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Malotilate
CAS No. 59937-28-9
Malotilate( Malotilate | CL-1500 | NKK 105 | NKK-105 )
Catalog No. M15231 CAS No. 59937-28-9
Malotilate, diisopropyl 1,3-dithiol-2-ylidenemalonate, is a drug used for the treatment of liver cirrhosis.
Purity : >98% (HPLC)
COA
Datasheet
HNMR
HPLC
MSDS
Handing Instructions
| Size | Price / USD | Stock | Quantity |
| 1 mL x 10 mM in DMSO | 28 | In Stock |
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| 10MG | 29 | In Stock |
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| 25MG | 46 | In Stock |
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| 50MG | 63 | In Stock |
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| 100MG | 91 | In Stock |
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| 200MG | Get Quote | In Stock |
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| 500MG | 221 | In Stock |
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| 1G | Get Quote | In Stock |
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Biological Information
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Product NameMalotilate
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NoteResearch use only, not for human use.
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Brief DescriptionMalotilate, diisopropyl 1,3-dithiol-2-ylidenemalonate, is a drug used for the treatment of liver cirrhosis.
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DescriptionMalotilate, diisopropyl 1,3-dithiol-2-ylidenemalonate, is a drug used for the treatment of liver cirrhosis.(In Vitro):Malotilate reduces collagen synthesis and cell migration activity of fibroblasts in vitro.Malotilate, an anti-fibrotic substance, selectively inhibited the 5-lipoxygenase, whereas both the 12- and the 15-lipoxygenase pathways are stimulated. Malotilate has been shown to prevent acute experimental liver injury induced by several hepatotoxic compounds, including Ahyl alcohot, Bromobenzene, Carbon tetrachloride, ChIoroform, Dimethylnitrosamine and Thioacetamide.(In Vivo):Malotilate (100 mg/kg; p.o.; daily for 3 days) treatment in rats with hypocholesterolemia results in a rapid normalization of lowered serum cholesterol.
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In VitroMalotilate reduces collagen synthesis and cell migration activity of fibroblasts in vitro.Malotilate, an anti-fibrotic substance, selectively inhibited the 5-lipoxygenase, whereas both the 12- and the 15-lipoxygenase pathways are stimulated. Malotilate has been shown to prevent acute experimental liver injury induced by several hepatotoxic compounds, including Ahyl alcohot, Bromobenzene, Carbon tetrachloride, ChIoroform, Dimethylnitrosamine and Thioacetamide.
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In VivoMalotilate (100 mg/kg; p.o.; daily for 3 days) treatment in rats with hypocholesterolemia results in a rapid normalization of lowered serum cholesterol. Animal Model:Male rats of the SLC-SD strain (rats with carbon tetrachloride-induced liver damage)Dosage:100 mg/kg Administration:P.o.; daily for 3 days Result:The triglyceride secretion from livers in rats given CCI4 was inhibited to about 40% of the level in the control rats. This inhibition of the triglyceride secretion was completely normalized in response to malotilate administration for 3 days.
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SynonymsMalotilate | CL-1500 | NKK 105 | NKK-105
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PathwayOthers
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TargetOther Targets
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RecptorOthers
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Research AreaCancer
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Indication——
Chemical Information
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CAS Number59937-28-9
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Formula Weight288.38
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Molecular FormulaC12H16O4S2
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Purity>98% (HPLC)
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SolubilityEthanol: 58 mg/mL (201.12 mM); DMSO: 58 mg/mL (201.12 mM)
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SMILESO=C(OC(C)C)/C(C(OC(C)C)=O)=C1SC=CS/1
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Chemical Name1,3-Dithiol-2-ylidenepropanedioic acid, bis(1-methylethyl) ester
Shipping & Storage Information
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Storage(-20℃)
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ShippingWith Ice Pack
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Stability≥ 2 years
Reference
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PAR-3 (1-6) amide (m...
SFNGGP-NH2 is a biological active peptide. (PAR-3 is a high-affinity thrombin receptor. PAR-3 mRNA is expressed in the cutaneous mast cells of humans. Protease-Activated Receptors (PARs) have been studied for their roles in itch and their itch-associated response through histamine-dependent/independent pathways have been reported. PAR-3 has been shown not to induce itching alone but possibly in conjunction with PAR-4. Co-expression of PAR-3 and PAR-4 enhances thrombin action suggesting that PAR-3 alone does not mediate transmembrane signaling but instead functions as a cofactor to activate PAR-4.)
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TFIIH Modulator-19
TFIIH Modulator-19 induces the dimerization of trichothiodystrophy group A protein to modulate TFIIH transcriptional activity.
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KRA-533
KRA-533 is a potent KRAS agonist. KRA-533 binds to the GTP/GDP binding pocket in the KRAS protein to prevent GTP cleavage, resulting in the accumulation of constitutively active GTP-bound KRAS that triggers both apoptotic and autophagic cell death pathways in cancer cells.
