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Paederosidic acid methyl ester


  • Brand : BIOFRON

  • Catalogue Number : BD-P0670

  • Specification : 98.0%(HPLC)

  • CAS number : 122413-01-8

  • Formula : C19H26O12S

  • Molecular Weight : 478.47

  • PUBCHEM ID : 6325269

  • Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight




Botanical Source

Structure Type



Standards;Natural Pytochemical;API




Cyclopenta[c]pyran-4-carboxylic acid, 1-(β-D-glucopyranosyloxy)-1,4a,5,7a-tetrahydro-5-hydroxy-7-[[[(methylthio)carbonyl]oxy]methyl]-, methyl ester, (1S,4aS,5R,7aS)-/Methyl (1S,4aS,5S,7aS)-1-(β-D-glucopyranosyloxy)-5-hydroxy-7-({[(methylsulfanyl)carbonyl]oxy}methyl)-1,4a,5,7a-tetrahydrocyclopenta[c]pyran-4-carboxylate/paederosidic acid methyl ester/Cyclopenta[c]pyran-4-carboxylic acid, 1-(β-D-glucopyranosyloxy)-1,4a,5,7a-tetrahydro-5-hydroxy-7-[[[(methylthio)carbonyl]oxy]methyl]-, methyl ester, (1S,4aS,5S,7aS)-/Methyl (1S,4aS,5R,7aS)-1-(β-D-glucopyranosyloxy)-5-hydroxy-7-({[(methylsulfanyl)carbonyl]oxy}methyl)-1,4a,5,7a-tetrahydrocyclopenta[c]pyran-4-carboxylate


methyl (1S,4aS,5S,7aS)-5-hydroxy-7-(methylsulfanylcarbonyloxymethyl)-1-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-1,4a,5,7a-tetrahydrocyclopenta[c]pyran-4-carboxylate



1.6±0.1 g/cm3


Methanol; Water

Flash Point

383.9±35.7 °C

Boiling Point

711.2±70.0 °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#:122413-01-8) 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.




Latent tuberculosis infection is attributed in part to the existence of Mycobacterium tuberculosis in a persistent non-replicating dormant state that is associated with tolerance to host defence mechanisms and antibiotics. We have recently reported that vitamin C treatment of M. tuberculosis triggers the rapid development of bacterial dormancy. Temporal genome-wide transcriptome analysis has revealed that vitamin C-induced dormancy is associated with a large-scale modulation of gene expression in M. tuberculosis.

An updated transcriptional regulatory network of M.tuberculosis (Mtb-TRN) consisting of 178 regulators and 3432 target genes was constructed. The temporal transcriptome data generated in response to vitamin C was overlaid on the Mtb-TRN (vitamin C Mtb-TRN) to derive insights into the transcriptional regulatory features in vitamin C-adapted bacteria. Statistical analysis using Fisher’s exact test predicted that 56 regulators play a central role in modulating genes which are involved in growth, respiration, metabolism and repair functions. Rv0348, DevR, MprA and RegX3 participate in a core temporal regulatory response during 0.25 h to 8 h of vitamin C treatment. Temporal network analysis further revealed Rv0348 to be the most prominent hub regulator with maximum interactions in the vitamin C Mtb-TRN. Experimental analysis revealed that Rv0348 and DevR proteins interact with each other, and this interaction results in an enhanced binding of DevR to its target promoter. These findings, together with the enhanced expression of devR and Rv0348 transcriptional regulators, indicate a second-level regulation of target genes through transcription factor- transcription factor interactions.

Temporal regulatory analysis of the vitamin C Mtb-TRN revealed that there is involvement of multiple regulators during bacterial adaptation to dormancy. Our findings suggest that Rv0348 is a prominent hub regulator in the vitamin C model and large-scale modulation of gene expression is achieved through interactions of Rv0348 with other transcriptional regulators.


