ldn212854 Search Results


ldn 212854  (MedChemExpress)
94
MedChemExpress ldn 212854
ACVR1 signaling promotes G1 arrest and apoptosis and facilitates the anti‐lymphoma activity of PRC2 inhibitors. A) Proliferation of WSU‐DLCL2 and SU‐DHL‐4 cells treated with MAK683 (1.2 µM) <t>and/or</t> <t>LDN‐212854</t> at the indicated concentrations. Viable cells were counted every 3 days (mean ± s.d., n = 2). B,C) RT‐qPCR analysis of the indicated genes and western blot analysis of SMADs and H3K27me3 in WSU‐DLCL2 cells treated with MAK683 (5 µM) and/or LDN‐212854 at the indicated concentrations for 6 days. All data were normalized to GAPDH and DMSO was arbitrarily set as 1 (mean ± s.d., n = 3) in (B). D) Statistic description of CFSE in SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 10 days (mean ± s.d., n = 4). E) Cell cycle analysis of SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 9 days (mean ± s.d., n = 3). F) EdU incorporation analysis of WSU‐DLCL2 and SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 6 or 12 days respectively (mean ± s.d., n ≥ 3). G) Cell apoptosis in WSU‐DLCL2 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 9 days, determined by sub G1‐content from PI staining and FACS (mean ± s.d., n = 4). H,I) Western blots and EdU incorporation analysis (mean ± s.d., n = 3) of the C4 clone of EZH2‐DD‐KI (DD‐KI) cells treated with shield (0.5 µ m ) and/or LDN‐212854 for 9 days. J) Cell apoptosis in WSU‐DLCL2 cells treated with LDN‐214117 and/or MAK683 (5 µ m ) for 9 days, determined by sub G1‐content from PI staining and FACS (mean ± s.d., n = 4). K) Proliferation of SU‐DHL‐4 cells treated with LDN‐214117 and/or MAK683 (1.2 µ m ). Viable cells were counted every 3 days (mean ± s.d., n = 2). All cellular experiments were performed at least two times and representative data are shown here. Statistical analysis was performed using one‐way ANOVA ( * , p < 0.05; ** , p < 0.01; *** , p < 0.001; **** , < 0.0001).
Ldn 212854, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ldn 212854 trihydrochloride  (MuseChem Chemicals)
N/A
Potent ALK2-biased BMP type I receptor kinase inhibitor (IC50 values 2.4 nM, 1.3 nM, and 85.8 nM for ALK1, 2, and 3 resp.), showing nearly 4 orders of selectivity for BMP versus the closely related
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ldn  (Selleck Chemicals)
93
Selleck Chemicals ldn
ACVR1 signaling promotes G1 arrest and apoptosis and facilitates the anti‐lymphoma activity of PRC2 inhibitors. A) Proliferation of WSU‐DLCL2 and SU‐DHL‐4 cells treated with MAK683 (1.2 µM) <t>and/or</t> <t>LDN‐212854</t> at the indicated concentrations. Viable cells were counted every 3 days (mean ± s.d., n = 2). B,C) RT‐qPCR analysis of the indicated genes and western blot analysis of SMADs and H3K27me3 in WSU‐DLCL2 cells treated with MAK683 (5 µM) and/or LDN‐212854 at the indicated concentrations for 6 days. All data were normalized to GAPDH and DMSO was arbitrarily set as 1 (mean ± s.d., n = 3) in (B). D) Statistic description of CFSE in SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 10 days (mean ± s.d., n = 4). E) Cell cycle analysis of SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 9 days (mean ± s.d., n = 3). F) EdU incorporation analysis of WSU‐DLCL2 and SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 6 or 12 days respectively (mean ± s.d., n ≥ 3). G) Cell apoptosis in WSU‐DLCL2 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 9 days, determined by sub G1‐content from PI staining and FACS (mean ± s.d., n = 4). H,I) Western blots and EdU incorporation analysis (mean ± s.d., n = 3) of the C4 clone of EZH2‐DD‐KI (DD‐KI) cells treated with shield (0.5 µ m ) and/or LDN‐212854 for 9 days. J) Cell apoptosis in WSU‐DLCL2 cells treated with LDN‐214117 and/or MAK683 (5 µ m ) for 9 days, determined by sub G1‐content from PI staining and FACS (mean ± s.d., n = 4). K) Proliferation of SU‐DHL‐4 cells treated with LDN‐214117 and/or MAK683 (1.2 µ m ). Viable cells were counted every 3 days (mean ± s.d., n = 2). All cellular experiments were performed at least two times and representative data are shown here. Statistical analysis was performed using one‐way ANOVA ( * , p < 0.05; ** , p < 0.01; *** , p < 0.001; **** , < 0.0001).
Ldn, supplied by Selleck Chemicals, 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/product/ldn212854/LDN-212854/pmc08835914-103-6-10
Average 93 stars, based on 1 article reviews
ldn - by Bioz Stars, 2026-10
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smad2/3 inhibitor ldn212854  (Topscience Co Ltd)
90
Topscience Co Ltd smad2/3 inhibitor ldn212854
ACVR1 signaling promotes G1 arrest and apoptosis and facilitates the anti‐lymphoma activity of PRC2 inhibitors. A) Proliferation of WSU‐DLCL2 and SU‐DHL‐4 cells treated with MAK683 (1.2 µM) <t>and/or</t> <t>LDN‐212854</t> at the indicated concentrations. Viable cells were counted every 3 days (mean ± s.d., n = 2). B,C) RT‐qPCR analysis of the indicated genes and western blot analysis of SMADs and H3K27me3 in WSU‐DLCL2 cells treated with MAK683 (5 µM) and/or LDN‐212854 at the indicated concentrations for 6 days. All data were normalized to GAPDH and DMSO was arbitrarily set as 1 (mean ± s.d., n = 3) in (B). D) Statistic description of CFSE in SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 10 days (mean ± s.d., n = 4). E) Cell cycle analysis of SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 9 days (mean ± s.d., n = 3). F) EdU incorporation analysis of WSU‐DLCL2 and SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 6 or 12 days respectively (mean ± s.d., n ≥ 3). G) Cell apoptosis in WSU‐DLCL2 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 9 days, determined by sub G1‐content from PI staining and FACS (mean ± s.d., n = 4). H,I) Western blots and EdU incorporation analysis (mean ± s.d., n = 3) of the C4 clone of EZH2‐DD‐KI (DD‐KI) cells treated with shield (0.5 µ m ) and/or LDN‐212854 for 9 days. J) Cell apoptosis in WSU‐DLCL2 cells treated with LDN‐214117 and/or MAK683 (5 µ m ) for 9 days, determined by sub G1‐content from PI staining and FACS (mean ± s.d., n = 4). K) Proliferation of SU‐DHL‐4 cells treated with LDN‐214117 and/or MAK683 (1.2 µ m ). Viable cells were counted every 3 days (mean ± s.d., n = 2). All cellular experiments were performed at least two times and representative data are shown here. Statistical analysis was performed using one‐way ANOVA ( * , p < 0.05; ** , p < 0.01; *** , p < 0.001; **** , < 0.0001).
