Propyzamide
(Synonyms: Kerb; RH 315)
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Propyzamide (Kerb) is an orally active inhibitor of β-tubulin and AHR signaling pathways. Propyzamide binds β-tubulin at the intradimer interface, disrupting microtubule assembly, leading to mitotic arrest and multipolar spindle formation. Propyzamide enhances C/EBPβ and NF-κB signaling, promoting colitogenic helper T cell differentiation and interleukin-17/interferon gamma-expressing colonic T cells. Propyzamide can be used in research on colitis, inflammatory bowel disease, and liver cancer.
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- Pureté : 99.77%
- CAS No.: 23950-58-5
- Formule: C12H11Cl2NO
- Masse moléculaire:256.13
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Stockage:
Store at room temperature 3 years.
In solvent -80°C, 2 years , -20°C, 1 year
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Activité biologique
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Chemical Information
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Solvant et solubilité
- Protocole
- Pureté et documentation
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Activité biologique
Description
Propyzamide (Kerb) is an orally active inhibitor of β-tubulin and AHR signaling pathways. Propyzamide binds β-tubulin at the intradimer interface, disrupting microtubule assembly, leading to mitotic arrest and multipolar spindle formation. Propyzamide enhances C/EBPβ and NF-κB signaling, promoting colitogenic helper T cell differentiation and interleukin-17/interferon gamma-expressing colonic T cells. Propyzamide can be used in research on colitis, inflammatory bowel disease, and liver cancer[1][2][3][4][5][6].
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β-Tubulin |
AhR |
NF-κB |
C/EBPβ |
IL-17 |
interferon gamma |
In Vitro
Adaptive ImmunityCytokines & ChemokinesCell Cycle RegulationInnate ImmunityLipid MetabolismOxidative StressAnti-cancerOthers
Adaptive Immunity
Cytokines & Chemokines
Cell Cycle Regulation
Propyzamide (20 μM; 48-72 h) arrests Vigna radiata root meristem cells in prophase (83.41% at 48 h; 73.26% at 72 h) and disrupts spindle microtubules[5].
Propyzamide (100 μM; 6 days) inhibits Nicotiana tabacum cv. BY-2 cell division, reaching 53% inhibition in the conductivity assay[6].
Propyzamide (0.75 μM-0.1 M; 24 h) causes complete depolymerization of cortical and spindle microtubules and induces multipolar spindle formation in Nicotiana tabacum cv. BY-2 cells[6].
Propyzamide (100 μM; 6 days) inhibits Nicotiana tabacum cv. BY-2 cell division, reaching 53% inhibition in the conductivity assay[6].
Propyzamide (0.75 μM-0.1 M; 24 h) causes complete depolymerization of cortical and spindle microtubules and induces multipolar spindle formation in Nicotiana tabacum cv. BY-2 cells[6].
Innate Immunity
Adaptive Immunity
Innate Immunity
Adaptive Immunity
Cytokines & Chemokines
Propyzamide (2 µM) promotes C/EBPβ recruitment to Ifng, Il12rb1, and Rorc promoters in mouse T cells[2].
Innate Immunity
Cytokines & Chemokines
Lipid Metabolism
Oxidative Stress
Cytokines & Chemokines
Propyzamide (50 μM; 24 h) activates xenobiotic metabolism and nuclear receptor signaling pathways in differentiated HepaRG cells, with predicted PXR, CAR, NRF2, and PP2A subunit induction[3].
Oxidative Stress
Propyzamide (3.13-50 μM; 24 h) induces CYP2B6 and CYP3A4 expression in differentiated HepaRG cells from 6.25 μM, with 3.4- and 3.0-fold increases at 50 μM[3].
Propyzamide (3.13-50 μM; 24 h)-induced CYP1A2, CYP2B6, and CYP3A4 expression in differentiated HepaRG cells is suppressed by MC-LA or MC-LR at 0.6 μM, demonstrating functional antagonism[3].
Propyzamide (3.13-50 μM; 24 h)-induced CYP1A2, CYP2B6, and CYP3A4 expression in differentiated HepaRG cells is suppressed by MC-LA or MC-LR at 0.6 μM, demonstrating functional antagonism[3].
Oxidative Stress
Cytokines & Chemokines
Anti-cancer
Propyzamide (50 μM; 24 h) combined with MC-LR (0.6 μM) produces transcriptional profiles in differentiated HepaRG cells that largely resemble MC-LR alone while adding HCC- and inflammation-related DEGs[3].
