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Homoharringtonine
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Product Name Homoharringtonine
Price: $50 / 20mg
CAS No.: 26833-87-4
Catalog No.: CFN98110
Molecular Formula: C29H39NO9
Molecular Weight: 545.61 g/mol
Purity: >=98%
Type of Compound: Alkaloids
Physical Desc.: Cryst.
Source: The branches of Cephalotaxus fortunei Hook.f.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Download: COA    MSDS    SDF    Manual
Similar structural: Comparison (Web)  (SDF)
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Related Screening Libraries
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10 mM * 1 mL in DMSO / Inquiry / In-stock
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Biological Activity
Description: Homoharringtonine, a plant alkaloid with antitumor and antileukemic properties, inhibit protein translation by preventing the initial elongation step of protein synthesis via an interaction with the ribosomal A-site. Homoharringtonine might have clinical activity in some patients with myelodysplastic syndrome.
Targets: Caspase | PARP | Bcl-2/Bax | MEK | ERK
In vitro:
Am J Hematol. 2004 Jul;76(3):199-204.
Homoharringtonine mediates myeloid cell apoptosis via upregulation of pro-apoptotic bax and inducing caspase-3-mediated cleavage of poly(ADP-ribose) polymerase (PARP).[Pubmed: 15224352 ]
Homoharringtonine (HHT) is a plant alkaloid with antileukemia activity that is currently being used for treatment of acute, chronic leukemias and MDS.
METHODS AND RESULTS:
In this study, we show that HHT can induce apoptosis in a variety of human myeloid leukemia cell lines (U937, HL-60, HEL, THP, and K562). U937 and HL60 cells undergo rapid apoptosis on treatment with HHT, as indicated by increased annexin V binding capacity, caspase-3 activation, and cleavage of poly(ADP-ribose) polymerase (PARP). In addition, the expression of bax is upregulated during HHT-induced cell death, whereas the expression of bcl-2 is only slightly decreased. Importantly, treatment of primary leukemic cells, obtained from acute myeloid leukemia patients, resulted in rapid apoptosis.
CONCLUSIONS:
Thus, our data provide the mechanism of HHT and justify the use of HHT in the treatment of human myeloid leukemia.
Sci Rep. 2015 Jul 13;5:8477.
Homoharringtonine induces apoptosis and inhibits STAT3 via IL-6/JAK1/STAT3 signal pathway in Gefitinib-resistant lung cancer cells.[Pubmed: 26166037]
Tyrosine kinase inhibitors (TKIs) are mostly used in non-small cell lung cancer (NSCLC) treatment. Unfortunately, treatment with Gefitinib for a period of time will result in drug resistance and cause treatment failure in clinic.
METHODS AND RESULTS:
Therefore, exploring novel compounds to overcome this resistance is urgently required. Here we investigated the antitumor effect of Homoharringtonine (HHT), a natural compound extracted from Cephalotaxus harringtonia, on Gefitinib-resistant NSCLC cell lines in vitro and in vivo. NCI-H1975 cells with EGFR T790M mutation are more sensitive to HHT treatment compared with that of A549 cells with wild type EGFR. HHT inhibited cells growth, cell viability and colony formation, as well as induced cell apoptosis through mitochondria pathway. Furthermore, we explored the mechanism of HHT inhibition on NSCLC cells. Higher level of interleukin-6 (IL-6) existed in lung cancer patients and mutant EGFR and TGFβ signal requires the upregulation of IL-6 through the gp130/JAK pathway to overactive STAT3, an oncogenic protein which has been considered as a potential target for cancer therapy. HHT reversiblely inhibited IL-6-induced STAT3 Tyrosine 705 phosphorylation and reduced anti-apoptotic proteins expression. Gefitinib-resistant NSCLC xenograft tests also confirmed the antitumor effect of HHT in vivo.
CONCLUSIONS:
Consequently, HHT has the potential in Gefitinib-resistant NSCLC treatment.
In vivo:
Lancet Oncol. 2013 Jun;14(7):599-608.
Homoharringtonine-based induction regimens for patients with de-novo acute myeloid leukaemia: a multicentre, open-label, randomised, controlled phase 3 trial.[Pubmed: 23664707]
Homoharringtonine-based induction regimens have been widely used in China for patients with acute myeloid leukaemia. However, their efficacy has not been tested in a multicentre randomised controlled trial in a large population. We assessed the efficacy and safety of Homoharringtonine-based induction treatment for management of newly diagnosed acute myeloid leukaemia.
METHODS AND RESULTS:
This open-label, randomised, controlled, phase 3 study was done in 17 institutions in China between September, 2007, and July, 2011. Untreated patients aged 14-59 years with acute myeloid leukaemia were randomly assigned (by a computer-generated allocation schedule without stratification) to receive one of three induction regimens in a 1:1:1 ratio: Homoharringtonine 2 mg/m(2) per day on days 1-7, cytarabine 100 mg/m(2) per day on days 1-7, and aclarubicin 20 mg/day on days 1-7 (HAA); Homoharringtonine 2 mg/m(2) per day on days 1-7, cytarabine 100 mg/m(2) per day on days 1-7, and daunorubicin 40 mg/m(2) per day on days 1-3 (HAD); or daunorubicin 40-45 mg/m(2) per day on days 1-3 and cytarabine 100 mg/m(2) per day on days 1-7 (DA). Patients in complete remission were offered two cycles of intermediate-dose cytarabine (2 g/m(2) every 12 h on days 1-3). The primary endpoints were the proportion of patients who achieved complete remission after two cycles of induction treatment and event-free survival in the intention-to-treat population. The trial is registered in the Chinese Clinical Trial Register, number ChiCTR-TRC-06000054. We enrolled 620 patients, of whom 609 were included in the intention-to-treat analysis. 150 of 206 patients (73%) in the HAA group achieved complete remission versus 125 of 205 (61%) in the DA group (p=0.0108); 3-year event-free survival was 35.4% (95% CI 28.6-42.2) versus 23.1% (95% CI 17.4-29.3; p=0.0023). 133 of 198 patients (67%) in the HAD group had complete remission (vs DA, p=0·20) and 3-year event-free survival was 32.7% (95% CI 26.1-39.5; vs DA, p=0.08). Adverse events were much the same in all groups, except that more patients in the HAA (12 of 206 [5.8%]) and HAD (13 of 198 [6.6%]) groups died within 30 days than in the DA group (two of 205 [1%]; p=0.0067 vs HAA; p=0.0030 vs HAD).
