Anisomelic acid
Anisomelic acid is a human papillomavirus HPV16 E6 and HPV E7 depletor. Anisomelic acid directly interacts with HPV16 E6, promotes its ubiquitination and proteasomal degradation by recruiting E3 ubiquitin ligase, downregulates E6 and facilitates E7 degradation. Anisomelic acid induces endogenous mitochondrial apoptosis, activates caspase-3, causes cleavage of PARP, and triggers p53-independent endogenous apoptosis by depleting cIAP2. Anisomelic acid can be used in research related to HPV-positive cancers and cervical cancer.
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- CAS. Nr.: 59632-76-7
- Formel: C20H26O4
- Molecular Weight:330.42
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Speicherung:
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Biologische Aktivität
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Chemical Information
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Biologische Aktivität
Anisomelic acid (40 μM; 24 h) induces proteasome-dependent degradation of exogenous HPV16 E6 in transfected SiHa cells by enhancing E6 ubiquitination[1].
Anisomelic acid (20-40 μM; 12-24 h) downregulates the HPV16-E6 and HPV16-E7 oncoproteins and stabilizes p53 and p21 in SiHa cervical cancer cells[3].
Anisomelic acid (20-40 μM; 12-24 h) mainly induces apoptosis in SiHa cervical cancer cells by activating caspase-9, accompanied by subsequent cleavage of caspase-3 and PARP, as well as delayed cleavage of caspase-8[3].
Anisomelic acid (40 μM; 12 h) downregulates the expression of E6 and cIAP2 in SiHa cervical cancer cells, and this process is mediated by the proteasomal degradation pathway[3].
Anisomelic acid (10-40 μM; 24 h) induces concentration-dependent cell death and apoptosis in NOK16 cells by downregulating HPV16 E6[1].
Anisomelic acid (20 µM; 24 h) induces apoptosis in human cervical cancer SiHa cells; among the formulations tested, anisomelic acid loaded onto folate-chitosan coated rod-like mesoporous silica nanoparticles induces the highest level of apoptosis, which is approximately 3.2 times that of free anisomelic acid[2].
Anisomelic acid (20 µM; 24 h) activates the apoptotic machinery in SiHa human cervical cancer cells via cleavage of procaspase-3 and PARP[2].
Anisomelic acid (20-40 μM; 48 h) induces dose-dependent apoptotic DNA fragmentation in SiHa cervical cancer cells[3].
Anisomelic acid (20-40 μM; 24 h) downregulates the expression level of cIAP2 protein in SiHa cervical cancer cells[3].
Anisomelic acid (40 μM; 48 h) preferentially induces apoptosis in HPV-positive cervical cancer cells (SiHa, CaSki, HeLa) compared with HPV-negative cervical cancer cells (c33a), breast cancer cells (MCF7, MDA-MB-231), and non-cancerous MEF cells[3].
Anisomelic acid (20-40 μM; 8-48 h) induces time- and dose-dependent mitochondrial membrane depolarization in SiHa cervical cancer cells[3].
Anisomelic acid (20-40 μM; 24 h) induces G2/M phase cell cycle arrest in synchronized SiHa cervical cancer cells[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:SiHa cells (HPV16-positive cervical cancer cell line) expressing HPV16 E6-FLAG-HA
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Concentration:40 μM (anisomelic acid); 20 μM (MG132 (HY-13259))
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Incubation Time:24 h (anisomelic acid incubation); 2 h (MG132 pretreatment)
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Result:Decreased HPV16 E6 protein levels.
Increased levels of ubiquitinated E6 compared to untreated samples.
Showed even greater accumulation of ubiquitinated E6 when combined with MG132.
Had its E6-decreasing effect blocked by MG132 pretreatment.
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Cell Line:NOK16 cells (normal oral keratinocytes stably expressing HPV16 FLAG-tag E6), pWPI control cells
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Concentration:10, 20 and 40 μM
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Incubation Time:24 h
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Result:Increased the percentage of dead cells in NOK16 cells in a concentration-dependent manner, with significantly higher cell death at 10 μM, 20 μM, and 40 μM compared to DMSO-treated NOK16 cells and pWPI control cells.
Markedly decreased HPV16 E6 levels in NOK16 cells treated with 10 μM and 20 μM, along with PARP cleavage and decreased caspase-3 levels.
Resulted in higher E6 levels in NOK16 cells at 40 μM, potentially due to stress-induced cellular responses.
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Cell Line:SiHa
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Concentration:20 and 40 μM
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Incubation Time:48 h
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Result:Induced ~26% TUNEL-positive cells at 20 μM after 48 h.
Induced ~55% TUNEL-positive cells at 40 μM after 48 h.
