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  • Brand : BIOFRON

  • Catalogue Number : AV-C10257

  • Specification : 98%

  • CAS number : 34399-44-5

  • Formula : C16H24N2O

  • Molecular Weight : 260.38

  • PUBCHEM ID : 46218452

  • Volume : 5mg

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Catalogue Number


Analysis Method






Molecular Weight




Botanical Source

Structure Type



Standards;Natural Pytochemical;API




(1R,9S,10R,16R)-16-Methyl-6,14-diazatetracyclo[,10.02,7]heptadec-2(7)-en-5-one/1H-5,10b-Propano-1,7-phenanthrolin-8(7H)-one, 2,3,4,4a,5,6,9,10-octahydro-12-methyl-, (4aR,5S,10bR,12R)-




1.2±0.1 g/cm3


Autosomal recessive hyper-IgE syndrome, human gene mutation, DOCK8, primary immunodeficiency, molluscum contagiosum, recurrent infection, T cells, TH17 cells, eosinophils, IgE regulation, copy number variations, genomic deletions

Flash Point

189.7±28.9 °C

Boiling Point

488.2±45.0 °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#:34399-44-5) 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.




The genetic etiologies of the hyper-IgE syndromes are diverse. Approximately 60-70% of patients with hyper-IgE syndrome have dominant mutations in STAT3, and a single patient was reported to have a homozygous TYK2 mutation. In the remaining hyper-IgE syndrome patients, the genetic etiology has not yet been identified.

We performed genome-wide single nucleotide polymorphism analysis for nine subjects with autosomal recessive hyper-IgE syndrome to locate copy number variations and homozygous haplotypes. Homozygosity mapping was performed with twelve subjects from seven additional families. The candidate gene was analyzed by genomic and cDNA sequencing to identify causative alleles in a total of 27 patients with autosomal recessive hyper-IgE syndrome.

Subtelomeric microdeletions were identified in six subjects at the terminus of chromosome 9p. In all patients the deleted interval involved DOCK8, encoding a protein implicated in the regulation of the actin cytoskeleton. Sequencing of subjects without large deletions revealed 16 patients from nine unrelated families with distinct homozygous mutations in DOCK8 causing premature termination, frameshift, splice site disruption, single exon- and micro-deletions. DOCK8 deficiency was associated with impaired activation of CD4+ and CD8+ T cells.

Autosomal recessive mutations in DOCK8 are responsible for many, though not all, cases of autosomal recessive hyper-IgE syndrome. DOCK8 disruption is associated with a phenotype of severe cellular immunodeficiency characterized by susceptibility to viral infections, atopic eczema, defective T cell activation and TH17 cell differentiation; and impaired eosinophil homeostasis and dysregulation of IgE.


Autosomal recessive hyper-IgE syndrome, human gene mutation, DOCK8, primary immunodeficiency, molluscum contagiosum, recurrent infection, T cells, TH17 cells, eosinophils, IgE regulation, copy number variations, genomic deletions


Large Deletions and Point Mutations Involving DOCK8 in the Autosomal Recessive Form of the Hyper-IgE Syndrome


Dr Karin R. Engelhardt,1,* Sean McGhee, MD,2,* Sabine Winkler, MSc,1 Atfa Sassi, PhD,3 Cristina Woellner, MSc,1 Gabriela Lopez-Herrera, PhD,1 Andrew Chen,2 Hong Sook Kim, PhD,2 Maria Garcia Lloret, MD,2 Ilka Schulze, MD,4 Stephan Ehl, MD,4 Jens Thiel, MD,4 Dr Dietmar Pfeifer,5 Hendrik Veelken, MD,5 Tim Niehues, MD,6 Kathrin Siepermann, MD,6 Sebastian Weinspach, MD,7 Ismail Reisli, MD,8 Sevgi Keles, MD,8 Ferah Genel, MD,9 Necil Kutukculer, MD,10 Yildiz Camcioglu, MD,11 Ayper Somer, MD,12 Elif Karakoc Aydiner, MD,13 Isil Barlan, MD,13 Andrew Gennery, MD,14 Ayse Metin, MD, PhD,15 Aydan Degerliyurt, MD,15 Maria C. Pietrogrande, MD,16 Mehdi Yeganeh, MD,17 Zeina Baz, MD,18 Salem Al-Tamemi, MD,19 Christoph Klein, MD, PhD,20 Jennifer M. Puck, MD,21 Steven M. Holland, MD,22 Edward R. B. McCabe, MD, PhD,23 Bodo Grimbacher, MD,1,*# and Talal Chatila, MD, MSc2,*#

Publish date

2010 Dec 1.




The hyper-IgE syndrome (HIES) is a primary immunodeficiency characterized by infections of the lung and skin, elevated serum IgE, and involvement of the soft and tissues. Recently, HIES has been associated with heterozygous dominant-negative mutations in STAT3 and severe reductions of Th17 cells.

To determine whether there is a correlation between the genotype and phenotype of HIES patients and to establish diagnostic criteria to distinguish between STAT3 mutated and STAT3 wild-type patients.

