Art. -Nr.: HY-N1988

Cucurbitacin IIa

(Synonyms: Hemslecin A)

1 Cited Publications

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Cucurbitacin IIa (Hemslecin A) is an orally active, blood-brain barrier-permeable EGFR inhibitor with an IC₅₀ of 1.455 nM against human EGFR. Cucurbitacin IIa induces caspase-3-dependent apoptosis, downregulates survivin expression, enhances autophagy levels, disrupts the actin cytoskeleton via actin aggregation, arrests the cell cycle at the G2/M phase, and exerts anti-inflammatory activity by inhibiting the EGFR-MAPK signaling pathway. Cucurbitacin IIa can be used in the research of inflammation-related diseases, depression, and cancers such as non-small cell lung cancer.

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Reinheit: 99.90%
CAS. Nr.: 58546-34-2
Formel: C₃₂H₅₀O₈
Molecular Weight:562.73

Speicherung:

4°C, protect from light

* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Cucurbitacin IIa Chemical Structure

CAS. Nr.: 58546-34-2

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Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Publications (1)
Lösungsmittel & Löslichkeit
- In Vitro
- In Vivo
Reinheit & Dokumentation
Verweise
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

IC₅₀ & Target^[4]^[1]^[3]

EGFR

1.455 nM (IC₅₀)

Caspase 3

CaMK IIα

ERK1

MEK1

STAT3

ERK2

Alle EGFR Isoform-spezifische Produkte anzeigen :

Alle Caspase Isoform-spezifische Produkte anzeigen :

Alle p38 MAPK Isoform-spezifische Produkte anzeigen :

Alle MEK Isoform-spezifische Produkte anzeigen :

Alle Raf Isoform-spezifische Produkte anzeigen :

Alle ERK Isoform-spezifische Produkte anzeigen :

Alle STAT Isoform-spezifische Produkte anzeigen :

Alle CaMK Isoform-spezifische Produkte anzeigen :

Cellular Effect

Cell Line	Type	Value	Description	References
COLO 205	IC₅₀	1.09 μg/mL Compound: 4	Cytotoxicity against human COLO205 cells after 48 hrs by MTT assay Cytotoxicity against human COLO205 cells after 48 hrs by MTT assay	[PMID: 24717151]
HepG2 2.2.15	CC₅₀	66.2 μM Compound: 1	Cytotoxicity against human HepG2.2.15 cells Cytotoxicity against human HepG2.2.15 cells	[PMID: 23385212]
HepG2 2.2.15	IC₅₀	>66.2 μM Compound: 1	Antiviral activity against HBV infected in human HepG2.2.15 cells assessed as inhibition of viral e antigen production Antiviral activity against HBV infected in human HepG2.2.15 cells assessed as inhibition of viral e antigen production	[PMID: 23385212]
HepG2 2.2.15	IC₅₀	>66.2 μM Compound: 1	Antiviral activity against HBV infected in human HepG2.2.15 cells assessed as inhibition of viral surface antigen production Antiviral activity against HBV infected in human HepG2.2.15 cells assessed as inhibition of viral surface antigen production	[PMID: 23385212]
HepG2 2.2.15	IC₅₀	11.2 μM Compound: 1	Antiviral activity against HBV infected in human HepG2.2.15 cells assessed as inhibition of viral DNA replication Antiviral activity against HBV infected in human HepG2.2.15 cells assessed as inhibition of viral DNA replication	[PMID: 23385212]
NCI-H460	IC₅₀	11.53 μg/mL Compound: 4	Cytotoxicity against human H460 cells after 48 hrs by MTT assay Cytotoxicity against human H460 cells after 48 hrs by MTT assay	[PMID: 24717151]
SW-620	IC₅₀	1.11 μg/mL Compound: 4	Cytotoxicity against human SW620 cells after 48 hrs by MTT assay Cytotoxicity against human SW620 cells after 48 hrs by MTT assay	[PMID: 24717151]

