1. Medicarpin, a legume phytoalexin, acts as an estrogen receptor (ER) agonist, can stimulate osteoblast differentiation likely via ERβ, promote achievement of peak bone mass, and is devoid of uterine estrogenicity; in addition, given its excellent oral bioavailability, it can be potential osteogenic agent. |
2. Medicarpin exhibits no uterine estrogenicity, however it can inhibit osteoclastogenesis and has nonestrogenic bone conserving effect in ovariectomized mice.
3. Medicarpin and maackiain and two of their biosynthetic precursors inhibit the constitutive and phenobarbital (PB)-induced types of AHH, but have little effect on the 3-methylcholanthrene (MC)-induced type of AHH.
4. Medicarpin sensitizes myeloid leukemia cells to TRAIL-induced apoptosis through the induction of DR5 and activation of the ROS-JNK-CHOP pathway.
5. Medicarpin has antifungal activity.
|Targets:||ROS | JNK | Bcl-2/Bax | TNF-α | NF-kB | p65 | P450 (e.g. CYP17)|
|Source:||The herb of Hedysarum polybotrys Hand. -Mazz.|
|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: firstname.lastname@example.org
|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.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||3.6996 mL||18.498 mL||36.9959 mL||73.9919 mL||92.4898 mL|
|5 mM||0.7399 mL||3.6996 mL||7.3992 mL||14.7984 mL||18.498 mL|
|10 mM||0.37 mL||1.8498 mL||3.6996 mL||7.3992 mL||9.249 mL|
|50 mM||0.074 mL||0.37 mL||0.7399 mL||1.4798 mL||1.8498 mL|
|100 mM||0.037 mL||0.185 mL||0.37 mL||0.7399 mL||0.9249 mL|
Environ Sci Pollut Res Int. 2014 Dec;21(24):14091-8.
|Effect of lead treatment on medicarpin accumulation and on the gene expression of key enzymes involved in medicarpin biosynthesis in Medicago sativa L.[Pubmed: 25053287]|
|The present study was undertaken to determine the effect of Pb treatment on Medicarpin production and accumulation in Medicago sativa L. To this aim, 7- and 30-day-old plants were treated with 0, 120, 240, 500, and 1,000 μM Pb during 10 days. The content of Medicarpin was determined by HPLC, and the extent of Medicarpin production was deduced from the result of semiquantitative RT-PCR performed on PAL, CHS, and VR genes. HPLC results indicated that Medicarpin concentration has been reduced in the roots, while its exudation to the culture medium has been increased.Overall, q-PCR results suggest that Medicarpin biosynthesis has been induced in the shoots and reduced in the roots of the plants treated with a toxic concentration of Pb.|
Cell Death Dis. 2014 Oct 16;5:e1465.
|Medicarpin, a legume phytoalexin sensitizes myeloid leukemia cells to TRAIL-induced apoptosis through the induction of DR5 and activation of the ROS-JNK-CHOP pathway.[Pubmed: 25321472]|
|Medicarpin (Med), a naturally occurring phytoalexin sensitizes myeloid leukemia cells to TRAIL-induced apoptosis. Combination of Medicarpin and TRAIL induced significantly higher apoptosis compared with that of the individual treatments of either agent alone through activation of both the extrinsic and the intrinsic cell death pathways characterized by the activation of caspases 8, 9, 3, and 7. Medicarpin treatment downregulated antiapoptotic proteins (Survivin, Bcl2, Bcl-xL, XIAP, and c-FLIP), upregulated pro-apoptotic proteins (Bax, Cytochrome C, Smac/Diablo, Bid, truncated Bid (tBid), p-eIF2α, Bip, and CHOP (CCAAT-enhancer binding protein homologous protein)), induced G2/M cell-cycle arrest, and increased the expression of the functional TRAIL receptor DR5 through activation of the ROS-JNK-CHOP pathway. Gain and loss of function studies clearly indicated that DR5 expression was critical for Medicarpin-induced TRAIL sensitization. The Medicarpin-induced TRAIL sensitization did not involve the NFkB signaling pathway or redistribution of DR5 in lipid rafts. The concomitant treatment with Med and TRAIL showed robust apoptotic effects in primary myeloid leukemia cells but had no toxic effects in primary human peripheral blood mononuclear cells (PBMCs). In conclusion, our results suggest that Medicarpin sensitizes myeloid leukemia cells to TRAIL-induced apoptosis through the upregulation of DR5 through activation of the ROS-JNK-CHOP pathway.|
Mol Cell Endocrinol. 2010 Aug 30;325(1-2):101-9.