We collected clinical data, determined Th17 cell numbers, and sequenced STAT3 100 patients with a strong clinical suspicion of HIES and serum IgE >1000 IU/mL. explored diagnostic criteria by using a machine-learning approach to identify which features best predict a STAT3 mutation.

In 64 patients we identified 31 different STAT3 mutations, 18 of which are novel. These included mutations at splice sites and outside the previously implicated DNA-binding and SH2 domains. A combination of five clinical features predicted STAT3 mutations with 85% accuracy. Th17 cells were profoundly reduced in patients harboring STAT3 mutations, while 10 out of 13 patients without mutations had low (<1%) Th17 cells but were distinct markedly reduced IFN-γ producing CD4+ T cells. Conclusions We propose the following diagnostic guidelines for STAT3-deficient HIES: Possible: IgE >1000 IU/mL plus a weighted score of clinical features >30 based on recurrent pneumonia, newborn rash, pathologic bone fractures, characteristic face, and high palate. Probable: Above plus lack of Th17 cells or a family history for definitive HIES. Definitive: Above plus a dominant-negative heterozygous mutation in STAT3.


Hyper-IgE Syndrome, HIES, Job syndrome, Th17 cells, STAT3-mutations, diagnostic guidelines


Mutations in the signal transducer and activator of transcription 3 (STAT3) and diagnostic guidelines for the Hyper-IgE Syndrome


Cristina Woellner, MSc,1 E. Michael Gertz, PhD,2 Alejandro A. Schaffer, PhD,2 Macarena Lagos, MD,3 Mario Perro, MSc,1 Erik-Oliver Glocker, MD,1 Maria C. Pietrogrande, MD,4 Fausto Cossu, MD,5 Jose L. Franco, MD, PhD,6 Nuria Matamoros, MD,7 Barbara Pietrucha, MD, PhD,8 Edyta Heropolita?ska-Pliszka, MD,8 Mehdi Yeganeh, MD,9 Mostafa Moin, MD,9 Teresa EspaNol, MD, PhD,10 Stephan Ehl, MD,11 Andrew R. Gennery, MD,12 Mario Abinun, MD, PhD,12 Anna Br?borowicz, MD,13 Tim Niehues, MD,14 Sara Sebnem Kilic, MD,15 Anne Junker, MD,16 Stuart E. Turvey, MD, PhD,16 Alessandro Plebani, MD,17 Berta Sanchez, PhD,18 Ben-Zion Garty, MD,19 Claudio Pignata, MD,20 Caterina Cancrini, MD,21 Jiri Litzman, MD,22 ozden Sanal, MD,23 Ulrich Baumann, MD,24 Rosa Bacchetta, MD,25 Amy P. Hsu, BA,26 Joie N. Davis, CRNP,26 Lennart Hammarstrom, MD,27 E. Graham Davies, MD,28 Efrem Eren, MD,29 Peter D. Arkwright, MD, PhD,30 Jukka S. Moilanen, MD,31 Dorothee Viemann, MD,32 Sujoy Khan, MRCP,33 Laszlo Marodi, MD,34 Andrew J. Cant, MD,12 Alexandra F. Freeman, MD,26 Jennifer M. Puck, MD,35 Steven M. Holland, MD,26 and Bodo Grimbacher, MD1

Publish date

2011 Feb 1.


Hysteroscopy is increasingly performed in an outpatient setting. Pain is the primary reason for abandonment of procedure or incomplete assessment. There is no consensus upon routine use of analgesia during hysteroscopy.

To assess the effectiveness and safety of pharmacological interventions for pain relief in women undergoing outpatient hysteroscopy, compared with placebo, no treatment or other pharmacological therapies.

Search methods
In September 2016 we searched the Cochrane Gynaecology and Fertility (CGF) Trials Register, CENTRAL, MEDLINE, Embase, PsycINFO, CINAHL and two trials registers (ClinicalTrials.gov and WHO ICTRP), together with reference checking and contact with study authors and experts.

Selection criteria
We included randomised controlled trials (RCTs) comparing use of pharmacological interventions with other pharmacological interventions and pharmacological interventions versus placebo or no treatment.

Data collection and analysis
We used standard methodological procedures expected by Cochrane. Our primary outcome was mean pain score.

Main results
We included 32 RCTS (3304 participants), of which only 19 reported data suitable for analysis. Most studies were at unclear or high risk of bias in most of the domains assessed. The evidence was low or very low quality, mainly due to risk of bias and imprecision. Baseline pain scores were relatively low in all groups.

