Parbendazole
Based on 8 publication(s) in Google Scholar
Parbendazole (SKF‑29044) is an orally active benzimidazole carbamate compound with multiple biological activities. Parbendazole binds to free tubulin and inhibits microtubule polymerization; it also activates the JNK/c‑Jun signaling axis and upregulates the expression of the downstream axonal repulsion factor Sema3A. Parbendazole upregulates KAL-1 mRNA expression, reduces nerve growth factor levels, and promotes the terminal differentiation of normal human epidermal keratinocytes. Parbendazole induces apoptosis in differentiated acute myeloid leukemia monocytes and exerts antileukemic activity in a mouse xenograft model of acute myeloid leukemia. Parbendazole exhibits broad-spectrum anthelmintic activity against various animal nematodes. Parbendazole is used in research related to acute myeloid leukemia and parasitic infections.
For research use only. We do not sell to patients.
- Purity : 99.92%
- CAS No.: 14255-87-9
- Formula: C13H17N3O2
- Molecular Weight:247.29
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Storage:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 2 years , -20°C, 1 year
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Protocols
- Purity & Documentation
- References
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Help & FAQs
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Fenbendazole (Standard)Antibiotic
Publications Citing Use of MedChemExpress (MCE) Parbendazole
More- EBioMedicine. 2021 Mar:65:103276. [Abstract]
- RSC Adv. 2021 May 25;11(31):18938-18944. [Abstract]
- Commun Biol. 2024 Jan 24;7(1):123. [Abstract]
- Int J Mol Sci. 2023 Jun 30;24(13):10972. [Abstract]
- Molecules. 2026 Mar 5;31(5):864. [Abstract]
- Cancers (Basel). 2022 Nov 28;14(23):5854. [Abstract]
- Indian J Ophthalmol. 2026 Feb 1;74(2):250-258. [Abstract]
- Heinrich-Heine-Universität Düsseldorf. April 2021.
All Parasite Isoforms
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Biological Activity
Description
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JNK |
β-Tubulin |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| CAL-27 | IC50 |
173 nM
Compound: Parbendazole
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Antiproliferative activity against human CAL-27 cells assessed as cell growth inhibition incubated for 72 hrs by CCK-8 assay
Antiproliferative activity against human CAL-27 cells assessed as cell growth inhibition incubated for 72 hrs by CCK-8 assay
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[PMID: 35576703] |
| FaDu | IC50 |
160 nM
Compound: Parbendazole
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Antiproliferative activity against human FaDu cells assessed as cell growth inhibition incubated for 72 hrs by CCK-8 assay
Antiproliferative activity against human FaDu cells assessed as cell growth inhibition incubated for 72 hrs by CCK-8 assay
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[PMID: 35576703] |
| HFF-1 | IC50 |
>20 μM
Compound: Parbendazole
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Cytotoxicity against human HFF-1 clls assessed as reduction in cell viability incubated for 72 hrs by CCK-8 assay
Cytotoxicity against human HFF-1 clls assessed as reduction in cell viability incubated for 72 hrs by CCK-8 assay
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[PMID: 35576703] |
| HN-6 | IC50 |
102 nM
Compound: Parbendazole
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Antiproliferative activity against human HN-6 cells assessed as cell growth inhibition incubated for 72 hrs by CCK-8 assay
Antiproliferative activity against human HN-6 cells assessed as cell growth inhibition incubated for 72 hrs by CCK-8 assay
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[PMID: 35576703] |
In Vitro
Parbendazole (PBZ) exhibits extremely potent anti-survival activity against THP-1 acute myeloid leukemia cells, with an IC50 of 0.6 nM at 48 h and an IC50 of 0.3 nM at 72 h. At concentrations ≥50 nM, it effectively induces rapid monocytic differentiation of THP-1 acute myeloid leukemia cells, followed by apoptosis, which is accompanied by upregulation of the KLF4/DPYSL2A differentiation axis[1].