|Medicarpin inhibits osteoclastogenesis and has nonestrogenic bone conserving effect in ovariectomized mice.[Pubmed: 20570709]|
|Medicarpin, a pterocarpan class of naturally occurring benzopyran furanobenzene compound was synthesized in gram scale to investigate its effects on murine bone cells and in ovariectomized (OVx) mice. Medicarpin, at as low as 10(-10)M suppressed osteoclastogenesis in bone marrow cells (BMCs). Medicarpin-induced apoptosis of mature osteoclasts isolated from long bones. Effects of Medicarpin in osteoclasts appear to be independent of estrogen receptor (ER) activation as ICI 180,782 failed to abrogate its effects on osteoclasts. In calvarial osteoblasts, Medicarpin (10(-10)M) blocked nuclear factor kappaB (NF-kappaB) signaling assessed by tumor necrosis factor alpha (TNFalpha)-stimulated nuclear translocation of p65 subunit of NF-kappaB. Medicarpin also inhibited the expression of TNFalpha in mouse calvarial osteoblasts. This effect was ER dependent as ICI 180,782 reversed the suppressive effect of Medicarpin on TNFalpha mRNA levels in osteoblasts. In addition, like 17beta-estradiol, presence of Medicarpin inhibited TNFalpha-induced upregulation of interleukin-1, and -6 mRNA levels in osteoblasts. In co-cultures consisting of calvarial osteoblasts and BMCs, presence of Medicarpin increased osteoprotegerin (OPG)/receptor activator of NF-kappaB ligand (RANKL) ratio and reduced mRNA levels of osteoclast markers including tartrate-resistant acid phosphatase and RANK. OVx mice administered Medicarpin (10.0mgkg(-1)day(-1)) orally for 30days had reduced formation of osteoclasts but increased formation of osteoprogenitor cells in BMCs compared with OVx+vehicle group. Medicarpin treatment to OVx mice maintained parameters of trabecular microarchitecure. Medicarpin exhibited no uterine estrogenicity. Our findings point towards direct and indirect inhibitory effects of Medicarpin on osteoclastogenesis in vitro that contribute to its bone sparing effect in OVx mice.|
J Nutr Biochem. 2012 Jan;23(1):27-38.
|Medicarpin, a legume phytoalexin, stimulates osteoblast differentiation and promotes peak bone mass achievement in rats: evidence for estrogen receptor β-mediated osteogenic action of medicarpin.[Pubmed: 21333515]|
|We have evaluated osteogenic effect of Medicarpin (Med); a phytoalexin that is structurally related to isoflavones and is found in dietary legumes. Medicarpin stimulated osteoblast differentiation and mineralization at as low as 10⁻¹⁰ M. Studies with signal transduction inhibitors demonstrated involvement of a p38 mitogen activated protein kinase-ER-bone morphogenic protein-2 pathway in mediating Medicarpin action in osteoblasts. Co-activator interaction studies demonstrated that Medicarpin acted as an estrogen receptor (ER) agonist; however, in contrast to 17β-estradiol, Medicarpin had no uterine estrogenicity and blocked proliferation of MCF-7 cells. Medicarpin increased protein levels of ERβ in osteoblasts. Selective knockdown of ERα and ERβ in osteoblasts established that osteogenic action of Medicarpin is ERβ-dependent. Female Sprague-Dawley (weaning) rats were administered Medicarpin at 1.0- and 10.0 mg.kg⁻¹ doses by gavage for 30 days along with vehicle control. Medicarpin treatment resulted in increased formation of osteoporgenitor cells in the bone marrow and osteoid formation (mineralization surface, mineral apposition/bone formation rates) compared with vehicle group. In addition, Medicarpin increased cortical thickness and bone biomechanical strength. In pharmacokinetic studies, Medicarpin exhibited oral bioavailability of 22.34% and did not produce equol. Together, our results demonstrate Medicarpin stimulates osteoblast differentiation likely via ERβ, promotes achievement of peak bone mass, and is devoid of uterine estrogenicity. In addition, given its excellent oral bioavailability, Medicarpin can be potential osteogenic agent.|
Int. Biodeter. Biodegr., 2012, 69(4):38-40.
|Medicarpin, an antifungal compound identified in hexane extract of Dalbergia congestiflora Pittier heartwood.[Reference: WebLink]|
|The Dalbergia congestiflora Pittier tree, known in Mexico as campinceran, is a species from the tropical and mountain deciduous forests of western Mexico. Its heartwood is considered to have great beauty and is highly valued in the international market due to its excellent physical and mechanical properties, and its natural resistance to fungal attack. In the present work, the antifungal effect of various extracts from the D. congestiflora Pittier heartwood were evaluated against the Trametes versicolor fungus. A hexane extract (250 mg l−1) caused 100% growth inhibition, as did a crystalline substance isolated from the same extract (150 mg l−1) characterized as (+)-3-hydroxy-9-methoxypterocarpan or (+)-Medicarpin by MS and NMR spectroscopy.|
|Specificity of medicarpin and related isoflavonoids in inhibition of rat hepatic mixed function oxidase activity.[Pubmed: 3877941]|
|The cytochromes P-450 of the mixed function oxidase system metabolize a wide variety of endogenous compounds to either nontoxic products or toxic metabolites. A number of natural products, such as flavonoids, influence this metabolism. Exposure to these compounds may therefore be a factor in animal and human responsiveness to cytochrome P-450 substrates. We have examined the effect of the pterocarpan Medicarpin on the cytochrome P-450-dependent aryl hydrocarbon hydroxylase (AHH) and ethoxycoumarin deethylase (ECD) activities of rat liver microsomes. Medicarpin and maackiain and two of their biosynthetic precursors inhibit the constitutive and phenobarbital (PB)-induced types of AHH, but have little effect on the 3-methylcholanthrene (MC)-induced type of AHH. This is in contrast to the effect of the commonly used cytochrome P-450 inhibitor 7,8-benzoflavone, which inhibits the hepatic AHH of MC-treated rats and has no effects on the AHH of control or PB-treated rats. However, Medicarpin inhibited the constitutive as well as the PB- and MC-induced ECD. The specific modulatory effect as well as its relative availability suggests the utility of Medicarpin as a probe for different forms of cytochrome P-450 in animal tissues.|