In Vitro

Cucurbitacin IIa (0.1-1000 μM; 24-48 h) dose-dependently inhibits the proliferation of RAW 264.7 macrophages, with an IC₅₀ value of 122.32 μM at 24 h and 6.42 μM at 48 h^[1].
Cucurbitacin IIa (2.5-40 μM; 24 h) dose-dependently inhibits the migration of RAW 264.7 macrophages^[1].
Cucurbitacin IIa (2.5-40 μM; 5 h) does not inhibit LPS (HY-D1056)-induced TNF-α expression in RAW 264.7 macrophages^[1].
Cucurbitacin IIa (2.5-40 μM; 5 h) does not inhibit LPS-induced phosphorylation of MAPK (p38, ERK1/2, JNK) or phosphorylation of NF-κB pathway components (IκBα, p65) in RAW 264.7 macrophages^[1].
Cucurbitacin IIa (2.5-40 μM; 6-24 h) induces caspase-3-dependent apoptosis in LPS-stimulated (but not unstimulated) RAW 264.7 macrophages, which is evidenced by an increased population of cells at the sub-G0/G1 phase, elevated levels of activated caspase-3, and decreased expression of survivin^[1].
Cucurbitacin IIa (2.5-40 μM; 6-24 h) dose-dependently enhances LPS-induced autophagy in RAW 264.7 macrophages, which is evidenced by increased LC3B-II levels and enhanced LC3 puncta formation^[1].
Cucurbitacin IIa disrupts the actin cytoskeleton of RAW 264.7 macrophages by inducing actin aggregation, which is evidenced by the altered G-actin/F-actin ratio and abnormal actin distribution in treated cells^[1].
Cucurbitacin IIa (0.1-100 μg/mL; 48 h) reduces the viability and inhibits the growth of human prostate cancer cells CWR22Rv-1, PC-3 as well as human lung cancer cells NCI-H1299^[2].
Cucurbitacin IIa (10 μg/mL; 2 h) induces irreversible aggregation of filamentous actin in mouse NIH 3T3 cells transfected with EGFP-actin^[2].
Cucurbitacin IIa (50 μg/mL; 48 h) disrupts the actin cytoskeleton in human prostate cancer CWR22Rv-1 cells, but does not affect their microtubule cytoskeleton^[2].
Cucurbitacin IIa (10 μg/mL; 16 h) induces G2/M phase cell cycle arrest and increases the proportion of sub-G1 phase (apoptotic) cell population in parental human prostate cancer CWR22Rv-1 cells; however, these effects are inhibited in CWR22Rv-1 cells with δ-catenin overexpression^[2].
Cucurbitacin IIa (1-50 μg/mL; 16 h) reduces the expression levels of phosphorylated histone H3 and survivin, increases the level of cleaved PARP, and decreases the phosphorylation level of RhoA at serine 188 in human prostate cancer CWR22Rv-1 and PC-3 cells as well as human lung cancer NCI-H1299 cells, without inhibiting the phosphorylation of JAK2/STAT3^[2].
Cucurbitacin IIa (5-40 μg/mL; 72 h) induces apoptotic DNA fragmentation in human prostate cancer PC-3 and CWR22Rv-1 cells^[2].
Cucurbitacin IIa (1-50 μg/mL; 16 h) reduces the phosphorylation level of RhoA at serine 188 in human prostate cancer CWR22Rv-1 cells^[2].
Cucurbitacin IIa (50 μg/mL; 48 h) induces F-actin aggregation without altering the subcellular localization of STAT3 in human lung cancer NCI-H1299 cells^[2].
Cucurbitacin IIa (40-80 μM; 36 h) potently inhibits the proliferation of A549 cells, with an IC₅₀ of 60 μM after 36 h of treatment^[4].
Treatment of A549 cells with Cucurbitacin IIa (50-70 μM; 36 h) induces dose-dependent apoptosis in the cells^[4].
Treatment of A549 cells with Cucurbitacin IIa (50-70 μM; 36 h) induces G₂/M cell cycle arrest^[4].
Cucurbitacin IIa (60 μM; 1-5 h) alters the transcription levels of EGFR-MAPK pathway and apoptosis/cell cycle-related genes in A549 cells; significant upregulation of Raf1 and STAT3, as well as significant downregulation of MEK1 and ERK1, are observed at all time points^[4].
Cucurbitacin IIa (60 μM; 1-24 h) regulates the accumulation and phosphorylation of EGFR-MAPK pathway-related proteins, apoptosis-related proteins, and cell cycle-related proteins in A549 cells, including the continuous degradation of survivin, the continuous reduction of phosphorylated MEK1/2, and the continuous increase of phosphorylated BRAF^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Migration Assay^[1]

Cell Line:

mouse RAW 264.7 macrophage cells
Concentration:

2.5, 10, 40 μM
Incubation Time:

24 h
Result:

Markedly inhibited RAW 264.7 cell migration in a dose-dependent manner.
Reduced migrated cell numbers significantly at all tested concentrations compared to control.