Parbendazole (100 nM; 48 h) exerts broad and potent differentiation-inducing and pro-apoptotic effects on acute myeloid leukemia cell lines with different subtypes and genetic backgrounds, while exhibiting limited toxicity to normal human hematopoietic progenitor cells; it effectively induces monocytic differentiation, triggers apoptosis, and upregulates the KLF4/DPYSL2A axis in primary human AML-PDX cells[1].
Parbendazole (0.01-1 μM; 48 h) induces the expression of the Sema3A gene and protein in normal human epidermal keratinocytes in a dose-dependent manner[2].
Parbendazole (1 μM; 48 h) downregulates NGF mRNA expression and upregulates KAL‑1 mRNA expression in normal human epidermal keratinocytes (NHEKs)[2].
Parbendazole (1 μM; 24 h) promotes the phosphorylation of JNK and c‑Jun in normal human epidermal keratinocytes (NHEKs)[2].
Parbendazole (1-10 μM; 24 h) increases the mRNA and protein expression levels of Sema3A in an in vitro reconstructed human epidermis (RHE) model[2].
Parbendazole hydrochloride: Wild-type Physarum polycephalum CLd-AXE tubulin completely inhibits in vitro microtubule assembly at 2-5 μM parbendazole, whereas mutant BEN210-AXE tubulin retains full microtubule assembly capacity even at parbendazole concentrations as high as 50 μM[3].
Parbendazole inhibits the growth of wild-type Physarum polycephalum CLd‑AXE myxamoebae and the in vitro assembly of their tubulin.
Parbendazole exhibits significant pH-dependent ultraviolet absorption characteristics, and shows a pronounced red shift in alkaline methanol medium compared to neutral and acidic methanol conditions[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Normal human epidermal keratinocytes (NHEKs)
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Concentration:0.01 μM, 0.1 μM, 1 μM
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Incubation Time:48 h
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Result:Dose‑dependently increases Sema3A mRNA levels.
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Cell Line:Normal human epidermal keratinocytes (NHEKs)
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Concentration:0.01 μM, 0.1 μM, 1 μM
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Incubation Time:48 h
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Result:Dose‑dependently increases secreted Sema3A protein levels.
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Cell Line:Normal human epidermal keratinocytes (NHEKs)
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Concentration:0.01 μM, 0.1 μM, 1 μM
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Incubation Time:48 h
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Result:Reduces cell viability at 1 μM; decreased mitochondrial dehydrogenase activity partially attributes to keratinocyte differentiation rather than simple cytotoxicity.
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Cell Line:Normal human epidermal keratinocytes (NHEKs)
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Concentration:1 μM
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Incubation Time:48 h
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Result:Down‑regulates NGF mRNA expression and up‑regulates KAL‑1 mRNA expression.
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Cell Line:Normal human epidermal keratinocytes (NHEKs)
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Concentration:1 μM
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Incubation Time:24 h
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Result:Promotes phosphorylation of JNK and c‑Jun.
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Cell Line:Normal human epidermal keratinocytes (NHEKs)
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Concentration:1 μM
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Incubation Time:24 h
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Result:Fails to induce Sema3A up‑regulation when JNK or c‑Jun is inhibited.
In Vivo
Parbendazole (5 mg/kg; i.v.; single injection) exhibits rapid distribution, a long elimination half-life of 720.0 min, and very low total excretion via urine and feces over 5 days in healthy goats[4].
Parbendazole (100 mg/kg; p.o.; daily; 28 consecutive days) exerts significant in vivo anti-leukemic activity in the AML PDX model by reducing leukemia burden, inducing leukemic cell monocytic differentiation, and prolonging animal survival[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 J mice (female, 14 weeks old)[1]
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Dosage:10 mg/kg; 50 mg/kg; 100 mg/kg
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Administration:p.o.; daily; 28 days
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Result:Showed no significant alterations in peripheral blood cell counts across the 28-day observation period.
Showed no significant alterations in individual body weight across the 28-day observation period at all tested doses up to 100 mg/kg.
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Animal Model:NOD/Shi-scid, IL-2RγKO (NOG) mice (male, 28 weeks old, acute myeloid leukemia PDX model induced by intravenous injection of 1.0 × 106 KMT2A-rearranged AML-PDX cells)[1]
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Dosage:100 mg/kg
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Administration:p.o.; daily; 28 consecutive days
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Result:Significantly reduced bone marrow AML cell chimerism percentage.
