Cyclopamine

Hedgehog (Hh) signaling Inhibitor CAS# 4449-51-8

Cyclopamine

Catalog No. BCN2964----Order now to get a substantial discount!

Product Name & Size Price Stock
Cyclopamine: 5mg Please Inquire In Stock
Cyclopamine: 10mg Please Inquire In Stock
Cyclopamine: 20mg Please Inquire Please Inquire
Cyclopamine: 50mg Please Inquire Please Inquire
Cyclopamine: 100mg Please Inquire Please Inquire
Cyclopamine: 200mg Please Inquire Please Inquire
Cyclopamine: 500mg Please Inquire Please Inquire
Cyclopamine: 1000mg Please Inquire Please Inquire
Related Products

Quality Control of Cyclopamine

Number of papers citing our products

Chemical structure

Cyclopamine

3D structure

Chemical Properties of Cyclopamine

Cas No. 4449-51-8 SDF Download SDF
PubChem ID 442972 Appearance White powder
Formula C27H41NO2 M.Wt 411.6
Type of Compound Alkaloids Storage Desiccate at -20°C
Synonyms 11-Deoxojervine
Solubility Ethanol : 16.67 mg/mL (40.50 mM; Need ultrasonic)
DMSO : 5 mg/mL (12.15 mM; Need ultrasonic and warming)
H2O : < 0.1 mg/mL (insoluble)
Chemical Name (3S,3'R,3'aS,6'S,6aS,6bS,7'aR,9R,11aS,11bR)-3',6',10,11b-tetramethylspiro[2,3,4,6,6a,6b,7,8,11,11a-decahydro-1H-benzo[a]fluorene-9,2'-3a,4,5,6,7,7a-hexahydro-3H-furo[3,2-b]pyridine]-3-ol
SMILES CC1CC2C(C(C3(O2)CCC4C5CC=C6CC(CCC6(C5CC4=C3C)C)O)C)NC1
Standard InChIKey QASFUMOKHFSJGL-LAFRSMQTSA-N
Standard InChI InChI=1S/C27H41NO2/c1-15-11-24-25(28-14-15)17(3)27(30-24)10-8-20-21-6-5-18-12-19(29)7-9-26(18,4)23(21)13-22(20)16(27)2/h5,15,17,19-21,23-25,28-29H,6-14H2,1-4H3/t15-,17+,19-,20-,21-,23-,24+,25-,26-,27-/m0/s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Cyclopamine

The herbs of Veratrum nigrum L.

Biological Activity of Cyclopamine

DescriptionCyclopamine is a Hedgehog (Hh) pathway antagonist with an IC50 of 46 nM in the Hh cell assay, it can increase levels of p27, and decreases both expression of IGF-II and activation of Akt in PC-3 prostate cancer cells. Cyclopamine as a novel, potent inhibitor of human breast cancer proliferation and estrogen responsiveness that could potentially be developed into a promising therapeutic agent for the treatment of breast cancer. Cyclopamine also can suppress the growth of leukemia and lymphoma cells.
TargetsCdk | Akt | MAPK | ERK | NF-kB | MMP(e.g.TIMP) | Estrogen receptor | Progestogen receptor | Hedgehog
In vitro

Cyclopamine and quercetin suppress the growth of leukemia and lymphoma cells.[Pubmed: 20032413]

Anticancer Res. 2009 Nov;29(11):4629-32.

Hedgehog (Hh) and Wnt signaling pathways are involved in the stimulation of growth of leukemia and lymphoma cells. In the present study, whether or not the Hh inhibitor, Cyclopamine, and the Wnt inhibitor, quercetin, suppress cell growth was investigated.
METHODS AND RESULTS:
The effects of Cyclopamine and quercetin on the in vitro growth and protein expression of ten acute leukemia and B-cell lymphoma cell lines were examined. Cyclopamine and quercetin suppressed cell growth and induced apoptosis in seven and eight cell lines respectively. Cyclopamine decreased the level of Gli1 protein, a target gene product of Hh signaling. Quercetin decreased the level of Notch1 protein and its active fragment in the DND-41 T-lymphoblastic leukemia cell line with constitutive Notch activation.
CONCLUSIONS:
Cyclopamine and quercetin suppress the growth of a number of leukemia and lymphoma cells. This finding suggests the potential use of these compounds in molecularly-targeted therapy for leukemia and lymphoma.

