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Fig. 1 · Structure
Cat. No.
A10249
CAS No.
4449-51-8
Formula
C27H41NO2
Mol. Weight
411.6

Documents & Downloads

Cyclopamine

Cat. No. A10249 CAS 4449-51-8

Hedgehog signaling inhibitor

Cyclopamine is a Smo or hedgehog signaling pathway inhibitor.

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Biological Activity

Target & Activity

Target Activity Value
Smoothened (TM3Hh12 cells) 46 nM

Cellular Effect

Cell Line Activity Value Description Reference
A549 IC50 49 μM Anticancer activity against human A549 cells by MTS assay [PMID: 18221872]
C3H 10T1/2 EC50 0.17 μM Inhibition of Hedgehog pathway-dependent oxysterol-induced mouse C3 H10T1/2 cell differentiation assessed as alkaline phosphatase production after 72 hrs [PMID: 18842035]
C3H 10T1/2 IC50 0.6 μM Inhibition of human Shh-induced mouse C3H10T1/2 cell differentiation after 48 hrs by alkaline phosphatase reporter assay [PMID: 23074541]
C3H 10T1/2 IC50 0.6 μM Inhibition of N-terminal SHH activated pathway in mouse C3H10T1/2 cells assessed as SAG-induced cell differentiation by alkaline phosphatase assay [PMID: 21592788]
C3H 10T1/2 IC50 0.62 μM Inhibition of SAG-induced differentiation of mouse mesenchymal pluripotent C3H10T1/2 cells to alkaline phosphatase positive oeseoblasts after 6 hrs [PMID: 22268551]
CHO IC50 1200 nM Antagonist activity at mouse Smo receptor expressed in CHO cells by [3H]Hh-Ag binding assay [PMID: 19091559]
CHO IC50 280 nM Antagonist activity at human Smo receptor expressed in CHO cells by [3H]Hh-Ag binding assay [PMID: 19091559]
Daoy IC50 0.16 μM Inhibition of Hedgehog signaling in human DaOY cells assessed as downregulation of Gli1 mRNA expression after 48 hrs by RT-PCR analysis [PMID: 24900716]
HEK293 IC50 64 nM Displacement of BODIPY-labelled cyclopamine from human Smo receptor expressed in HEK293 cells after 2 hrs by fluorescence microscopy [PMID: 22268551]
Medulloblastoma cell EC50 1 μM Antiproliferative activity against mouse medulloblastoma cells harboring heterozygous ptch1 gene by MTT assay [PMID: 17417631]
MEF IC50 1.9 μM Inhibition of Smo in mouse Ptch-deficient MEF cells assessed as inhibition of Shh-induced Gli-responsive betagalactosidase activity after 30 hrs by BetaGLo assay [PMID: 23074541]
Shh Light II IC50 0.3 μM Inhibition of SHH pathway in mouse Shh Light2 cells after 40 hrs by Gli-dependent luciferase reporter gene assay [PMID: 21592788]
Shh Light II IC50 0.3 μM Inhibition of Smo-mediated Hh signaling in human Shh-light2 cells by luciferase reporter gene assay [PMID: 22268551]
Shh Light II IC50 1312 nM Inhibition of SHH in mouse Shh-Light2 cells after 48 hrs by Gli1 reporter gene assay in presence of SAG [PMID: 19541490]
Shh Light II IC50 484 nM Antagonist activity at Smo in mouse Shh-Light 2 cells assessed as inhibition of Shh-induced Gli1-reporter activity after 2 days by dual-luciferase reporter gene method [PMID: 23063522]
Shh Light II EC50 500 nM Inhibition of SHH in mouse Shh Light2 cells by GLI-responsive firefly luciferase reporter gene assay [PMID: 19309080]
TM3 IC50 46 nM Inhibition of Hedgehog signaling pathway in mouse TM3 cells bearing pTA-8xGli-Luc reporter construct assessed as transcriptional modulation of Gli after 48 hrs by luciferase assay [PMID: 19091559]
U-87MG ATCC IC50 22.5 μM Antiproliferative activity against human U87MG cells after 72 hrs by MTS assay [PMID: 22226657]

18 records · Scroll to view more

In Vitro Studies

Cyclopamine exposure caused a small but consistent decrease in viable HGC-27 tumorsphere cell numbers, with a greater effect on cell death in adherent cells. In primary cultures from patient CC samples, Cyclopamine reduced average BrdU incorporation compared with control compound tomatidine. In dissociated HGC-27 tumorsphere cells, Cyclopamine treatment, compared with control tomatidine, significantly reduced sub-tumorsphere formation capacity in a dose-dependent fashion, with no such effect observed in adherent cells. [1,2]