Induced partial monocytic differentiation of residual PDX leukemic cells evidenced by elevated CD11b and CD14 monocyte marker expression and characteristic monocyte morphological changes.
Extended overall survival of treated mice.
Chemical Information
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CAS No. 14255-87-9
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Appearance Solid
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Molecular Weight 247.29
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Formula C13H17N3O2
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Color White to light yellow
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SMILES
O=C(OC)NC1=NC2=CC=C(CCCC)C=C2N1
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Synonyms
SKF 29044
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year
Publications (8)
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Journal Impact Factor
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Most Recent
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EBioMedicine
Identification of novel myelin repair drugs by modulation of oligodendroglial differentiation competence. [Abstract]2021 Mar:65:103276. PMID: 33714029 -
RSC Adv
Structural insights into targeting of the colchicine binding site by ELR510444 and parbendazole to achieve rational drug design. [Abstract]2021 May 25;11(31):18938-18944. PMID: 35478655 -
Commun Biol
Parbendazole as a promising drug for inducing differentiation of acute myeloid leukemia cells with various subtypes. [Abstract]2024 Jan 24;7(1):123. PMID: 38267545 -
Int J Mol Sci
A Novel Ex Vivo Model to Study Therapeutic Treatments for Myelin Repair following Ischemic Damage. [Abstract]2023 Jun 30;24(13):10972. PMID: 37446147 -
Molecules
2026 Mar 5;31(5):864. PMID: 41828851 -
Cancers (Basel)
Drug Repurposing Applications to Overcome Male Predominance via Targeting G2/M Checkpoint in Human Esophageal Squamous Cell Carcinoma. [Abstract]2022 Nov 28;14(23):5854. PMID: 36497337 -
Indian J Ophthalmol
Ranitidine protects Müller cells against ferroptosis in diabetic retinopathy by regulating the AKT1/GSK3β pathway. [Abstract]2026 Feb 1;74(2):250-258. PMID: 41581041 -
Solvent & Solubility
In Vitro:
DMSO : 4 mg/mL (16.18 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.
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.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: 0.4 mg/mL (1.62 mM); Suspended solution; Need ultrasonic
This protocol yields a suspended solution of 0.4 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (4.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: 0.4 mg/mL (1.62 mM); Suspended solution; Need ultrasonic
This protocol yields a suspended solution of 0.4 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (4.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocols
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RT-PCR
Reverse transcription technology uses RNA as a template to synthesize DNA. RT-PCR is simple, specific and sensitive, and can be used to detect gene expression levels and expression differences in cells; detect RNA virus content; clone cDNA sequences of specific genes.
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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Patient-Derived Xenograft (PDX)
Patient-derived xenograft (PDX) models are generated by engrafting primary human tumor tissue directly into immunodeficient mice, allowing in vivo propagation of patient tumor biology without initial in vitro adaptation. These models are used to preserve key histopathological and molecular characteristics of the original tumor and enable assessment of tumor growth dynamics and therapeutic response in a living organism. The biological readout is tumor engraftment and subsequent growth in the murine host, which reflects the ability of human tumor cells to survive, vascularize, and expand in an immunocompromised microenvironment.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Splenic/Portal-Vein Liver Metastasis Xenograft
Splenic and portal-vein liver metastasis xenograft models deliver tumor cells into the portal circulation so that cells reach the liver first and form hepatic metastatic lesions; splenic injection uses the spleen as an access route to the portal system, while direct portal-vein injection introduces cells into the portal vein without requiring splenectomy. The assay detects liver colonization, intrahepatic tumor growth, tumor distribution, treatment response, survival, and liver-metastasis microenvironment changes; readouts include bioluminescence or fluorescence imaging, gross liver nodule counts, liver weight or tumor burden, histology, and survival.