Cyclopamine increases the cytotoxic effects of paclitaxel and radiation but not cisplatin and gemcitabine in Hedgehog expressing pancreatic cancer cells.[Pubmed: 16552573 ]

Cancer Chemother Pharmacol. 2006 Dec;58(6):765-70.

The hedgehog signaling pathway (Hh) is frequently over expressed in pancreatic adenocarcinomas. We studied the potential cytotoxic interactions between Cyclopamine, a Hh pathway inhibitor and paclitaxel, cisplatin, gemcitabine and ionizing radiation (IR).
METHODS AND RESULTS:
In vitro clonogenic survival analysis was performed with Cyclopamine alone or Cyclopamine in combination with paclitaxel, gemcitabine, cisplatin and IR in Hh expressing human pancreatic tumor cells and Hh non-expressing colon cancer cells. Relative cytotoxicity was assessed in combination treatment compared with exposure to single agents. Assays of apoptosis (annexin V) were performed in the presence of Cyclopamine, chemotherapeutic agents, and IR. We report that Cyclopamine increased the cytotoxic effects of paclitaxel and IR in Hh expressing pancreatic carcinoma cells. These effects were not observed in Hh non-expressing cells. Cyclopamine did not significantly increase killing by cisplatin or gemcitabine in Hh expressing pancreatic cancer cells.
CONCLUSIONS:
These data suggest strategies to combine Hh inhibitors with radiotherapy and chemotherapeutic agents, specifically paclitaxel and related compounds in the treatment of pancreatic cancer.

Protocol of Cyclopamine

Kinase Assay

Cyclopamine is a novel Hedgehog signaling inhibitor with significant anti-proliferative, anti-invasive and anti-estrogenic potency in human breast cancer cells.[Pubmed: 23599805 ]

The hedgehog pathway inhibitor cyclopamine increases levels of p27, and decreases both expression of IGF-II and activation of Akt in PC-3 prostate cancer cells.[Pubmed: 17602833 ]

Cancer Lett. 2007 Oct 8;255(2):300-6.

The hedgehog signalling inhibitor Cyclopamine has been shown to induce growth inhibition and cell cycle arrest in prostate cancer cell lines, but the mechanism of action has not been clearly defined, and observations between laboratories have not always been consistent.
METHODS AND RESULTS:
We first observed that albumin can protect PC-3 prostate cancer cells from Cyclopamine-induced growth inhibition, suggesting that Cyclopamine binds to albumin, and that only free Cyclopamine is active. We then conducted a phospho-site protein kinase screen to elucidate the mechanism of Cyclopamine-induced growth inhibition. Treatment of PC-3 cells with 5 or 10 microM Cyclopamine for 72h resulted in a decrease in cell viability of approximately 50% and approximately 75%, respectively. A phospho-site protein kinase screen showed that Cyclopamine decreased levels of phospho-Thr(187)-p27 by 71%. This phospho-site on p27 positively regulates its ubiquitin degradation; therefore a decrease in phospho-Thr(187)-p27 should correlate with increased levels of p27. Consistent with this hypothesis, treatment of PC-3 cells with Cyclopamine resulted in a approximately 3-fold increase in p27 protein levels. Cdk-2 phosphorylates Thr(187)-p27, and immunoblotting demonstrated that Cyclopamine treatment of PC-3 cells reduces the expression of cdk-2. Furthermore, Cyclopamine decreased the levels of phosphorylated (activated) Akt, which is known to increase p27 degradation via Skp-2-induced ubiquitination. The mechanism by which Cyclopamine decreases phosphorylated Akt is currently under investigation, but it may involve our observed Cyclopamine-induced reduction in IRS-1 and IGF-II expression.
CONCLUSIONS:
These results demonstrate novel molecular correlates of Cyclopamine-induced growth inhibition of prostate cancer cells.

Oncol Lett. 2013 Apr;5(4):1417-1421.