Smad2/3 Inhibitor Ldn212854, supplied by Topscience Co 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/ldn212854/smad2+3+inhibitor+ldn212854/10__1097_slash_fjc__0000000000000655-35-7-13
Average 90 stars, based on 1 article reviews
smad2/3 inhibitor ldn212854 - by Bioz Stars, 2026-10
90/100 stars
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ldn212854  (Glycomimetics inc)
90
Glycomimetics inc ldn212854
ACVR1 signaling promotes G1 arrest and apoptosis and facilitates the anti‐lymphoma activity of PRC2 inhibitors. A) Proliferation of WSU‐DLCL2 and SU‐DHL‐4 cells treated with MAK683 (1.2 µM) <t>and/or</t> <t>LDN‐212854</t> at the indicated concentrations. Viable cells were counted every 3 days (mean ± s.d., n = 2). B,C) RT‐qPCR analysis of the indicated genes and western blot analysis of SMADs and H3K27me3 in WSU‐DLCL2 cells treated with MAK683 (5 µM) and/or LDN‐212854 at the indicated concentrations for 6 days. All data were normalized to GAPDH and DMSO was arbitrarily set as 1 (mean ± s.d., n = 3) in (B). D) Statistic description of CFSE in SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 10 days (mean ± s.d., n = 4). E) Cell cycle analysis of SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 9 days (mean ± s.d., n = 3). F) EdU incorporation analysis of WSU‐DLCL2 and SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 6 or 12 days respectively (mean ± s.d., n ≥ 3). G) Cell apoptosis in WSU‐DLCL2 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 9 days, determined by sub G1‐content from PI staining and FACS (mean ± s.d., n = 4). H,I) Western blots and EdU incorporation analysis (mean ± s.d., n = 3) of the C4 clone of EZH2‐DD‐KI (DD‐KI) cells treated with shield (0.5 µ m ) and/or LDN‐212854 for 9 days. J) Cell apoptosis in WSU‐DLCL2 cells treated with LDN‐214117 and/or MAK683 (5 µ m ) for 9 days, determined by sub G1‐content from PI staining and FACS (mean ± s.d., n = 4). K) Proliferation of SU‐DHL‐4 cells treated with LDN‐214117 and/or MAK683 (1.2 µ m ). Viable cells were counted every 3 days (mean ± s.d., n = 2). All cellular experiments were performed at least two times and representative data are shown here. Statistical analysis was performed using one‐way ANOVA ( * , p < 0.05; ** , p < 0.01; *** , p < 0.001; **** , < 0.0001).
Ldn212854, supplied by Glycomimetics inc, 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/ldn212854/ldn212854/pm39492001-270-6-14
Average 90 stars, based on 1 article reviews
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bmp15 inhibitor ldn-212854 cat# m00946  (MedBio Publications)
90
MedBio Publications bmp15 inhibitor ldn-212854 cat# m00946
ACVR1 signaling promotes G1 arrest and apoptosis and facilitates the anti‐lymphoma activity of PRC2 inhibitors. A) Proliferation of WSU‐DLCL2 and SU‐DHL‐4 cells treated with MAK683 (1.2 µM) <t>and/or</t> <t>LDN‐212854</t> at the indicated concentrations. Viable cells were counted every 3 days (mean ± s.d., n = 2). B,C) RT‐qPCR analysis of the indicated genes and western blot analysis of SMADs and H3K27me3 in WSU‐DLCL2 cells treated with MAK683 (5 µM) and/or LDN‐212854 at the indicated concentrations for 6 days. All data were normalized to GAPDH and DMSO was arbitrarily set as 1 (mean ± s.d., n = 3) in (B). D) Statistic description of CFSE in SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 10 days (mean ± s.d., n = 4). E) Cell cycle analysis of SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 9 days (mean ± s.d., n = 3). F) EdU incorporation analysis of WSU‐DLCL2 and SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 6 or 12 days respectively (mean ± s.d., n ≥ 3). G) Cell apoptosis in WSU‐DLCL2 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 9 days, determined by sub G1‐content from PI staining and FACS (mean ± s.d., n = 4). H,I) Western blots and EdU incorporation analysis (mean ± s.d., n = 3) of the C4 clone of EZH2‐DD‐KI (DD‐KI) cells treated with shield (0.5 µ m ) and/or LDN‐212854 for 9 days. J) Cell apoptosis in WSU‐DLCL2 cells treated with LDN‐214117 and/or MAK683 (5 µ m ) for 9 days, determined by sub G1‐content from PI staining and FACS (mean ± s.d., n = 4). K) Proliferation of SU‐DHL‐4 cells treated with LDN‐214117 and/or MAK683 (1.2 µ m ). Viable cells were counted every 3 days (mean ± s.d., n = 2). All cellular experiments were performed at least two times and representative data are shown here. Statistical analysis was performed using one‐way ANOVA ( * , p < 0.05; ** , p < 0.01; *** , p < 0.001; **** , < 0.0001).
Bmp15 Inhibitor Ldn 212854 Cat# M00946, supplied by MedBio Publications, 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/ldn212854/BMP15+inhibitor+LDN+212854+Cat++M00946/pm36071342-110-31-34
Average 90 stars, based on 1 article reviews
bmp15 inhibitor ldn-212854 cat# m00946 - by Bioz Stars, 2026-10
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ldn 212854  (Tocris)
N/A
Potent bone morphogenetic protein type I ALK inhibitor
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ldn 212854  (Cayman Chemical)
N/A
Activation of bone morphogenetic protein BMP type I receptors also known as activin receptor like kinases ALK1 7 leads to the assembly of SMAD complexes which translocate to the nucleus to induce transcriptional activation important
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ldn212854  (Cayman Chemical)
N/A
LDN212854
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ldn 212854 trihydrochloride  (Biosynth Carbosynth)
N/A
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ldn-212854  (TargetMol)
N/A
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ldn 212854  (Aladdin Scientific Corporation)
N/A
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Image Search Results