CONCLUSIONS:
A regimen of Homoharringtonine, cytarabine, and aclarubicin is a treatment option for young, newly diagnosed patients with acute myeloid leukaemia.
Homoharringtonine Description
Source: The branches of Cephalotaxus fortunei Hook.f.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Calculate Dilution Ratios(Only for Reference)
1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.8328 mL 9.1641 mL 18.3281 mL 36.6562 mL 45.8203 mL
5 mM 0.3666 mL 1.8328 mL 3.6656 mL 7.3312 mL 9.1641 mL
10 mM 0.1833 mL 0.9164 mL 1.8328 mL 3.6656 mL 4.582 mL
50 mM 0.0367 mL 0.1833 mL 0.3666 mL 0.7331 mL 0.9164 mL
100 mM 0.0183 mL 0.0916 mL 0.1833 mL 0.3666 mL 0.4582 mL
* Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
Protocol
Kinase Assay:
Eur J Pharm Biopharm. 2015 Jan;89:232-8.
Homoharringtonine increases intestinal epithelial permeability by modulating specific claudin isoforms in Caco-2 cell monolayers.[Pubmed: 25513955]
Homoharringtonine (HHT), a natural alkaloid produced by various Cephalotaxus species, has antileukemic activity in acute and chronic myelogenous leukemia. However, Homoharringtonine can also induce unanticipated effects in the gastrointestinal tract, such as diarrhea and nausea/vomiting, but the mechanism behind these adverse effects has not been clarified.
METHODS AND RESULTS:
In the present study, we show that Homoharringtonine affects the epithelial permeability of intestinal Caco-2 cell monolayers. Homoharringtonine reduced the transepithelial electrical resistance (TER) of Caco-2 cells in a dose- and time-dependent manner. The Homoharringtonine effect was reversible and no cytotoxicity was observed at the concentrations used. Homoharringtonine simultaneously increased the paracellular flux of the 4 kDa and 40 kDa FITC-dextrans associated with the TER reduction. Immunoblotting analysis revealed that Homoharringtonine decreased the protein expression of TJ components such as claudin-3, -5, and -7. However, the transcription levels of these claudins were not repressed by Homoharringtonine treatment. Homoharringtonine also disturbed the cellular localization of claudin-1 and -4. These changes coincided with the reduced barrier function.
CONCLUSIONS:
Our findings suggest that Homoharringtonine enhances the paracellular permeability of Caco-2 cell monolayers by modulating the protein expression and localization of claudin isoforms; these actions might be responsible for the gastrointestinal effects of Homoharringtonine .
Med Oncol. 2014 Feb;31(2):836.
Homoharringtonine contributes to imatinib sensitivity by blocking the EphB4/RhoA pathway in chronic myeloid leukemia cell lines.[Pubmed: 24415355 ]
The purpose was to investigate the role of EphB4 in imatinib (IM) resistance and the mechanism responsible for Homoharringtonine (HHT) contributing to imatinib sensitivity for a chronic myeloid leukemia (CML) cell lines.
METHODS AND RESULTS:
We established cell lines from a patient with CML at the time of first diagnosis and relapsed phase and designated them as NPhA1 and NPhA2, respectively. Stable underexpressing EphB4 cells (NPhA2-sh) were obtained. The activated signal proteins in cells were tested by Western blot. The EphB4 was overexpressed in IM-resistant NPhA2 in comparison with the NPhA1 cell line, but the expression of EphB4 mRNA and protein significantly decreased in knockdown NPhA2-EphB4-sh cells compared with NPhA2 and NPhA1 (P < 0.001) cell lines. NPhA2-EphB4-sh cells were sensitive to IM (IC50 0.93 mg/L), and NPhA2 showed IM resistance (IC50 5.45 mg/L) (P < 0.001). Meanwhile, phospho-Rac1/cdc42 was significantly increased in NPhA2 cells compared to NPhA2-EphB4-sh (P < 0.001). The apoptosis rate reached 58.71 ± 2.39 % with NPhA2 cells incubated with HHT + IM, which was higher than NPhA2 cells incubated with IM alone (P = 0.002). IC50 of NPhA2 cells incubated with IM was 5.45 mg/L. However, co-stimulation with HHT + IM decreased the IC50 of NPhA2 cells from 5.45 to 1.17 mg/L (P < 0.001). Furthermore, HHT blocked the expressions of EphB4/RhoA, but did not down-regulate the phospho-MEK/ERK in NPhA2 cells. The overexpression of EphB4 contributed to IM resistance in CML line cells.
CONCLUSIONS:
EphB4/RhoA may be a new marker of IM resistance. HHT + IM gained more treatment advantages than IM alone by blocking EphB4/RhoA pathways in CML cell lines.
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