Western Blot Analysis^[1]

Cell Line:

LPS-stimulated mouse RAW 264.7 macrophage cells
Concentration:

2.5, 10, 40 μM
Incubation Time:

1 h pretreatment, followed by 1 h LPS stimulation (MAPK analysis); 1 h pretreatment, followed by 4 h LPS stimulation (NF-κB analysis)
Result:

Did not suppress LPS-induced phosphorylation of p38, ERK1/2, JNK, IκBα, or p65.
Slightly increased MAPK phosphorylation levels at high doses.

Apoptosis Analysis^[1]

Cell Line:

LPS-stimulated mouse RAW 264.7 macrophage cells
Concentration:

2.5, 10, 40 μM
Incubation Time:

6 h (WB); 24 h (morphological observation, flow cytometry, WB)
Result:

Reduced the arborized morphology of LPS-activated cells and induced cell fragmentation.
Elevated sub-G0/G1 apoptotic cell populations in LPS-stimulated cells to 17.55% (2.5 μM), 24.64% (10 μM), and 33.28% (40 μM), with no increase in apoptotic cells observed with treatment alone.
Significantly increased cleaved caspase-3 levels in LPS-stimulated cells, with higher levels at 24 h than 6 h.
Decreased survivin expression significantly in LPS-stimulated cells treated with 2.5 and 10 μM at 24 h.

Cell Autophagy Assay^[1]

Cell Line:

LPS-stimulated mouse RAW 264.7 macrophage cells
Concentration:

2.5, 10, 40 μM
Incubation Time:

6 h, 24 h (western blot); 24 h (immunofluorescence microscopy, chloroquine combined treatment)
Result:

Dose-dependently enhanced LPS-induced increases in LC3B-II levels, with greater effects at 24 h than 6 h.
Further increased LC3B-II levels in LPS + Cucurbitacin IIa-treated cells when combined with chloroquine, confirming enhanced autophagic flux.
Increased LC3B-II levels alone, but this effect was significantly lower than the LPS + Cucurbitacin IIa treatment at 24 h. Induced more LC3 puncta in LPS + Cucurbitacin IIa-treated cells than LPS alone-treated cells.

Immunofluorescence^[2]

Cell Line:

human prostate cancer CWR22Rv-1 cells
Concentration:

50 μg/mL
Incubation Time:

48 h
Result:

Caused severe clustering of F-actin.
Showed no significant changes in microtubule structure compared to untreated cells.

Cell Cycle Analysis^[2]

Cell Line:

human prostate cancer CWR22Rv-1 cells (parental and δ-catenin-overexpressing)
Concentration:

10 μg/mL
Incubation Time:

16 h
Result:

Caused a 46% reduction in G1 phase, a decrease in S phase to 20%, a 5.5-fold increase in G2/M phase, and a 2.7-fold increase in sub-G1 phase in parental CWR22Rv-1 cells.
Caused only a moderate decrease in S phase and a slight increase in G2/M phase, with no significant changes in G1 or sub-G1 phases in δ-catenin-overexpressing CWR22Rv-1 cells.

Western Blot Analysis^[2]

Cell Line:

human prostate cancer CWR22Rv-1 and PC-3 cells, human lung cancer NCI-H1299 cells
Concentration:

1, 50 μg/mL
Incubation Time:

16 h
Result:

Reduced levels of phospho-Histone H3 and survivin, and increased levels of cleaved PARP in all three cell lines.
Reduced serine 188 phosphorylation of RhoA but did not alter total RhoA levels, total or phosphorylated STAT3, total or phosphorylated JAK2, or total or phosphorylated ERK1/2 in CWR22Rv-1 cells.
Had no significant effect on total or phosphorylated STAT3 or JAK2, and only marginally reduced JAK2 phosphorylation in NCI-H1299 cells.

Apoptosis Analysis^[2]

Cell Line:

human prostate cancer PC-3 and CWR22Rv-1 cells
Concentration:

5, 40 μg/mL
Incubation Time:

72 h
Result:

Induced clear DNA fragmentation, a hallmark of apoptosis, in both cell lines.