Others
Propyzamide (300-1,000 µM; overnight at 4 °C) competes with [3H]TCDD for binding to mouse and human AHR in cell-free assays[2].
Propyzamide (10 µM) inhibits FICZ-induced AHR activation in HEK293FT/DC2.4 AHR reporter cells[2].
Propyzamide (10 µM) activates VCAM1 and C/EBPβ-dependent pro-inflammatory promoters in reporter assays[2].
Propyzamide (3.13-50 μM; 24 h) alone is not cytotoxic in differentiated HepaRG cells up to 50 μM, whereas combined with 0.6 μM MCs it reduces viability to approximately 80% at 50 μM[3].
Propyzamide (50 μM; 24 h) weakly inhibits PP2A activity in differentiated HepaRG cells, with a relative activity of 0.84[3].
Propyzamide (50 µM; 48 h) disrupts β-tubulin immunolocalization in C. vulgaris spermatids, reducing signals at stages IV-VI and eliminating them from stages VII-X, with nuclear distortion at stages V, VII, and VIII[4].
Propyzamide (50 µM; 48 h) induces extensive ultrastructural abnormalities in C. vulgaris spermatids, including nuclear envelope invagination/fragmentation, disturbed chromatin condensation, dilated ER and autolytic vacuoles, and fragmented microtubular manchette, while flagella remain largely correctly formed[4].
Propyzamide (20 μM; 24-72 h) inhibits Vigna radiata seedling root elongation by approximately 20-25%[5].
Propyzamide (20 μM; 24-72 h) impairs lateral root development and causes root tip thickening in Vigna radiata seedlings[5].
Propyzamide (10 µM) inhibits FICZ-induced AHR activation in HEK293FT/DC2.4 AHR reporter cells[2].
Propyzamide (10 µM) activates VCAM1 and C/EBPβ-dependent pro-inflammatory promoters in reporter assays[2].
Propyzamide (3.13-50 μM; 24 h) alone is not cytotoxic in differentiated HepaRG cells up to 50 μM, whereas combined with 0.6 μM MCs it reduces viability to approximately 80% at 50 μM[3].
Propyzamide (50 μM; 24 h) weakly inhibits PP2A activity in differentiated HepaRG cells, with a relative activity of 0.84[3].
Propyzamide (50 µM; 48 h) disrupts β-tubulin immunolocalization in C. vulgaris spermatids, reducing signals at stages IV-VI and eliminating them from stages VII-X, with nuclear distortion at stages V, VII, and VIII[4].
Propyzamide (50 µM; 48 h) induces extensive ultrastructural abnormalities in C. vulgaris spermatids, including nuclear envelope invagination/fragmentation, disturbed chromatin condensation, dilated ER and autolytic vacuoles, and fragmented microtubular manchette, while flagella remain largely correctly formed[4].
Propyzamide (20 μM; 24-72 h) inhibits Vigna radiata seedling root elongation by approximately 20-25%[5].
Propyzamide (20 μM; 24-72 h) impairs lateral root development and causes root tip thickening in Vigna radiata seedlings[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[3]
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Cell Line:differentiated HepaRG cells
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Concentration:3.13, 6.25, 12.5, 25, 50 μM (PRO alone); 3.13, 6.25, 12.5, 25, 50 μM (combined with 0.6 μM MCs)
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Incubation Time:24 h
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Result:Did not reduce cell viability at the highest tested concentration (50 μM).
Mixtures of PRO (3.13-50 μM) with MCs (0.6 μM) reduced cell viability to approximately 80% at 50 μM PRO + 0.6 μM MCs.
Real Time qPCR[3]
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Cell Line:differentiated HepaRG cells
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Concentration:3.13, 6.25, 12.5, 25, 50 μM
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Incubation Time:24 h
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Result:Induced expression of all marker genes.
Significant effects on CYP2B6 and CYP3A4 were found from 6.25 μM (BMDL 11.3 and 14.6 μM, respectively).
At the highest tested concentration, expression was increased by 3.4-fold for CYP2B6 and 3.0-fold for CYP3A4.
CYP1A2 and GPX2 appeared to increase in a concentration-dependent manner, but the effects were not significant.
Real Time qPCR[3]
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Cell Line:differentiated HepaRG cells
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Concentration:3.13, 6.25, 12.5, 25, 50 μM combined with 0.6 μM MC-LA or 0.6 μM MC-LR
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Incubation Time:24 h
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Result:In both mixtures, MCs predominantly drove the observed effects.