Stimulation of Hedgehog (Hh) signaling induces carcinogenesis or promotes cell survival in cancers of multiple organs. In epithelial cancer with aberrant Hedgehog activation, abrogation of Hedgehog signaling by Cyclopamine, a naturally occurring Hedgehog-specific small-molecule inhibitor, causes profound inhibition of tumor growth.
METHODS AND RESULTS:
In the present study, Cyclopamine displayed a significant potency in suppressing the proliferation of both estrogen-responsive (MCF-7) and estrogen-independent (MDA-MB-231) human breast cancer cells. Cyclopamine induced a robust G1 cell cycle arrest and elicited notable effects on the expression of cyclin D1 through modulation of the MAPK/ERK signaling pathway. Cyclopamine also inhibited the invasive ability of both breast cancer cell lines by suppressing the expression levels of NF-κB, MMP2 and MMP9 protein. Furthermore, in estrogen-responsive MCF-7 cells, Cyclopamine significantly downregulated the production of estrogen receptor-α protein.
CONCLUSIONS:
Our results implicate Cyclopamine as a novel, potent inhibitor of human breast cancer proliferation and estrogen responsiveness that could potentially be developed into a promising therapeutic agent for the treatment of breast cancer.

Cyclopamine Dilution Calculator

Concentration (start)
x
Volume (start)
=
Concentration (final)
x
Volume (final)
 
 
 
C1
V1
C2
V2

calculate

Cyclopamine Molarity Calculator

Mass
=
Concentration
x
Volume
x
MW*
 
 
 
g/mol

calculate

Preparing Stock Solutions of Cyclopamine

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.4295 mL 12.1477 mL 24.2954 mL 48.5909 mL 60.7386 mL
5 mM 0.4859 mL 2.4295 mL 4.8591 mL 9.7182 mL 12.1477 mL
10 mM 0.243 mL 1.2148 mL 2.4295 mL 4.8591 mL 6.0739 mL
50 mM 0.0486 mL 0.243 mL 0.4859 mL 0.9718 mL 1.2148 mL
100 mM 0.0243 mL 0.1215 mL 0.243 mL 0.4859 mL 0.6074 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

Organizitions Citing Our Products recently

 
 
 

Calcutta University

University of Minnesota

University of Maryland School of Medicine

University of Illinois at Chicago

The Ohio State University

University of Zurich

Harvard University

Colorado State University

Auburn University

Yale University

Worcester Polytechnic Institute

Washington State University

Stanford University

University of Leipzig

Universidade da Beira Interior

The Institute of Cancer Research

Heidelberg University

University of Amsterdam

University of Auckland
TsingHua University
TsingHua University
The University of Michigan
The University of Michigan
Miami University
Miami University
DRURY University
DRURY University
Jilin University
Jilin University
Fudan University
Fudan University
Wuhan University
Wuhan University
Sun Yat-sen University
Sun Yat-sen University
Universite de Paris
Universite de Paris
Deemed University
Deemed University
Auckland University
Auckland University
The University of Tokyo
The University of Tokyo
Korea University
Korea University

Background on Cyclopamine

Cyclopamine is a naturally occurring Hedgehog (Hh)?specific small?molecule signaling steroidal alkaloid inhibitor, causes a profound inhibition of tumor growth, has significant anti?invasive, anti?proliferative and anti?estrogenic potency in human breast cancer cells [2] [1]. The EC50 of cyclopamine is 10.57 μM, it was identified by an FXR-bla (farnesoid X receptor- b-lactamase) assay [3].

Hh signaling pathway plays a critical role in embryonic development and tumorigenesis [4]. Hh signaling pathway shows saliency in regulating cellular proliferation and differentiation in a wide array of human tissues. It is related to aberrant cell survival in numerous human malignancies, ranging from BCCs and medulloblastomas to small cell lung, gastrointestinal, breast and prostate tumors [1].