Immunofluorescence^[2]

Cell Line:

human prostate cancer CWR22Rv-1 cells
Concentration:

1, 50 μg/mL
Incubation Time:

16 h
Result:

Significantly reduced RhoA phosphorylation at serine 188, with a more pronounced reduction observed at 50 μg ml⁻1 compared to 1 μg ml⁻1.

Immunofluorescence^[2]

Cell Line:

human lung cancer NCI-H1299 cells
Concentration:

50 μg/mL
Incubation Time:

48 h
Result:

Induced F-actin clustering but did not alter the mixed nuclear and cytoplasmic distribution of STAT3 compared to untreated cells.

Cell Viability Assay^[4]

Cell Line:

A549
Concentration:

40, 50, 60, 70, 80 μM
Incubation Time:

36 h
Result:

Inhibited A549 cell proliferation in a dose-dependent manner, with an IC₅₀ value of approximately 60 μM at 36 h.
Caused statistically significant reductions in cell viability relative to vehicle control across all tested concentrations.

Apoptosis Analysis^[4]

Cell Line:

A549
Concentration:

50, 60, 70 μM
Incubation Time:

36 h
Result:

Induced apoptosis in A549 cells in a dose-dependent manner.

Cell Cycle Analysis^[4]

Cell Line:

A549
Concentration:

50, 60, 70 μM
Incubation Time:

36 h
Result:

Arrested A549 cells at the G2/M phase, with the G2/M phase cell population increasing to approximately one-third of total cells across all tested concentrations.

Real Time qPCR^[4]

Cell Line:

A549
Concentration:

60 μM
Incubation Time:

1, 2, 3, 4, 5 h
Result:

Caused significant, time-dependent changes in the transcription of EGFR-MAPK pathway and related genes.
Upregulated Raf1 and STAT3 significantly at all time points. Downregulated MEK1 and ERK1 significantly at all time points.
Upregulated BRAF, ERK2, and survivin across all treatments.
Downregulated cyclinB1 across all treatments.
Slightly upregulated EGFR at 3 h and downregulated EGFR at other time points.

Western Blot Analysis^[4]

Cell Line:

A549
Concentration:

60 μM
Incubation Time:

1, 2, 4, 8, 12, 24 h
Result:

Caused time-dependent changes in protein accumulation and phosphorylation in the EGFR-MAPK pathway and related proteins. Decreased total EGFR accumulation within 8 h, then increased; increased phosphorylated EGFR significantly, then dropped after 12 h.
Decreased total BRAF and Raf1 accumulation initially, then increased after 12 h and 24 h, respectively; increased phosphorylated BRAF continuously, while decreased phosphorylated Raf1 to a minimum at 12 h. Kept total MEK1/2 accumulation constant; decreased phosphorylated MEK1/2 continuously.
Reduced total and phosphorylated ERK1/2 to a trough at 4 h, then increased gradually.
Decreased STAT3 accumulation within 12 h, then recovered to baseline.
Degraded survivin completely over time. Suppressed cyclinB1 accumulation in early treatments, then recovered in later treatments.

In Vivo

Cucurbitacin IIa (30-90 mg/kg; i.p., p.o., i.v.; once daily; 10 days) dose-dependently suppresses H₂₂ hepatocellular carcinoma tumour growth in C57 mice, with the highest inhibition efficiency (57.05%) achieved at 90 mg/kg administered intraperitoneally daily for 10 days^[2].
Cucurbitacin IIa dose-dependently suppresses Lewis lung carcinoma tumour growth in C57 mice^[2].
Cucurbitacin IIa (2.5-5 mg/kg; i.p.; once daily; 5 weeks) exerts dose-dependent antidepressant-like effects in CUMS-exposed mice, with the 5 mg/kg dose fully restoring behavioral, synaptic receptor expression, and CaMKII-CREB-BDNF pathway marker levels to normal, and these effects are dependent on BDNF signaling^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

C57 mice^[2]
Dosage:

30-90 mg/kg (i.p.); 30-90 mg/kg (p.o.); 5-15 mg/kg (i.v.)
Administration:

i.p.; daily; 10 days; p.o.; daily; 10 days; i.v.; daily; 10 days
Result:

Reduced mean tumour weight.