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

Cyclopamine reduces viable tumorsphere cell numbers

Cell-based study · HGC-27 tumorsphere cells [1]

HGC-27 tumorsphere cells exposed to Cyclopamine at 2.5 uM, 5 uM, and 10 uM for 48 hours showed a small but consistent decrease in viable cell number. The effect on cell death was greater in adherent cells.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Percentage of cell viabilityReported result Cyclopamine (2.5 uM, 5 uM, 10 uM), 48 hours: cyclopamine alone to tumorsphere cells could make a small but consistent decrease in the viable cell number. Compared with HGC-27 tumorsphere cells, the effect of cyclopamine on cell death to adherent cells was more significance.[1]

Literature-Reported Treatment Conditions

Treatment concentration
2.5 uM, 5 uM, 10 uM
Exposure duration
48 hours
Method
exposure to different concentrations of cyclopamine
Reported limits
Not stated in the sentences used: vehicle.
Methods and source locations

Compound reported in the paper: Cyclopamine

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

Results > 4. SHH pathway blocking reduced the self-renewing capacity and chemoresistance of HGC-27 tumorsphere cells (S42, S43, S44); Figure 5 legend (S157, S158)

Percentage of cell viability: Percentage of cell viability; comparator: tomatidine — Results > 4. SHH pathway blocking reduced the self-renewing capacity and chemoresistance of HGC-27 tumorsphere cells (S42, S43, S44); Figure 5 legend (S157)

BrdU incorporation in Primary cultures from patient CC samples

Cell-based study · Primary cultures from patient CC samples [2]

Model: Primary cultures from patient CC samples. Treatment: 5 and 10 µM. Result: Cyclopamine treatment produced 1.9-fold (p < 0.01) and 3.5-fold (p < 0.01) less BrdU incorporation on average at 5 and 10 µM as compared with the control compound tomatidine (10 µM). An insensitive sample (CC11) and rescue by GLI1 (see below) indicate specificity..

Measured endpoints — not treatment concentrations
EndpointReported resultReference
BrdU incorporationBrdU incorporation 1.9-fold (p < 0.01) and 3.5-fold (p < 0.01) less BrdU incorporation[2]

Literature-Reported Treatment Conditions

Treatment concentration
5 and 10 µM
Exposure duration
48 h
Co-treatment
Other interventions in this design: EGF 10 ng/ml. Compound effect isolated by the comparison: as compared with the control compound tomatidine (10 µM).
Reported limits
Not stated in the sentences used: route, vehicle.
Methods and source locations

Compound reported in the paper: Cyclopamine

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

RESULTS > Human CC cells require HH-GLI function for sustained proliferation and survival in vitro (S21); RESULTS > Cyclopamine treatment of CC cells in vitro enhances apoptosis and decreases proliferation (S35, S38); MATERIALS AND METHODS > Human CC specimens, primary cells and cell lines (S91); MATERIALS AND METHODS > In situ hybridization, immunohistochemistry and immunocytochemistry (S97)

BrdU incorporation: BrdU incorporation; comparator: control compound tomatidine (10 µM) — RESULTS > Cyclopamine treatment of CC cells in vitro enhances apoptosis and decreases proliferation (S35, S38)

Cyclopamine reduces sub-tumorsphere formation

Cell-based study · HGC-27 tumorsphere cells [1]

Dissociated HGC-27 tumorsphere cells were treated with Cyclopamine at 2.5 µM, 5 µM, and 10 µM for 2 weeks, with tomatidine as the control. Cyclopamine significantly reduced sub-tumorsphere formation capacity in a dose-dependent fashion; no such effect was observed in adherent cells.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
formation of sub-tumorspheresReported result Cyclopamine (2.5 µM, 5 µM, 10 µM): cyclopamine treatment led to a significantly reduction in capacity for the formation of sub-tumorspheres in HGC-27 tumorsphere cells in a dose-dependent fashion, but no such effect was observed in adherent cells.[1]

Literature-Reported Treatment Conditions

Treatment concentration
2.5 µM, 5 µM, 10 µM
Exposure duration
2 weeks
Method
treated the dissociated cells
Co-treatment
Other interventions in this design: human FGF-2 20 ng/ml; EGF 100 ng/ml. Compound effect isolated by the comparison: cyclopamine or control tomatidine.
Reported limits
Not stated in the sentences used: vehicle.
Methods and source locations