Analgesic versus placebo or no treatment

Local anaesthetics

Local anaesthetics reduced mean pain scores during the procedure [(SMD) ?0.29, 95% CI ?0.39 to ?0.19, 10 RCTs, 1496 women, I2 = 80%, low?quality evidence)] and within 30 minutes (SMD 0.50, 95% CI ?0.67 to ?0.33, 5 RCTs, 545 women, I2 = 43%, low?quality evidence). This translates to a difference of up to 7 mm on a 0?10 cm visual analogue scale (VAS) during the procedure and up to 13 mm within 30 minutes, which is unlikely to be clinically meaningful. There was no clear evidence of a difference between the groups in mean pain scores after > 30 minutes (SMD ?0.11, 95% CI ?0.30 to 0.07, 4 RCTs, 450 women, I2 = 0%, low?quality evidence), or in rates of vasovagal reactions (OR 0.70, 95% CI 0.43 to 1.13, 8 RCTs, 1309 women, I2 = 66%, very low?quality evidence). There was insufficient evidence to determine whether there was a difference in rates of non?pelvic pain (OR 1.76, 95% CI 0.53 to 5.80, 1 RCT, 99 women, very low?quality evidence).

Nonsteroidal anti?inflammatory drugs (NSAIDs)

There was insufficient evidence to determine whether there was a difference between the groups in mean pain scores during the procedure (SMD ?0.18, 95% CI ?0.35 to 0.00, 3 RCTs, 521 women, I2 = 81%, low?quality evidence). Pain scores were lower in the NSAIDs group within 30 minutes (SMD ?0.25, 95% CI ?0.46 to ?0.04, 2 RCTs, 340 women, I2=29%, low?quality evidence) and at over 30 minutes (SMD ?0.27, 95% CI ?0.49 to ?0.05, 2 RCTs, 321 women, I2 = 78%, low?quality evidence). This equates to maximum differences of under 7.5 mm on a 0?10 cm scale, which are unlikely to be clinically significant. One RCT (181 women) reported adverse events: there was insufficient evidence to determine whether there was a difference between the groups in vasovagal reactions (OR 0.76, 95% CI 0.20 to 2.94, very low?quality evidence). For other reported adverse events (non pelvic pain and allergic reactions) evidence was lacking.


One RCT utilised sublingual buprenorphine and one utilised oral tramadol. Data on pain scores during the procedure were unsuitable for pooling due to inconsistency. Tramadol was associated with a benefit of up to 22 mm on a 0?10 cm scale (SMD ?0.76, 95% CI ?1.10 to ?0.42, 1 RCT, 140 women). However, the effect estimate for this outcome for sublingual opioids did not support a benefit from the intervention (SMD 0.08, 95% CI ?0.22 to 0.39, 164 women). Compared with placebo, the pain score within 30 minutes of the procedure was reduced in the tramadol group, with a difference of up to 17mm on a 0?10cm scale (SMD ?0.57, 95% CI ?0.91 to ?0.23 , 1 RCT, 140 women, low?quality evidence. There was no clear evidence of a difference between the tramadol and placebo groups at over 30 minutes (SMD ?0.17, 95% CI ?0.51 to 0.16, 1 RCT, 140 women, low?quality evidence). Nausea and vomiting occurred in 39% of the buprenorphine group, and in none of the placebo group (OR 107.55, 95% CI 6.44 to 1796.46)

Analgesic versus any other analgesic

Some comparisons did not report pain scores at all time frames of interest, and none reported data on adverse events.

One RCT (84 women) compared local intracervical anaesthesia versus combined intracervical and paracervical anaesthesia. Pain scores were higher in the group with local intracervical anaesthesia during the procedure (SMD 4.27, 95% CI 3.49 to 5.06, very low?quality evidence), within 30 minutes (SMD 1.55, 95% CI 1.06 to 2.05, very low?quality evidence) and at more than 30 minutes (SMD 3.47, 95% CI 2.78 to 4.15, very low?quality evidence). This translates to a possible benefit in the combined group of up to 12 mm on a 0?10 cm scale during the procedure. Benefits at longer follow?up were smaller.

One RCT compared antispasmodic + NSAID versus local paracervical anaesthesia. Pain scores were lower in the NSAID group than in the local anaesthesia group (during procedure: SMD ?1.40, 95% CI ?1.90 to ?0.91; >30 minutes after procedure: SMD ?0.87, 95% CI ?1.33 to ?0.41; 80 women, very low?quality evidence). This suggests a possible benefit of during the procedure of up to 23 mm on a 0?10 VAS scale and up to 11 mm >30 minutes after the procedure.

Other comparisons included local intracervical anaesthesia versus combined intracervical, paracervical and topical anaesthesia, and opioid versus NSAIDs. Findings were inconclusive.

Authors’ conclusions
There was no consistent good?quality evidence of a clinically meaningful difference in safety or effectiveness between different types of pain relief compared with each other or with placebo or no treatment in women undergoing outpatient hysteroscopy.


Female, Humans, Ambulatory Surgical Procedures, Ambulatory Surgical Procedures/adverse effects, Analgesia, Analgesia/methods, Anesthetics, Local, Anesthetics, Local/therapeutic use, Hysteroscopy, Hysteroscopy/adverse effects, Pain, Postoperative, Pain, Postoperative/drug therapy


Pain relief for outpatient hysteroscopy


Gaity Ahmad, Sushant Saluja, Helena O'Flynn, Alessandra Sorrentino, Daniel Leach, and Andrew Watson

Publish date

2017 Oct

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