Animal Model:

BALB/c (adult male, 18-22 g, chronic unpredictable mild stress-induced)^[3]
Dosage:

2.5 mg/kg; 5 mg/kg (CUMS mice); 5 mg/kg (naive mice)
Administration:

i.p.; daily; 5 weeks (1 hour before CUMS procedures/behavioral tests); i.p. (naive mice)
Result:

Restored the behavioral indicators, synaptic receptor expression levels, and levels of CaMKII-CREB-BDNF pathway markers in mice to normal states.

Chemical Information

CAS. Nr. 58546-34-2
Appearance Solid
Molecular Weight 562.73
Formel C₃₂H₅₀O₈
Color White to off-white
SMILES

C[C@@]([C@@](CC=C1[C@@]2([H])C[C@H](O)[C@@H](O)C1(C)C)([H])[C@@]2(C)C3=O)(C[C@@H](O)[C@]4([H])[C@@](C)(O)C(CCC(C)(C)OC(C)=O)=O)[C@@]4(C3)C
Synonyms

Hemslecin A
Structure Classification
- Terpenoids
- Triterpenes
Initial Source
Versand

Room temperature in continental US; may vary elsewhere.
Speicherung

4°C, protect from light

* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Publications (1)

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Vet Microbiol

The Chinese medicine monomer Schisandrin C inhibits PRRSV infection by regulating the OGT-PI3K/AKT/mTOR signaling pathway. [Abstract]

2026 May:316:110992. PMID: 41865607

Lösungsmittel & Löslichkeit

In Vitro:

DMSO : 25 mg/mL (44.43 mM; ultrasonic and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

1.7771 mL

8.8853 mL

17.7705 mL

5 mM

0.3554 mL

1.7771 mL

3.5541 mL

10 mM

0.1777 mL

0.8885 mL

1.7771 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, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

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.

Protocol 1

Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline

Solubility: ≥ 1 mg/mL (1.78 mM); Clear solution

This protocol yields a clear solution of ≥ 1 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (10.0 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.

Protocol 2

Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)

Solubility: ≥ 1 mg/mL (1.78 mM); Clear solution

This protocol yields a clear solution of ≥ 1 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (10.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

Protocol 3

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 1 mg/mL (1.78 mM); Clear solution

This protocol yields a clear solution of ≥ 1 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (10.0 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

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g
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
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Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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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

Reinheit & Dokumentation

Select Batch:

Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (306 KB)
SDS (393 KB)
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- Portuguese - PT (393 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
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Other Report (2659 KB)
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Verweise

[1]. He J, et al. Cucurbitacin IIa induces caspase-3-dependent apoptosis and enhances autophagy in lipopolysaccharide-stimulated RAW 264.7 macrophages. Int Immunopharmacol. 2013;16(1):27-34. [Content Brief]

[2]. Boykin C, et al. Cucurbitacin IIa: a novel class of anti-cancer drug inducing non-reversible actin aggregation and inhibiting survivin independent of JAK2/STAT3 phosphorylation. Br J Cancer. 2011;104(5):781-789. [Content Brief]

[3]. Zhou SM, et al. Cucurbitacin IIa exerts antidepressant-like effects on mice exposed to chronic unpredictable mild stress. Neuroreport. 2017;28(5):259-267. [Content Brief]

[4]. Zhang J, et al. Cucurbitacin IIa interferes with EGFR-MAPK signaling pathway leads to proliferation inhibition in A549 cells. Food Chem Toxicol. 2019;132:110654. [Content Brief]

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	1.7771 mL	8.8853 mL	17.7705 mL	44.4263 mL
	5 mM	0.3554 mL	1.7771 mL	3.5541 mL	8.8853 mL
	10 mM	0.1777 mL	0.8885 mL	1.7771 mL	4.4426 mL
	15 mM	0.1185 mL	0.5924 mL	1.1847 mL	2.9618 mL
	20 mM	0.0889 mL	0.4443 mL	0.8885 mL	2.2213 mL
	25 mM	0.0711 mL	0.3554 mL	0.7108 mL	1.7771 mL
	30 mM	0.0592 mL	0.2962 mL	0.5924 mL	1.4809 mL
	40 mM	0.0444 mL	0.2221 mL	0.4443 mL	1.1107 mL

Cucurbitacin IIa

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Cucurbitacin IIa

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Alle EGFR Isoform-spezifische Produkte anzeigen

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