Marker gene expression patterns were largely comparable to those of the respective MC alone, opposing those of PRO, resulting in functional antagonism.
Both MCs suppressed the PRO-induced increased expression of CYP2B6, CYP3A4, and CYP1A2.
Cell Proliferation Assay[6]
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Cell Line:Nicotiana tabacum cv. Bright Yellow 2 (BY-2) suspension cells
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Concentration:100 μM
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Incubation Time:6 days
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Result:Inhibited BY-2 cell division by 53%.
Immunofluorescence[6]
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Cell Line:Nicotiana tabacum cv. BY-2 cells
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Concentration:0.1 M (Figure 1 legend); 0.1-100 μM (Figure 2 legend); 0.75 μM (Figure 2C)
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Incubation Time:24 h
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Result:Caused complete depolymerization of cortical and spindle microtubules at 0.1 M, induced deformed chromosome structures classified as prometaphases, and produced multinucleated cells.
Also induced multipolar spindle formation, with representative multipolar spindles shown at 0.75 μM.
In Vivo
Adaptive ImmunityCytokines & ChemokinesApoptosisInnate ImmunityOxidative Stress
Adaptive Immunity
Cytokines & Chemokines
Apoptosis
Propyzamide (100 mg kg−1; gavage; 7 days) worsens anti-CD3-induced enteritis and T cell-driven small intestinal inflammation in mice[2].
Adaptive Immunity
Innate Immunity
Propyzamide (100 mg kg−1; intraperitoneally for 3 days and/or oral gavage) does not initiate intestinal inflammation or alter baseline intestinal immune populations in healthy mice[2].
Adaptive Immunity
Innate Immunity
Cytokines & Chemokines
Adaptive Immunity
Oxidative Stress
Propyzamide (0.2-20 μM; in E3 medium; 24-72 h) amplifies TNBS-induced intestinal inflammation in zebrafish without initiating inflammation in naive larvae[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:AB wild-type and lck:gfp (7 days post-fertilization larvae)[2]
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Dosage:0.2, 1, 5, and 20 μM
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Administration:in E3 medium; co-administered with 25 μg/mL TNBS; 24-72 h starting at 7 d.p.f.
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Result:Boosted TNBS-induced intestinal inflammation in zebrafish, as indicated by intestinal scores and expression of pro-inflammatory genes.
In TNBS-exposed zebrafish, Propyzamide at 20 μM was tested in combination with TNBS; quantification of intestinal GFP-positive T cells in lck:gfp zebrafish was performed.
Did not induce intestinal inflammation in the absence of TNBS.
AHR activation by FICZ or NOS inhibition partially interfered with the worsening of TNBS-induced colitis by Propyzamide.
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Animal Model:C57BL/6J (male, 8 weeks old)[2]
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Dosage:100 mg/kg intraperitoneally; 100 mg/kg by oral gavage
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Administration:intraperitoneally for 3 days until TNBS presensitization; then oral gavage for 6 consecutive days until TNBS rectal challenge
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Result:Worsened intestinal pathology as indicated by weight loss, colon shortening, and histological evaluation.
Increased IL-17+ CD4+ T cells, IL-17+ RORγt+ CD4+ T cells, IFNγ+ CD4+ T cells, and IFNγ+ CD8+ T cells in the colon, but did not modify IL-17 production by CD8+ T cells and γδ T cells.
Increased colonic CD45+CD3+ lymphocyte counts normalized by colon tissue length compared with vehicle control TNBS mice.
Also increased Ifng and Il17a expression in lamina propria mononuclear cells (LPMC) from TNBS mice compared with vehicle control TNBS mice, whereas naive mice showed lower expression.
RNA-seq detected upregulation of pro-inflammatory pathways, including leukocyte extravasation, integrin signalling, and NF-κB activation.
Upstream regulator analysis identified decreased AHR suppression of NF-κB-driven C/EBPβ.
qPCR validation detected increased Rela and Cebpb expression and increased Tnf, Il1b, Il23, and Il6 in lamina propria mononuclear cells; no changes were detected in Il10 or Tgfb expression.
scRNA-seq showed expansion of T cell and dendritic cell clusters, upregulation of NF-κB-driven C/EBPβ pro-inflammatory gene expression, and decreased AHR signalling.
Increased Vcam1 expression in the colon of TNBS mice and increased T cell expression of Itga4, but not Itga1.
Reduced microbiome diversity in the ileum and caecum and expanded Sutterellaceae; however, germ-free recipients of faecal microbiota from Propyzamide- or vehicle-exposed mice developed comparable intestinal inflammation after TNBS administration.