Compound reported in the paper: Cyclopamine

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

Results > 4. SHH pathway blocking reduced the self-renewing capacity and chemoresistance of HGC-27 tumorsphere cells (S35); Materials and Methods > Culture of adherent cells, tumorspheres and sub-tumorspheres (S69, S73, S75); Figure 5 legend (S150)

formation of sub-tumorspheres: formation of sub-tumorspheres; comparator: control tomatidine — Results > 4. SHH pathway blocking reduced the self-renewing capacity and chemoresistance of HGC-27 tumorsphere cells (S35); Materials and Methods > Culture of adherent cells, tumorspheres and sub-tumorspheres (S75)

In Vivo Studies

HH st.18 chick embryos received Cyclopamine in ovo and were incubated for 24 h. Altered ventral patterning at thoracic levels occurred in 80% of exposed embryos, and the pMN domain was affected in 60% of samples, with fewer cells expressing Olig2. [3]

Cyclopamine alters ventral patterning in chick embryos

Animal study · HH st.18 chick embryos [3]

HH st.18 chick embryos received 25 µl of 1 mg/mL Cyclopamine solution in ovo and were incubated for 24 h. Altered ventral patterning at thoracic levels occurred in 80% of exposed embryos, while the pMN domain was affected in 60% of samples, with fewer cells expressing Olig2.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Nkx2.2 (green), Olig2 (red), and Arx (white) expression at anterior thoracic levelsventral patterning altered ventral patterning was observed in 80% of the embryos exposed to cyclopamine[3]

Conditions shared by the study groups

Route
in ovo
Treatment course
incubated for 24 h
Vehicle
45% 2-hydropropyl-β-cyclodextrin (HBC; Sigma)
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Cyclopamine 25 µl of 1 mg/mL solutionvehicle (HBC; i)HH st.18 embryos; 25 µl of 1 mg/mL solution of cyclopamine; in ovo and incubated for 24 h: At thoracic levels, altered ventral patterning was observed in 80% of the embryos exposed to cyclopamine. Furthermore, the pMN domain was affected in 60% of the samples, with fewer cells expressing Olig2 (n = 12).[3]
Cyclopamine 25 µl of 1 mg/mL solution
Model: HH st.18 chick embryos
Methods and source locations

Compound reported in the paper: Cyclopamine

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

Results > Prolonged Exposure to Shh Signalling Is Required In Vivo for Ventral Patterning (S104, S106); Materials and Methods > In Ovo Cyclopamine Treatment (S147); Figure 5 legend (S199, S201, S202)

Nkx2.2 (green), Olig2 (red), and Arx (white) expression at anterior thoracic levels: Nkx2.2 (green), Olig2 (red), and Arx (white) expression at anterior thoracic levels; comparator: vehicle (HBC; i) — Results > Prolonged Exposure to Shh Signalling Is Required In Vivo for Ventral Patterning (S104, S106); Materials and Methods > In Ovo Cyclopamine Treatment (S147); Figure 5 legend (S201, S202)

Cyclopamine 25 µl of 1 mg/mL solution · Results > Prolonged Exposure to Shh Signalling Is Required In Vivo for Ventral Patterning (S104, S106); Materials and Methods > In Ovo Cyclopamine Treatment (S147); Figure 5 legend (S201)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 4449-51-8
Applications Hedgehog signaling inhibitor
Formula C27H41NO2
Molecular Weight 411.6
Synonyms 11-deoxojervine
SMILES
C[C@H]1C[C@@H]2[C@H]([C@H]([C@]3(O2)CC[C@H]4[C@@H]5CC=C6C[C@H](CC[C@@]6([C@H]5CC4=C3C)C)O)C)NC1

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO Insoluble
Water DMF Warmed: 9 mg/mL (21.86 mM)
Ethanol Warmed: 2 mg/mL (4.85 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.

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] Song Z, Yue W, Wei B, et al. Sonic hedgehog pathway is essential for maintenance of cancer stem-like cells in human gastric cancer. PLoS One (2011). PMID: 21394208 DOI: 10.1371/journal.pone.0017687 Source material
  2. [2] Varnat F, Duquet A, Malerba M, et al. Human colon cancer epithelial cells harbour active HEDGEHOG-GLI signalling that is essential for tumour growth, recurrence, metastasis and stem cell survival and expansion. EMBO Mol Med (2009). PMID: 20049737 DOI: 10.1002/emmm.200900039 Source material
  3. [3] Dessaud E, Ribes V, Balaskas N, et al. Dynamic assignment and maintenance of positional identity in the ventral neural tube by the morphogen sonic hedgehog. PLoS Biol (2010). PMID: 20532235 DOI: 10.1371/journal.pbio.1000382 Source material

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