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Subcutaneous Cell-Line-Derived Xenograft
Subcutaneous cell-line-derived xenograft (CDX) models are established by implanting cultured human cancer cell lines into immunodeficient mice, where the injected cells form localized tumors that can be monitored in vivo as a measure of tumorigenic potential, growth kinetics, and treatment response. These models are widely used in oncology research because they allow reproducible tumor formation and enable comparative assessment of tumor growth between different cell lines or genetic manipulations in a controlled in vivo microenvironment. Subcutaneous implantation of cancer cells in immunodeficient mice is a standard approach for evaluating tumor growth behavior and therapeutic response across multiple cancer types, including prostate, esophageal, pancreatic, and colon cancer models.
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Real Time qPCR (Q-PCR)
Real-time quantitative PCR (qPCR) quantifies an amplifiable nucleic-acid target by monitoring fluorescence during PCR cycling rather than measuring product only after amplification. The increase in fluorescence tracks accumulation of PCR product, and the quantification cycle (Cq; historically also Ct/CP) is related to the initial amount of target: samples containing more starting target generally reach the defined fluorescence threshold in fewer cycles.
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Orthotopic Cell-Line Xenograft
Orthotopic cell-line xenograft models involve implantation of human cancer cell lines into the anatomically corresponding organ of immunodeficient mice to reproduce tumor growth within a native microenvironment, enabling more clinically relevant tumor behavior compared with subcutaneous models. These models are widely used because orthotopic placement better recapitulates tumor progression, including invasion and metastatic spread, which are often underrepresented in heterotopic implantation systems. Compared with conventional xenografts, orthotopic implantation is described as more technically complex but provides improved simulation of tumor-microenvironment interactions and metastatic behavior, making it particularly valuable for translational oncology research. Surgical orthotopic implantation approaches have been emphasized as enabling faithful reproduction of clinical cancer features, including metastasis and disease progression patterns that align with the tumor’s organ of origi
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Intraperitoneal/Peritoneal Dissemination Xenograft
Intraperitoneal (IP) or peritoneal dissemination xenograft models are based on the introduction of human cancer cells into the peritoneal cavity of immunodeficient mice, where they attach to peritoneal surfaces, form multicellular aggregates or spheroids, and progressively generate disseminated tumor nodules that mimic advanced peritoneal metastatic disease. These models are widely used to study ovarian cancer progression, tumor-microenvironment interactions, and intraperitoneal therapeutic responses, often incorporating bioluminescence or fluorescence imaging to longitudinally monitor tumor burden in vivo. The biological principle relies on the capacity of tumor cells such as SKOV3 or related ovarian carcinoma lines to survive in suspension, aggregate within ascites-like fluid, adhere to mesothelial surfaces, and invade peritoneal organs, thereby recapitulating human peritoneal carcinomatosis patterns observed in advanced disease.
Purity & Documentation
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Data Sheet (291 KB)
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SDS (419 KB)
- English - EN (419 KB)
- Français - FR (419 KB)
- Deutsch - DE (419 KB)
- Norwegian - NO (419 KB)
- Español - ES (419 KB)
- Swedish - SV (419 KB)
- Italian - IT (419 KB)
- Korean - KR (419 KB)
- Portuguese - PT (419 KB)
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Handling Instructions (2659 KB)
References
[1]. Matsuo H, et al. Parbendazole as a promising drug for inducing differentiation of acute myeloid leukemia cells with various subtypes. Communications biology. 2024 Jan 24;7(1):123. [Content Brief]
[3]. Foster KE, et al. A mutant beta-tubulin confers resistance to the action of benzimidazole-carbamate microtubule inhibitors both in vivo and in vitro. European journal of biochemistry. 1987 Mar 16;163(3):449-55. [Content Brief]
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 | 4.0438 mL | 20.2192 mL | 40.4384 mL | 101.0959 mL |
| 5 mM | 0.8088 mL | 4.0438 mL | 8.0877 mL | 20.2192 mL | |
| 10 mM | 0.4044 mL | 2.0219 mL | 4.0438 mL | 10.1096 mL | |
| 15 mM | 0.2696 mL | 1.3479 mL | 2.6959 mL | 6.7397 mL |
Parbendazole Related Classifications
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