Jervine hydriodide
Based on 3 publication(s) in Google Scholar
Jervine hydriodide is an orally active steroidal alkaloid and Hedgehog signaling pathway inhibitor. Jervine hydriodide can be isolated from Veratrum californicum. Jervine hydriodide regulates Wnt, inhibits the AKT/mTOR signaling pathway, and activates the AMPK signaling pathway. Jervine hydriodide induces DNA damage, Apoptosis, Autophagy, ROS production and Mitochondrial damage. Jervine hydriodide exhibits anti-cancer and anti-inflammatory activities. Jervine hydriodide reduces tumor growth rate and weight in xenograft models. Jervine hydriodide can be used in studies related to triple-negative breast cancer, nasopharyngeal carcinoma and non-small cell lung cancer.
For research use only. We do not sell to patients.
- CAS No.: 60326-37-6
- Formula: C27H40INO3
- Molecular Weight:553.52
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Biological Activity
Jervine (10-40 μM; 48 h) hydriodide dose-dependently represses Hedgehog signaling in 5-8F and C666-1 NPC cells, and suppression of GLI1 is necessary for Jervine-induced autophagy, as shown by increased LC3B-II conversion and puncta formation with GLI1 knockdown[2].
Jervine (1.25-20 μM; 1-4 days) time- and dose-dependently inhibits the proliferation of A549 and H1299 NSCLC cells, with 20 μM jervine causing the strongest reduction after 4 days of incubation[3].
Jervine (5-10 μM; 48 h) hydriodide significantly induces apoptosis in A549 and H1299 NSCLC cells, with 10 μM causing a stronger apoptotic response[3].
Jervine (5-10 μM; 48 h) hydriodide significantly induces apoptosis in A549 and H1299 NSCLC cells, as detected by Hoechst 33258 staining[3].
Jervine (5-10 μM; 48 h) hydriodide dose-dependently upregulates markers of apoptosis (cleaved Caspase-3, cleaved PARP) and autophagy (LC3II) in A549 and H1299 NSCLC cells[3].
Jervine (5-10 μM; 48 h) hydriodide dose-dependently represses AKT/mTOR signaling in A549 and H1299 NSCLC cells, as evidenced by reduced p-AKT and p-mTOR expression[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human NSCLC A549, H1299 cells
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Concentration:5 μM; 10 μM
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Incubation Time:48 h
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Result:Significantly increased the number of LC3-positive puncta per cell in both cell lines.
Increased LC3 puncta to approximately 30 per A549 cell and approximately 50 per H1299 cell at 5 μM.
Increased LC3 puncta to approximately 70 per A549 cell and approximately 50 per H1299 cell at 10 μM.
All increases were statistically significant (**p < 0.01 vs control).
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Cell Line:human NSCLC A549, H1299 cells
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Concentration:5 μM; 10 μM
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Incubation Time:48 h
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Result:Dose-dependently increased the expression of cleaved Caspase-3, cleaved PARP, and LC3II in both A549 and H1299 cells compared to control.
Jervine (20 mg/kg; p.o.; daily; 24 days) hydriodide's suppression of nasopharyngeal carcinoma xenograft tumor growth in BALB/c nude mice is largely dependent on induction of autophagy, as co-treatment with the autophagy inhibitor 3-MA (HY-19312) abrogates its anti-tumor effects[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c nude (male, 5 weeks old, 17−19 g, subcutaneous xenograft model via 5−8F cell injection)[2]
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Dosage:20 mg/kg
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Administration:p.o.; daily; 24 days
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Result:Significantly reduced tumor growth rate, with tumor volume reaching a significantly lower level than controls by day 28.
Significantly reduced final tumor weight compared to controls.
Significantly decreased Ki-67-positive area in tumor tissue.
Significantly increased TUNEL-positive area in tumor tissue.
Significantly increased LC3B-positive area in tumor tissue.
Significantly decreased SHH-positive area in tumor tissue.
Significantly reduced protein expression of PTCH1, SMO, and GLI1 in tumor tissue.
Significantly increased cleaved Caspase-3 in tumor tissue.
Showed no significant differences in mouse body weight, serum levels of AST, ALT, ALP, BUN, or CRE, or histology of major organs (liver, spleen, lung, kidney, heart) compared to controls.
Chemical Information
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CAS No. 60326-37-6
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Molecular Weight 553.52
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Formula C27H40INO3
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SMILES
CC1=C(C([C@@]2([H])[C@@]3([H])CC=C4[C@@]2(CC[C@@H](C4)O)C)=O)[C@@]3([H])CC[C@]15O[C@@]6([H])[C@](NC[C@H](C6)C)([H])[C@H]5C.I
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Synonyms
11-Ketocyclopamine hydriodide
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (3)
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Journal Impact Factor
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Most Recent
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Philos Trans R Soc Lond B Biol Sci
2023 Nov 20;378(1890):20220248. PMID: 37778388 -
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Biochem Biophys Res Commun
Jervine inhibits non-small cell lung cancer (NSCLC) progression by suppressing Hedgehog and AKT signaling via triggering autophagy-regulated apoptosis. [Abstract]2020 Dec 10;533(3):397-403. PMID: 32972750
Purity & Documentation
References
[1]. Eswaran A, et al. Jervine-induced suppression of triple-negative breast cancer (TNBC) cells growth through the regulation of Wnt signaling pathway- an in-silico and in-vitro approach. J Comput Aided Mol Des. 2026 Feb 5;40(1):57. [Content Brief]
[2]. Chen J, et al. Jervine exhibits anticancer effects on nasopharyngeal carcinoma through promoting autophagic apoptosis via the blockage of Hedgehog signaling. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. 2020 Dec;132:110898. [Content Brief]
[3]. Lei W, et al. Jervine inhibits non-small cell lung cancer (NSCLC) progression by suppressing Hedgehog and AKT signaling via triggering autophagy-regulated apoptosis. Biochemical and biophysical research communications. 2020 Dec 10;533(3):397-403. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Jervine hydriodide Related Classifications
HY-N0836A Related Classifications
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