A) AS86 at different concentrations (0.1 nM, 1 nM and 10 nM) was added to the plates coated with different proteins (0.1 μg TrkA, TrkB, TrkC, or p75 respectively), and ELISA was used to examine the binding capacity of AS86. (B, C) Cultured hippocampal neurons (DIV10) were pretreated with the Trk inhibitors k252a (300 nM) or <t>AZD-1332</t> (100 nM) for 60 min before incubation with mIgG (3 nM), BDNF (1 nM), or AS86 (3 nM) for 15 min (N = 2, n = 3). The Western blots of TrkB Y515 and Y816 sites activation (B) and the quantitative plots (C) are presented. Unless specifically indicated otherwise, statistical analyses in this and all other figures were carried out using one-way ANOVA followed by post hoc test. Symbols for P values (for both ANOVA and Student's t -test): *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: P < 0.0001. The quantification data in this and all other figures were presented as mean ± SEM.
Azd 1332, 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/product/az-23/AZD-1332/pmc07295064-282-22-23
Average 92 stars, based on 1 article reviews
azd 1332 - by Bioz Stars, 2026-11
92/100 stars
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az-23  (Axon Medchem LLC)
90
Axon Medchem LLC az-23
The specificity of TrkB agonistic antibody AS86. (A) AS86 at different concentrations (0.1 nM, 1 nM and 10 nM) was added to the plates coated with different proteins (0.1 μg TrkA, TrkB, TrkC, or p75 respectively), and ELISA was used to examine the binding capacity of AS86. (B, C) Cultured hippocampal neurons (DIV10) were pretreated with the Trk inhibitors k252a (300 nM) or <t>AZD-1332</t> (100 nM) for 60 min before incubation with mIgG (3 nM), BDNF (1 nM), or AS86 (3 nM) for 15 min (N = 2, n = 3). The Western blots of TrkB Y515 and Y816 sites activation (B) and the quantitative plots (C) are presented. Unless specifically indicated otherwise, statistical analyses in this and all other figures were carried out using one-way ANOVA followed by post hoc test. Symbols for P values (for both ANOVA and Student's t -test): *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: P < 0.0001. The quantification data in this and all other figures were presented as mean ± SEM.
Az 23, supplied by Axon Medchem LLC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/az-23/az+23/pmc06604814-297-29-32
Average 90 stars, based on 1 article reviews
az-23 - by Bioz Stars, 2026-11
90/100 stars
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az-23  (AstraZeneca ltd)
90
AstraZeneca ltd az-23
The specificity of TrkB agonistic antibody AS86. (A) AS86 at different concentrations (0.1 nM, 1 nM and 10 nM) was added to the plates coated with different proteins (0.1 μg TrkA, TrkB, TrkC, or p75 respectively), and ELISA was used to examine the binding capacity of AS86. (B, C) Cultured hippocampal neurons (DIV10) were pretreated with the Trk inhibitors k252a (300 nM) or <t>AZD-1332</t> (100 nM) for 60 min before incubation with mIgG (3 nM), BDNF (1 nM), or AS86 (3 nM) for 15 min (N = 2, n = 3). The Western blots of TrkB Y515 and Y816 sites activation (B) and the quantitative plots (C) are presented. Unless specifically indicated otherwise, statistical analyses in this and all other figures were carried out using one-way ANOVA followed by post hoc test. Symbols for P values (for both ANOVA and Student's t -test): *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: P < 0.0001. The quantification data in this and all other figures were presented as mean ± SEM.
Az 23, supplied by AstraZeneca ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/az-23/az+23/10__1158_slash_1078___0432__ccr___08___0651-124-43-38
Average 90 stars, based on 1 article reviews
az-23 - by Bioz Stars, 2026-11
90/100 stars
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az 23  (Biosynth Carbosynth)
N/A
Inhibitor of TrkA and TrkB kinases. Inhibitor of TrkA and TrkB kinases.
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az 23  (MuseChem Chemicals)
N/A
AZ-23(CAT:I003398) is an ATP-competitive and orally bioavailable inhibitor of tropomyosin receptor kinases (TrkA, TrkB, and TrkC) with high potency. It inhibits TrkA and TrkB with IC₅₀ values of 2 nM and 8 nM, respectively, while
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az-23  (Aladdin Scientific Corporation)
N/A
AZ-23 is an ATP-competitive and orally bioavailable Trk kinase A/B/C inhibitor with IC 50 s of 2 nM (TrkA), 8 nM (TrkB), 24 nM (FGFR1), 52 nM (Flt3), 55 nM (Ret), 84 nM (MuSk), 99
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az 23  (BOC Sciences)
N/A
AZ 23 is a potent and selective tyrosine kinase (Trk) inhibitor with the potential for therapeutic utility in neuroblastoma and multiple other cancer indications.
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Image Search Results


The specificity of TrkB agonistic antibody AS86. (A) AS86 at different concentrations (0.1 nM, 1 nM and 10 nM) was added to the plates coated with different proteins (0.1 μg TrkA, TrkB, TrkC, or p75 respectively), and ELISA was used to examine the binding capacity of AS86. (B, C) Cultured hippocampal neurons (DIV10) were pretreated with the Trk inhibitors k252a (300 nM) or AZD-1332 (100 nM) for 60 min before incubation with mIgG (3 nM), BDNF (1 nM), or AS86 (3 nM) for 15 min (N = 2, n = 3). The Western blots of TrkB Y515 and Y816 sites activation (B) and the quantitative plots (C) are presented. Unless specifically indicated otherwise, statistical analyses in this and all other figures were carried out using one-way ANOVA followed by post hoc test. Symbols for P values (for both ANOVA and Student's t -test): *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: P < 0.0001. The quantification data in this and all other figures were presented as mean ± SEM.

Journal: Theranostics

Article Title: Therapeutic potential of a TrkB agonistic antibody for Alzheimer's disease

doi: 10.7150/thno.44165

Figure Lengend Snippet: The specificity of TrkB agonistic antibody AS86. (A) AS86 at different concentrations (0.1 nM, 1 nM and 10 nM) was added to the plates coated with different proteins (0.1 μg TrkA, TrkB, TrkC, or p75 respectively), and ELISA was used to examine the binding capacity of AS86. (B, C) Cultured hippocampal neurons (DIV10) were pretreated with the Trk inhibitors k252a (300 nM) or AZD-1332 (100 nM) for 60 min before incubation with mIgG (3 nM), BDNF (1 nM), or AS86 (3 nM) for 15 min (N = 2, n = 3). The Western blots of TrkB Y515 and Y816 sites activation (B) and the quantitative plots (C) are presented. Unless specifically indicated otherwise, statistical analyses in this and all other figures were carried out using one-way ANOVA followed by post hoc test. Symbols for P values (for both ANOVA and Student's t -test): *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: P < 0.0001. The quantification data in this and all other figures were presented as mean ± SEM.

Article Snippet: The reagents included BDNF protein (Sino Biological Inc, 50240-MNAS), Mouse IgG (YEASEN, 3611ES10), and β-Amyloid protein (25-35) (Synpeptide), K252a (Bio Vision, 2013-500), AZD-1332 (Alomeone labs, A-495).

Techniques: Enzyme-linked Immunosorbent Assay, Binding Assay, Cell Culture, Incubation, Western Blot, Activation Assay

Cell survival function of AS86. ( A ) Attenuation of serum-deprivation induced cell death by AS86. Different doses of BDNF or AS86 were applied to serum-deprived cultures of hTrkB-PC12 cells in the absence or presence of Trk inhibitors (300 nM K252a or 50 nM AZD-1332) for 16 hours, and the levels of apoptosis were determined by the ratio of the number of caspase 3 positive cells to total number of cells, using a caspase 3-substrate kit. Survival rates were measured by the decreased apoptotic levels normalized to that of vehicle treatment (n = 3). ( B ) Attenuation of Aβ induced cell death by AS86. Hippocampal neurons were pretreated with AS86 or BDNF for 30 minutes, followed by treatment with Aβ (25-35) (5 µM). Cell viability was analyzed with ATP level quantification assay 48 hours later (N = 2 independent experiments, n = 6 samples). ( C, D ) Inhibition of Aβ induced apoptotic signals by AS86. Hippocampal neurons were pretreated with AS86 or BDNF for 30 minutes, followed by treatment with Aβ (25-35) (15 µM) for 24 hours. Total and cleaved caspase3 levels were measured using Western blotting (N = 3 independent experiments, n = 3 replicates). Representative Western blots (D) and quantitative plots (C) are presented.

Journal: Theranostics

Article Title: Therapeutic potential of a TrkB agonistic antibody for Alzheimer's disease

doi: 10.7150/thno.44165

Figure Lengend Snippet: Cell survival function of AS86. ( A ) Attenuation of serum-deprivation induced cell death by AS86. Different doses of BDNF or AS86 were applied to serum-deprived cultures of hTrkB-PC12 cells in the absence or presence of Trk inhibitors (300 nM K252a or 50 nM AZD-1332) for 16 hours, and the levels of apoptosis were determined by the ratio of the number of caspase 3 positive cells to total number of cells, using a caspase 3-substrate kit. Survival rates were measured by the decreased apoptotic levels normalized to that of vehicle treatment (n = 3). ( B ) Attenuation of Aβ induced cell death by AS86. Hippocampal neurons were pretreated with AS86 or BDNF for 30 minutes, followed by treatment with Aβ (25-35) (5 µM). Cell viability was analyzed with ATP level quantification assay 48 hours later (N = 2 independent experiments, n = 6 samples). ( C, D ) Inhibition of Aβ induced apoptotic signals by AS86. Hippocampal neurons were pretreated with AS86 or BDNF for 30 minutes, followed by treatment with Aβ (25-35) (15 µM) for 24 hours. Total and cleaved caspase3 levels were measured using Western blotting (N = 3 independent experiments, n = 3 replicates). Representative Western blots (D) and quantitative plots (C) are presented.

Article Snippet: The reagents included BDNF protein (Sino Biological Inc, 50240-MNAS), Mouse IgG (YEASEN, 3611ES10), and β-Amyloid protein (25-35) (Synpeptide), K252a (Bio Vision, 2013-500), AZD-1332 (Alomeone labs, A-495).

Techniques: Inhibition, Western Blot