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  • Brand : BIOFRON

  • Catalogue Number : AV-B03110

  • Specification : 95%

  • CAS number : 639-36-1

  • Formula : C21H24N2O3

  • Molecular Weight : 352.43

  • PUBCHEM ID : 15558574

  • Volume : 5mg

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Catalogue Number


Analysis Method






Molecular Weight




Botanical Source

Structure Type



Standards;Natural Pytochemical;API




Methyl (15α,19E)-17-hydroxysarpagan-16-carboxylate/Sarpagan-16-carboxylic acid, 17-hydroxy-, methyl ester, (15α)-


methyl (1S,12S,13S,14S,15E)-15-ethylidene-13-(hydroxymethyl)-3,17-diazapentacyclo[,10.04,9.012,17]octadeca-2(10),4,6,8-tetraene-13-carboxylate


1.3±0.1 g/cm3


Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

264.0±30.1 °C

Boiling Point

513.0±50.0 °C at 760 mmHg

Melting Point




InChl Key


WGK Germany


HS Code Reference

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:639-36-1) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.




ABT-639 is a selective T-type calcium channel blocker with efficacy in a wide range of preclinical models of nociceptive and neuropathic pain. In the current first-in-human (FIH) study, the pharmacokinetics, tolerability, and safety of ABT-639 after single- (up to 170 mg) and multiple doses (up to 160 mg BID) were evaluated in healthy volunteers in a randomized, double-blinded, placebo-controlled manner. ABT-639 demonstrated acceptable safety and pharmacokinetic profiles in human. Results from assessment of the routine laboratory variables showed an unexpected statistically significant and clinically relevant decrease in blood uric acid with the increase in ABT-639 dose, which is possibly due to inhibition in URAT1 transporter. Pharmacokinetic/pharmacodynamic models were constructed to characterize the relationship between ABT-639 exposure and uric acid response. The final model was a mechanism-based indirect response pharmacodynamic model with the stimulation of uric acid elimination by ABT-639. The model estimated Kin values in males and females were 10.2 and 7.13 μmol/h, respectively. The model estimated Kout was 0.033 1/h. ABT-639 concentration that can produce 50% stimulation in uric acid elimination was estimated to be 8,070 ng/mL. Based on the final model, further simulations were conducted to predict the effect of ABT-639 on uric acid in gout patients. The simulation results indicated that, if the urate-lowering response to ABT-639 in gout patients is similar to that in healthy subjects, ABT-639 BID doses of 140 mg or higher would be expected to provide clinically meaningful lowering of blood uric acid levels below the 380 μmol/L solubility limit of monosodium urate.


ABT-639, exposure-response analyses, uric acid, PK-PD modeling, population pharmacokinetics, URAT1 inhibition


Population Pharmacokinetics and Exposure-Uric Acid Analyses After Single and Multiple Doses of ABT-639, a Calcium Channel Blocker, in Healthy Volunteers


Guohua An, Wei Liu, W. Rachel Duan, Wolfram Nothaft, Walid Awni, Sandeep Dutta

Publish date

2015 Mar;




T-type Cav3.2 calcium channels represent a novel target for neuropathic pain modulation. Preclinical studies with ABT-639, a peripherally acting highly selective T-type Cav3.2 calcium channel blocker, showed dose-dependent reduction of pain in multiple pain models. ABT-639 also demonstrated an acceptable safety profile at single- and multiple-dose levels evaluated in a clinical phase 1 study in healthy volunteers. The primary objective of this phase 2, multicenter, randomized, double-blind, placebo-controlled, and active-controlled study was to compare the analgesic efficacy and safety of ABT-639 with placebo in the treatment of diabetic neuropathic pain. Pregabalin, an approved treatment for painful diabetic neuropathy, was included as a positive control. A total of 194 patients were randomized and treated for 6 weeks; 62 patients received ABT-639 (100 mg twice daily), 70 patients received pregabalin (150 mg twice daily), and 62 patients received placebo. When assessing the mean changes from baseline in patient-recorded pain scores at the end of week 6, there was no significant difference observed for ABT-639 compared with placebo (?2.28 vs ?2.36; P = 0.582). Pregabalin treatment resulted in a transient improvement in pain compared with placebo, which did not persist throughout the study. There were no significant safety issues identified with ABT-639. A majority of adverse events were considered mild to moderate in intensity. In conclusion, treatment with the highly selective T-type Cav3.2 calcium channel blocker ABT-639 100 mg twice daily for 6 weeks showed no safety signals that would preclude further investigation but did not reduce neuropathic pain in patients with diabetes (ClinicalTrials.gov identifier: NCT01345045).


Diabetic neuropathic pain, ABT-639, T-type calcium channels


A randomized double-blind, placebo-, and active-controlled study of T-type calcium channel blocker ABT-639 in patients with diabetic peripheral neuropathic pain

Publish date

2015 Oct




Breast cancer is characterised by an elevated capacity for tumour invasion and lymph node metastasis, but the cause remains to be determined. Recent studies suggest that microRNAs can regulate the evolution of malignant behaviours by regulating multiple target genes. In this study, we have first confirmed that miR-639 is up-regulated in metastatic breast cancer tissues and cell line with highly invasive capacity. Furthermore, we provided evidence to demonstrate that up-regulation of miR-639 contributes breast cancer invasion and metastasis. These data reveal a key role of miR-639 in breast cancer metastasis and support biological and clinical links between miR-639 and breast cancer.


miR-639, Breast cancer, Invasion, Metastases


miR-639 promotes the proliferation and invasion of breast cancer cell in vitro

Publish date

2015 Mar;

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