Treated with cyclopamine (10 or 20 μM) only and incubated for time periods ranging from 0 to10 days, MCF-7 cells and MDA?MB?231 cells displayed a significant reduction in proliferation rate compared with the control cells on days 3 and 6 (P<0.01). In the MCF?7 cells, cyclopamine significantly induced cell accumulation in the G1 phase (P<0.01) and a modest decrease in the S population percentage, from 22 to 16% (P<0.01). In the MDA?MB?231 cells, cyclopamine caused a significant increase in G1 cells. The invasion rate of cyclopamine?treated MCF?7 and MDA?MB?231cells significantly decreased compared with the CK [2].

Embryoes exposed to cyclopamine resulted in visible external defects, including cyclopia, proboscis formation, microphthalmia, thoracic lordosis, amelia and decreased body size. Examination of gastrointestinal organs revealed severe deficits, including less length of the gut tube and mesenchymal cell numbers in foregut-derived organs. Ectopic structures in duodenum, stomach, and dorsal pancreas were also found [5].

References:
[1].  Marc J. Meth and Jeffrey M. Weinberg. Cyclopamine: Inhibiting Hedgehog in the Treatment of Psoriasis. Continuing Medical Education, 2006, 78: 185-188.
[2].  Jun Che, Fu-Zheng Zhang, Chao-Qian Zhao, et al. Cyclopamine is a novel Hedgehog signaling inhibitor with significant anti?proliferative, anti?invasive and anti?estrogenic potency in human breast cancer cells. Oncology Letters, 2013, 5: 1417-1421.
[3].  Chia-Wen Hsu, Jinghua Zhao, Ruili Huang, et al. Quantitative High-Throughput Profiling of Environmental Chemicals and Drugs that Modulate Farnesoid X Receptor. Scientific Reports, 2014, 4: 6437.
[4].  Robert J. Lipinski, Paul R. Hutson, Paul W. Hannam, et al. Dose- and Route-Dependent Teratogenicity, Toxicity, and Pharmacokinetic Profiles of the Hedgehog Signaling Antagonist Cyclopamine in the Mouse. Toxicological Sciences, 2008, 104(1):189-197.
[5].  Seung K. Kim and Douglas A. Melton. Pancreas development is promoted by cyclopamine, a Hedgehog signaling inhibitor. Proc. Natl. Acad. Sci. USA, 1998, 95: 13036-13041.

Featured Products
New Products
 

References on Cyclopamine

Cyclopamine increases the cytotoxic effects of paclitaxel and radiation but not cisplatin and gemcitabine in Hedgehog expressing pancreatic cancer cells.[Pubmed:16552573]

Cancer Chemother Pharmacol. 2006 Dec;58(6):765-70.

INTRODUCTION: The hedgehog signaling pathway (Hh) is frequently over expressed in pancreatic adenocarcinomas. We studied the potential cytotoxic interactions between Cyclopamine, a Hh pathway inhibitor and paclitaxel, cisplatin, gemcitabine and ionizing radiation (IR). METHODS: In vitro clonogenic survival analysis was performed with Cyclopamine alone or Cyclopamine in combination with paclitaxel, gemcitabine, cisplatin and IR in Hh expressing human pancreatic tumor cells and Hh non-expressing colon cancer cells. Relative cytotoxicity was assessed in combination treatment compared with exposure to single agents. Assays of apoptosis (annexin V) were performed in the presence of Cyclopamine, chemotherapeutic agents, and IR. RESULTS: We report that Cyclopamine increased the cytotoxic effects of paclitaxel and IR in Hh expressing pancreatic carcinoma cells. These effects were not observed in Hh non-expressing cells. Cyclopamine did not significantly increase killing by cisplatin or gemcitabine in Hh expressing pancreatic cancer cells. CONCLUSIONS: These data suggest strategies to combine Hh inhibitors with radiotherapy and chemotherapeutic agents, specifically paclitaxel and related compounds in the treatment of pancreatic cancer.

Cyclopamine and quercetin suppress the growth of leukemia and lymphoma cells.[Pubmed:20032413]

Anticancer Res. 2009 Nov;29(11):4629-32.