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Animal Model:C57BL/6J (male, 8 weeks old)[2]
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Dosage:100 mg/kg by gavage; anti-CD3 monoclonal antibody 200 μg intraperitoneally
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Administration:by gavage for 7 days; then anti-CD3 monoclonal antibody intraperitoneally
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Result:Worsened intestinal pathology and T cell-driven inflammation in the anti-CD3 enteritis model, including worsened jejunal histopathology.
Transcriptomic analyses detected decreased AHR signalling, increased NF-κB activation, and increased expression of Cebpb and other pro-inflammatory molecules, as well as increased IL-17 and IFNγ production by CD4+ T cells.
Did not affect the number of small intestine immune cells or their transcriptional programs in the absence of anti-CD3.
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Animal Model:C57BL/6J (male, 8 weeks old)[2]
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Dosage:100 mg/kg intraperitoneally for 3 days and/or 100 mg/kg by oral gavage
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Administration:intraperitoneally for 3 days and/or oral gavage
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Result:Did not alter weight, colon length, CD4+ T cells, CD8+ T cells, γδ T cells, or innate lymphoid cell numbers in the absence of TNBS.
Did not affect the number of small intestine immune cells or their transcriptional programs in the absence of anti-CD3.
Chemical Information
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CAS No. 23950-58-5
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Appearance Solid
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Masse moléculaire 256.13
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Formule C12H11Cl2NO
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Color White to off-white
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SMILES
O=C(NC(C)(C)C#C)C1=CC(Cl)=CC(Cl)=C1
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Synonyms
Kerb; RH 315
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Store at room temperature 3 years
In solvent -80°C 2 years -20°C 1 year
Solvant et solubilité
In Vitro:
DMSO : 200 mg/mL (780.85 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
View the Complete Stock Solution Preparation Table
Preparing Stock Solutions
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Concentration
Solvent
Mass
1 mg
5 mg
10 mg
Concentration
Solvent
Mass
1 mM
3.9043 mL
19.5213 mL
39.0427 mL
5 mM
0.7809 mL
3.9043 mL
7.8085 mL
10 mM
0.3904 mL
1.9521 mL
3.9043 mL
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
Calculateur de molarité
Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)
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Pureté et documentation
Select Batch:
Pureté:
99.98%
Assay:
99.98%
ee.:
99.98%
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Fiche technique (303 KB)
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SDS (563 KB)
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Instruction de manipulation (2659 KB)
Références
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Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 3.9043 mL | 19.5213 mL | 39.0427 mL | 97.6067 mL |
| 5 mM | 0.7809 mL | 3.9043 mL | 7.8085 mL | 19.5213 mL | |
| 10 mM | 0.3904 mL | 1.9521 mL | 3.9043 mL | 9.7607 mL | |
| 15 mM | 0.2603 mL | 1.3014 mL | 2.6028 mL | 6.5071 mL | |
| 20 mM | 0.1952 mL | 0.9761 mL | 1.9521 mL | 4.8803 mL | |
| 25 mM | 0.1562 mL | 0.7809 mL | 1.5617 mL | 3.9043 mL | |
| 30 mM | 0.1301 mL | 0.6507 mL | 1.3014 mL | 3.2536 mL | |
| 40 mM | 0.0976 mL | 0.4880 mL | 0.9761 mL | 2.4402 mL | |
| 50 mM | 0.0781 mL | 0.3904 mL | 0.7809 mL | 1.9521 mL | |
| 60 mM | 0.0651 mL | 0.3254 mL | 0.6507 mL | 1.6268 mL | |
| 80 mM | 0.0488 mL | 0.2440 mL | 0.4880 mL | 1.2201 mL | |
| 100 mM | 0.0390 mL | 0.1952 mL | 0.3904 mL | 0.9761 mL |
Propyzamide Related Classifications
HY-B1883 Related Classifications
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Keywords
- Propyzamide
- 23950-58-5
- Kerb
- RH 315
- RH315
- RH 315
- RH-315
- Environmental Pollutants
- Aryl Hydrocarbon Receptor
- Microtubule/Tubulin
- NF-κB
- Interleukin Related
- AHR
- C/EBPβ
- colitogenic T helper differentiation
- inflammatory bowel disease
- interferon gamma
- interleukin-17
- microtubule assembly
- mitotic arrest
- β-tubulin
- Inhibitor
- inhibitor
- inhibit