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Cell Line:SiHa
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Concentration:20 and 40 μM
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Incubation Time:12 h; 24 h
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Result:Reduced HPV16-E6 protein levels to ~70% of control and HPV16-E7 levels to ~80% of control, while increasing p53 levels to ~120% of control and p21 levels to ~110% of control at 20 μM after 12 h.
Reduced HPV16-E6 protein levels to ~50% of control and HPV16-E7 levels to ~50% of control, while increasing p53 levels to ~160% of control and p21 levels to ~110% of control at 40 μM after 12 h.
Reduced HPV16-E6 protein levels to ~60% of control and HPV16-E7 levels to ~70% of control, while increasing p53 levels to ~140% of control and p21 levels to ~130% of control at 20 μM after 24 h.
Reduced HPV16-E6 protein levels to ~20% of control and HPV16-E7 levels to ~40% of control, while increasing p53 levels to ~190% of control and p21 levels to ~120% of control at 40 μM after 24 h.\nReduced procaspase-9 levels to ~75% of control, procaspase-3 levels to ~80% of control, and increased PARP cleavage (p85 fragment) to ~120% of control at 40 μM after 12 h.
Reduced procaspase-9 levels to ~60% of control, procaspase-3 levels to ~70% of control, procaspase-8 levels to ~90% of control, and increased PARP cleavage to ~130% of control at 40 μM after 24 h.
Induced abundant caspase-8 cleavage only after 24 h of treatment.
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Cell Line:SiHa
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Concentration:20-40 μM
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Incubation Time:24 h
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Result:Induced ~32% of cells to accumulate in the G2/M phase at 20 μM after 24 h.
Induced ~20% of cells to accumulate in the G2/M phase at 40 μM after 24 h.
Control cells showed ~15% of cells in G2/M phase.
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Cell Line:SiHa
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Concentration:20 and 40 μM
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Incubation Time:24 h
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Result:Reduced cIAP2 protein levels to ~50% of control at 20 μM after 24 h.
Reduced cIAP2 protein levels to ~40% of control at 40 μM after 24 h.
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Cell Line:SiHa
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Concentration:40 μM (preceded by 20 μM MG132 pre-incubation for 2 h)
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Incubation Time:12 h
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Result:Reduced E6 to ~60% of control and cIAP2 to ~70% of control without MG132 pre-incubation.
Maintained E6 levels at ~80% of control and cIAP2 at ~80% of control with MG132 pre-incubation.
Had its induced degradation of E6 and cIAP2 inhibited by MG132.
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Cell Line:HeLa, CaSki, c33a, MCF7, MDA-MB-231, MEF
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Concentration:40 μM
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Incubation Time:48 h
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Result:Induced ~41% caspase-3 activation in SiHa cells.
Induced ~37% caspase-3 activation in CaSki cells.
Induced ~34% caspase-3 activation in HeLa cells.
Induced ~15% caspase-3 activation in c33a cells.
Induced ~22% apoptotic cells (PI staining) in MDA-MB-231 cells.
Induced minimal apoptosis in MCF7 cells.
Induced ~18% caspase-3 activation in MEF cells.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:White Leghorn (embryos)[3]
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Dosage:2 mg/kg, 4 mg/kg, 8 mg/kg, 12 mg/kg, 20 mg/kg
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Administration:topical; daily; 5 days
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Result:Inhibited SiHa tumor growth in a dose-dependent manner.
Showed non-significant mean tumor weight reduction at 2 mg/kg compared to control.
Reduced mean tumor weight significantly at 4 mg/kg.
Reduced mean tumor weight significantly to less than half of control levels at 8 mg/kg and 12 mg/kg.
Caused no embryo toxicity at tested doses.
Chemical Information
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CAS. Nr. 59632-76-7
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Molecular Weight 330.42
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Formel C20H26O4
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SMILES
O=C(/C1=C\CC/C(C)=C/[C@]([C@@](CC/C(C)=C/CC1)([H])C2=C)([H])OC2=O)O
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Structure Classification
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Initial Source
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Verweise
[1]. Santos Silva M, et al. Anisomelic acid promotes proteasomal degradation of HPV16 E6 via E3 ligase recruitment: A mass spectrometry-based interactome study. Journal of proteomics. 2026 Jan 06;322:105536. [Content Brief]
[2]. Senthilkumar R, et al. Targeted delivery of a novel anticancer compound anisomelic acid using chitosan-coated porous silica nanorods for enhancing the apoptotic effect. Biomaterials science. 2015 Jan;3(1):103-11. [Content Brief]
[3]. Paul P, et al. Novel action modality of the diterpenoid anisomelic acid causes depletion of E6 and E7 viral oncoproteins in HPV-transformed cervical carcinoma cells. Biochemical pharmacology. 2014 May 15;89(2):171-84. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
Anisomelic acid Related Classifications
HY-N20712 Related Classifications
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