BACKGROUND: Hedgehog (Hh) and Wnt signaling pathways are involved in the stimulation of growth of leukemia and lymphoma cells. In the present study, whether or not the Hh inhibitor, Cyclopamine, and the Wnt inhibitor, quercetin, suppress cell growth was investigated. MATERIALS AND METHODS: The effects of Cyclopamine and quercetin on the in vitro growth and protein expression of ten acute leukemia and B-cell lymphoma cell lines were examined. RESULTS: Cyclopamine and quercetin suppressed cell growth and induced apoptosis in seven and eight cell lines respectively. Cyclopamine decreased the level of Gli1 protein, a target gene product of Hh signaling. Quercetin decreased the level of Notch1 protein and its active fragment in the DND-41 T-lymphoblastic leukemia cell line with constitutive Notch activation. CONCLUSION: Cyclopamine and quercetin suppress the growth of a number of leukemia and lymphoma cells. This finding suggests the potential use of these compounds in molecularly-targeted therapy for leukemia and lymphoma.

Cyclopamine is a novel Hedgehog signaling inhibitor with significant anti-proliferative, anti-invasive and anti-estrogenic potency in human breast cancer cells.[Pubmed:23599805]

Oncol Lett. 2013 Apr;5(4):1417-1421.

Stimulation of Hedgehog (Hh) signaling induces carcinogenesis or promotes cell survival in cancers of multiple organs. In epithelial cancer with aberrant Hedgehog activation, abrogation of Hedgehog signaling by Cyclopamine, a naturally occurring Hedgehog-specific small-molecule inhibitor, causes profound inhibition of tumor growth. In the present study, Cyclopamine displayed a significant potency in suppressing the proliferation of both estrogen-responsive (MCF-7) and estrogen-independent (MDA-MB-231) human breast cancer cells. Cyclopamine induced a robust G1 cell cycle arrest and elicited notable effects on the expression of cyclin D1 through modulation of the MAPK/ERK signaling pathway. Cyclopamine also inhibited the invasive ability of both breast cancer cell lines by suppressing the expression levels of NF-kappaB, MMP2 and MMP9 protein. Furthermore, in estrogen-responsive MCF-7 cells, Cyclopamine significantly downregulated the production of estrogen receptor-alpha protein. Our results implicate Cyclopamine as a novel, potent inhibitor of human breast cancer proliferation and estrogen responsiveness that could potentially be developed into a promising therapeutic agent for the treatment of breast cancer.

The hedgehog pathway inhibitor cyclopamine increases levels of p27, and decreases both expression of IGF-II and activation of Akt in PC-3 prostate cancer cells.[Pubmed:17602833]

Cancer Lett. 2007 Oct 8;255(2):300-6.

The hedgehog signalling inhibitor Cyclopamine has been shown to induce growth inhibition and cell cycle arrest in prostate cancer cell lines, but the mechanism of action has not been clearly defined, and observations between laboratories have not always been consistent. We first observed that albumin can protect PC-3 prostate cancer cells from Cyclopamine-induced growth inhibition, suggesting that Cyclopamine binds to albumin, and that only free Cyclopamine is active. We then conducted a phospho-site protein kinase screen to elucidate the mechanism of Cyclopamine-induced growth inhibition. Treatment of PC-3 cells with 5 or 10 microM Cyclopamine for 72h resulted in a decrease in cell viability of approximately 50% and approximately 75%, respectively. A phospho-site protein kinase screen showed that Cyclopamine decreased levels of phospho-Thr(187)-p27 by 71%. This phospho-site on p27 positively regulates its ubiquitin degradation; therefore a decrease in phospho-Thr(187)-p27 should correlate with increased levels of p27. Consistent with this hypothesis, treatment of PC-3 cells with Cyclopamine resulted in a approximately 3-fold increase in p27 protein levels. Cdk-2 phosphorylates Thr(187)-p27, and immunoblotting demonstrated that Cyclopamine treatment of PC-3 cells reduces the expression of cdk-2. Furthermore, Cyclopamine decreased the levels of phosphorylated (activated) Akt, which is known to increase p27 degradation via Skp-2-induced ubiquitination. The mechanism by which Cyclopamine decreases phosphorylated Akt is currently under investigation, but it may involve our observed Cyclopamine-induced reduction in IRS-1 and IGF-II expression. These results demonstrate novel molecular correlates of Cyclopamine-induced growth inhibition of prostate cancer cells.