Mtb-TRN (Mtb-transcriptional regulatory network), Dormancy, Vitamin C, Transcriptome, Mycobacterium tuberculosis


Multiple transcription factors co-regulate the Mycobacterium tuberculosis adaptation response to vitamin C


Malobi Nandi,1,2 Kriti Sikri,1 Neha Chaudhary,1,3 Shekhar Chintamani Mande,4 Ravi Datta Sharma,2 and Jaya Sivaswami Tyagicorresponding author1,5

Publish date





Among the several mechanisms that contribute to MDR (multidrug resistance), the overexpression of drug-efflux pumps belonging to the ABC (ATP-binding cassette) superfamily is the most frequent cause of resistance to antifungal agents. The multidrug transporter proteins Cdr1p and Cdr2p of the ABCG subfamily are major players in the development of MDR in Candida albicans. Because several genes coding for ABC proteins exist in the genome of C. albicans, but only Cdr1p and Cdr2p have established roles in MDR, it is implicit that the other members of the ABC family also have alternative physiological roles. The present study focuses on an ABC transporter of C. albicans, Mlt1p, which is localized in the vacuolar membrane and specifically transports PC (phosphatidylcholine) into the vacuolar lumen. Transcriptional profiling of the mlt1∆/∆ mutant revealed a down-regulation of the genes involved in endocytosis, oxidoreductase activity, virulence and hyphal development. High-throughput MS-based lipidome analysis revealed that the Mlt1p levels affect lipid homoeostasis and thus lead to a plethora of physiological perturbations. These include a delay in endocytosis, inefficient sequestering of reactive oxygen species (ROS), defects in hyphal development and attenuated virulence. The present study is an emerging example where new and unconventional roles of an ABC transporter are being identified.


ABC transporter, Candida albicans, MLT1, phosphotidylcholine, virulence


Pleiotropic effects of the vacuolar ABC transporter MLT1 of Candida albicans on cell function and virulence


Nitesh Kumar Khandelwal,* Philipp Kaemmer,† Toni M. Forster,† Ashutosh Singh,‡§ Alix T. Coste,║ David R. Andes,¶** Bernhard Hube,† Dominique Sanglard,║ Neeraj Chauhan,†† Rupinder Kaur,‡‡ Christophe d'Enfert,§§ Alok Kumar Mondal,* and Rajendra Prasad║║,1

Publish date

2016 Jun 1




Rapid proliferation of cancer cells assisted by endothelial cell-mediated angiogenesis and acquired inflammation at the tumor microenvironment (TME) lowers the success rate of chemotherapeutic regimens. Therefore, targeting these processes using localized delivery of a minimally toxic drug combination may be a promising strategy. Here, we present engineering of a biocompatible self-assembled lithocholic acid-dipeptide derived hydrogel (TRI-Gel) that can maintain sustained delivery of antiproliferating doxorubicin, antiangiogenic combretastatin-A4 and anti-inflammatory dexamethasone. Application of TRI-Gel therapy to a murine tumor model promotes enhanced apoptosis with a concurrent reduction in angiogenesis and inflammation, leading to effective abrogation of tumor proliferation and increased median survival with reduced drug resistance. In-depth RNA-sequencing analysis showed that TRI-Gel therapy induced transcriptome-wide alternative splicing of many genes responsible for oncogenic transformation including sphingolipid genes. We demonstrate that TRI-Gel therapy targets the reversal of a unique intron retention event in β-glucocerebrosidase 1 (Gba1), thereby increasing the availability of functional Gba1 protein. An enhanced Gba1 activity elevates ceramide levels responsible for apoptosis and decreases glucosylceramides to overcome drug resistance. Therefore, TRI-Gel therapy provides a unique system that affects the TME via post-transcriptional modulations of sphingolipid metabolic genes, thereby opening a new and rational approach to cancer therapy.


A Localized Chimeric Hydrogel Therapy Combats Tumor Progression through Alteration of Sphingolipid Metabolism


Sanjay Pal,†‡⊕ Nihal Medatwal,†§⊕ Sandeep Kumar,†§⊕ Animesh Kar,† Varsha Komalla,†⊖ Prabhu Srinivas Yavvari,∥⦶ Deepakkumar Mishra,† Zaigham Abbas Rizvi,⊥ Shiv Nandan,# Dipankar Malakar,∇ Manoj Pillai,∇ Amit Awasthi,⊥ Prasenjit Das,○ Ravi Datta Sharma,# Aasheesh Srivastava,∥ Sagar Sengupta,◆ Ujjaini Dasgupta,corresponding author*# and Avinash Bajajcorresponding author*†

Publish date

2019 Oct 23;