ACVR1 signaling promotes G1 arrest and apoptosis and facilitates the anti‐lymphoma activity of PRC2 inhibitors. A) Proliferation of WSU‐DLCL2 and SU‐DHL‐4 cells treated with MAK683 (1.2 µM) and/or LDN‐212854 at the indicated concentrations. Viable cells were counted every 3 days (mean ± s.d., n = 2). B,C) RT‐qPCR analysis of the indicated genes and western blot analysis of SMADs and H3K27me3 in WSU‐DLCL2 cells treated with MAK683 (5 µM) and/or LDN‐212854 at the indicated concentrations for 6 days. All data were normalized to GAPDH and DMSO was arbitrarily set as 1 (mean ± s.d., n = 3) in (B). D) Statistic description of CFSE in SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 10 days (mean ± s.d., n = 4). E) Cell cycle analysis of SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 9 days (mean ± s.d., n = 3). F) EdU incorporation analysis of WSU‐DLCL2 and SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 6 or 12 days respectively (mean ± s.d., n ≥ 3). G) Cell apoptosis in WSU‐DLCL2 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 9 days, determined by sub G1‐content from PI staining and FACS (mean ± s.d., n = 4). H,I) Western blots and EdU incorporation analysis (mean ± s.d., n = 3) of the C4 clone of EZH2‐DD‐KI (DD‐KI) cells treated with shield (0.5 µ m ) and/or LDN‐212854 for 9 days. J) Cell apoptosis in WSU‐DLCL2 cells treated with LDN‐214117 and/or MAK683 (5 µ m ) for 9 days, determined by sub G1‐content from PI staining and FACS (mean ± s.d., n = 4). K) Proliferation of SU‐DHL‐4 cells treated with LDN‐214117 and/or MAK683 (1.2 µ m ). Viable cells were counted every 3 days (mean ± s.d., n = 2). All cellular experiments were performed at least two times and representative data are shown here. Statistical analysis was performed using one‐way ANOVA ( * , p < 0.05; ** , p < 0.01; *** , p < 0.001; **** , < 0.0001).