Cyclopamine-mediated hedgehog pathway inhibition depletes stem-like cancer cells in glioblastoma.[Pubmed:17628016]

Stem Cells. 2007 Oct;25(10):2524-33.

Brain tumors can arise following deregulation of signaling pathways normally activated during brain development and may derive from neural stem cells. Given the requirement for Hedgehog in non-neoplastic stem cells, we investigated whether Hedgehog blockade could target the stem-like population in glioblastoma multiforme (GBM). We found that Gli1, a key Hedgehog pathway target, was highly expressed in 5 of 19 primary GBM and in 4 of 7 GBM cell lines. Shh ligand was expressed in some primary tumors, and in GBM-derived neurospheres, suggesting a potential mechanism for pathway activation. Hedgehog pathway blockade by Cyclopamine caused a 40%-60% reduction in growth of adherent glioma lines highly expressing Gli1 but not in those lacking evidence of pathway activity. When GBM-derived neurospheres were treated with Cyclopamine and then dissociated and seeded in media lacking the inhibitor, no new neurospheres formed, suggesting that the clonogenic cancer stem cells had been depleted. Consistent with this hypothesis, the stem-like fraction in gliomas marked by both aldehyde dehydrogenase activity and Hoechst dye excretion (side population) was significantly reduced or eliminated by Cyclopamine. In contrast, we found that radiation treatment of our GBM neurospheres increased the percentage of these stem-like cells, suggesting that this standard therapy preferentially targets better-differentiated neoplastic cells. Most importantly, viable GBM cells injected intracranially following Hedgehog blockade were no longer able to form tumors in athymic mice, indicating that a cancer stem cell population critical for ongoing growth had been removed. Disclosure of potential conflicts of interest is found at the end of this article.

Production of pancreatic hormone-expressing endocrine cells from human embryonic stem cells.[Pubmed:17053790]

Nat Biotechnol. 2006 Nov;24(11):1392-401.

Of paramount importance for the development of cell therapies to treat diabetes is the production of sufficient numbers of pancreatic endocrine cells that function similarly to primary islets. We have developed a differentiation process that converts human embryonic stem (hES) cells to endocrine cells capable of synthesizing the pancreatic hormones insulin, glucagon, somatostatin, pancreatic polypeptide and ghrelin. This process mimics in vivo pancreatic organogenesis by directing cells through stages resembling definitive endoderm, gut-tube endoderm, pancreatic endoderm and endocrine precursor--en route to cells that express endocrine hormones. The hES cell-derived insulin-expressing cells have an insulin content approaching that of adult islets. Similar to fetal beta-cells, they release C-peptide in response to multiple secretory stimuli, but only minimally to glucose. Production of these hES cell-derived endocrine cells may represent a critical step in the development of a renewable source of cells for diabetes cell therapy.

Inhibition of Hedgehog signaling by direct binding of cyclopamine to Smoothened.[Pubmed:12414725]

Genes Dev. 2002 Nov 1;16(21):2743-8.

The steroidal alkaloid Cyclopamine has both teratogenic and antitumor activities arising from its ability to specifically block cellular responses to vertebrate Hedgehog signaling. We show here, using photoaffinity and fluorescent derivatives, that this inhibitory effect is mediated by direct binding of Cyclopamine to the heptahelical bundle of Smoothened (Smo). Cyclopamine also can reverse the retention of partially misfolded Smo in the endoplasmic reticulum, presumably through binding-mediated effects on protein conformation. These observations reveal the mechanism of Cyclopamine's teratogenic and antitumor activities and further suggest a role for small molecules in the physiological regulation of Smo.

Description

Cyclopamine is a Hedgehog (Hh) pathway antagonist with an IC50 of 46 nM in the Hh cell assay.

Keywords:

Cyclopamine,4449-51-8,11-Deoxojervine,Natural Products,Hedgehog, buy Cyclopamine , Cyclopamine supplier , purchase Cyclopamine , Cyclopamine cost , Cyclopamine manufacturer , order Cyclopamine , high purity Cyclopamine

Online Inquiry for:

      Fill out the information below

      • Size:Qty: - +

      * Required Fields

                                      Result: