Fig. 1 · Structure

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Parthenolide ((-)-Parthenolide)

Cat. No. A10698 CAS 20554-84-1
Parthenolide ((-)-Parthenolide) is a sesquiterpene lactone which occurs naturally in the plant feverfew (Tanacetum parthenium).

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Biological Activity

Target & Activity

Target Activity Value
HDAC1

In Vitro Studies

In MDA-MB231 cells, Parthenolide progressively lowered intracellular GSH and decreased cell viability in separate assessments. In astroglial-enriched cultures prepared from ICR mice, Parthenolide pretreatment inhibited Tat±morphine-induced increases in TNF-α, MCP-1, and IL-6 release compared with Tat±morphine treatment without PAR. In murine immortalized macrophages stably expressing ASC-YFP, Parthenolide prevented LPS- and ATP-induced speck formation compared with DMSO. [1,2,3]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Reduced intracellular GSH in breast cancer cells

Cell-based study · MDA-MB231 cells [1]

In MDA-MB231 cells, exposure to 25 μM Parthenolide progressively lowered intracellular GSH, reaching 10–15% of control at 16 h.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
intracellular GSH contentGSH level 10–15% of control[1]

Literature-Reported Treatment Conditions

Treatment concentration
25 μM
Exposure duration
16 h
Method
diluted to final concentration in the culture medium
Vehicle
dimethyl sulfoxide (DMSO)
Methods and source locations

Compound reported in the paper: Parthenolide

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results > Parthenolide causes depletion of intracellular thiols (S55, S56); Materials and Methods > Chemicals and reagents (S108); Materials and Methods > Cell cultures (S111); Materials and Methods > Measurement of intracellular thiols and GSH content (S148); Figure 4 legend (S253)

intracellular GSH content: intracellular GSH content; comparator: untreated cells — Results > Parthenolide causes depletion of intracellular thiols (S56); Materials and Methods > Measurement of intracellular thiols and GSH content (S148)

Reduced cytokine release in astroglial cultures

Cell-based study · Astroglial-enriched cultures were prepared using 1–4-day-old ICR mice [2]

In astroglial-enriched cultures prepared from ICR mice, pretreatment with 10 µM and 20 µM Parthenolide inhibited Tat±morphine-induced increases in TNF-α, MCP-1, and IL-6 release at 12 h compared with Tat±morphine treatment without PAR.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
release of MCP-1, IL-6, and TNF-α by ELISAReported result Pretreatment with both 10 µM and 20 µM parthenolide inhibited Tat±morphine-induced increases in TNF-α, MCP-1, and IL-6 release at 12 h.[2]

Literature-Reported Treatment Conditions

Treatment concentration
10 µM and 20 µM
Exposure duration
for 15–20 min followed by incubation with HIV-Tat±morphine (Morph or MOR) for 12 h
Method
added to cells
Vehicle
culture medium
Co-treatment
Other interventions in this design: Tat1–72 100 nM; morphine sulfate 500 nM. Compound effect isolated by the comparison: Tat±morphine treatment without PAR.
Methods and source locations

Compound reported in the paper: Parthenolide

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Materials and Methods > Cell Culture (S6); Materials and Methods > Experimental Treatments (S21, S22); Results > NF-κB Inhibition Reduces Proinflammatory Cytokine and Chemokine Production (S84, S85); Figure 1 legend (S146, S147, S149)

release of MCP-1, IL-6, and TNF-α by ELISA: release of MCP-1, IL-6, and TNF-α by ELISA; comparator: Tat±morphine treatment without PAR — Results > NF-κB Inhibition Reduces Proinflammatory Cytokine and Chemokine Production (S85); Figure 1 legend (S147)

Speck formation prevention in immortalized macrophages

Cell-based study · Murine immortalized macrophages that stably express ASC-YFP [3]

Murine immortalized macrophages stably expressing ASC-YFP were treated with 10 µM Parthenolide. Compared with DMSO, Parthenolide prevented speck formation in response to LPS and ATP stimulation.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
formation of specksReported result 10 µM parthenolide prevented the formation of specks in response to stimulation with LPS and ATP[3]

Literature-Reported Treatment Conditions

Treatment concentration
10 µM
Exposure duration
stimulated with 10 ng/ml LPS for 3 h, treated with 50 µM CRID3 10 µM parthenolide or DMSO in serum free media for 30 min followed by addition of 5 mM ATP for 1 h
Method
in serum free media
Vehicle
DMSO
Co-treatment
Other interventions in this design: LPS 10 ng/ml; ATP 5 mM. Compound effect isolated by the comparison: DMSO.
Methods and source locations

Compound reported in the paper: Parthenolide

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results > CRID3 prevents NLRP3 and AIM2 dependent ASC oligomerisation (S30, S33); Figure 5 legend (S136)

formation of specks: formation of specks; comparator: DMSO — Results > CRID3 prevents NLRP3 and AIM2 dependent ASC oligomerisation (S33)

Decreased cell viability in breast cancer cells

Cell-based study · MDA-MB231 cells [1]

In MDA-MB231 cells, exposure to 25 μM Parthenolide for 16 h decreased cell viability by 64%, as assessed by MTT assay.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Cell viability was assessed by MTT assaycell viability cell viability decreased by 64%[1]

Literature-Reported Treatment Conditions

Treatment concentration
25 μM
Exposure duration
16 h of exposure
Method
diluted to final concentration in the culture medium
Vehicle
dimethyl sulfoxide (DMSO)
Methods and source locations

Compound reported in the paper: Parthenolide

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results > Parthenolide effect on cell viability and intracellular calcium level (S1, S2); Materials and Methods > Chemicals and reagents (S108); Materials and Methods > Cell viability and cell death assays (S115); Figure 1 legend (S200, S211)

Cell viability was assessed by MTT assay: Cell viability was assessed by MTT assay; comparator: untreated control — Results > Parthenolide effect on cell viability and intracellular calcium level (S2); Figure 1 legend (S200)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 20554-84-1
Formula C15H20O3
Molecular Weight 248.3
Synonyms (-)-Parthenolide
SMILES
C/C/1=C/CC[C@@]2([C@H](O2)[C@@H]3[C@@H](CC1)C(=C)C(=O)O3)C

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 49 mg/mL (197.32 mM)
Water Insoluble
Ethanol Warmed: 49 mg/mL (197.32 mM)

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration
9 mg/mL
Vehicle
2% DMSO+corn oil

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] D'Anneo A, Carlisi D, Lauricella M, et al. Parthenolide generates reactive oxygen species and autophagy in MDA-MB231 cells. A soluble parthenolide analogue inhibits tumour growth and metastasis in a xenograft model of breast cancer. Cell Death Dis (2013). PMID: 24176849 DOI: 10.1038/cddis.2013.415 Source material
  2. [2] El-Hage N, Bruce-Keller AJ, Yakovleva T, et al. Morphine exacerbates HIV-1 Tat-induced cytokine production in astrocytes through convergent effects on [Ca(2+)](i), NF-kappaB trafficking and transcription. PLoS One (2008). PMID: 19116667 DOI: 10.1371/journal.pone.0004093 Source material
  3. [3] Coll RC, Robertson A, Butler M, et al. The cytokine release inhibitory drug CRID3 targets ASC oligomerisation in the NLRP3 and AIM2 inflammasomes. PLoS One (2011). PMID: 22216309 DOI: 10.1371/journal.pone.0029539 Source material

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