Journal: Advanced Science

Article Title: BMP‐ACVR1 Axis is Critical for Efficacy of PRC2 Inhibitors in B‐Cell Lymphoma

doi: 10.1002/advs.202306499

Figure Lengend Snippet: ACVR1 signaling promotes G1 arrest and apoptosis and facilitates the anti‐lymphoma activity of PRC2 inhibitors. A) Proliferation of WSU‐DLCL2 and SU‐DHL‐4 cells treated with MAK683 (1.2 µM) and/or LDN‐212854 at the indicated concentrations. Viable cells were counted every 3 days (mean ± s.d., n = 2). B,C) RT‐qPCR analysis of the indicated genes and western blot analysis of SMADs and H3K27me3 in WSU‐DLCL2 cells treated with MAK683 (5 µM) and/or LDN‐212854 at the indicated concentrations for 6 days. All data were normalized to GAPDH and DMSO was arbitrarily set as 1 (mean ± s.d., n = 3) in (B). D) Statistic description of CFSE in SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 10 days (mean ± s.d., n = 4). E) Cell cycle analysis of SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 9 days (mean ± s.d., n = 3). F) EdU incorporation analysis of WSU‐DLCL2 and SU‐DHL‐4 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 6 or 12 days respectively (mean ± s.d., n ≥ 3). G) Cell apoptosis in WSU‐DLCL2 cells treated with MAK683 (5 µ m ) and/or LDN‐212854 at the indicated concentrations for 9 days, determined by sub G1‐content from PI staining and FACS (mean ± s.d., n = 4). H,I) Western blots and EdU incorporation analysis (mean ± s.d., n = 3) of the C4 clone of EZH2‐DD‐KI (DD‐KI) cells treated with shield (0.5 µ m ) and/or LDN‐212854 for 9 days. J) Cell apoptosis in WSU‐DLCL2 cells treated with LDN‐214117 and/or MAK683 (5 µ m ) for 9 days, determined by sub G1‐content from PI staining and FACS (mean ± s.d., n = 4). K) Proliferation of SU‐DHL‐4 cells treated with LDN‐214117 and/or MAK683 (1.2 µ m ). Viable cells were counted every 3 days (mean ± s.d., n = 2). All cellular experiments were performed at least two times and representative data are shown here. Statistical analysis was performed using one‐way ANOVA ( * , p < 0.05; ** , p < 0.01; *** , p < 0.001; **** , < 0.0001).

Article Snippet: WSU‐DLCL2, Karpas422, SU‐DHL‐1, Toledo, OCI‐Ly19, SU‐DHL‐4 and Pfeiffer cells were seeded in 12‐well plates at a density of 2 × 10 5 cells mL −1 with the indicated concentration of MAK683, LDN‐214117 (Med Chem Express # HY‐16712) and LDN‐212854 (Med Chem Express # HY‐15897).

Techniques: Activity Assay, Quantitative RT-PCR, Western Blot, Cell Cycle Assay, Staining