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2-Amino-6-ethoxybenzothiazole

$87

  • Brand : BIOFRON

  • Catalogue Number : BN-O1054

  • Specification : 99%(HPLC)

  • CAS number : 94-45-1

  • Formula : C9H10N2OS

  • Molecular Weight : 194.26

  • PUBCHEM ID : 7192

  • Volume : 5mg

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Catalogue Number

BN-O1054

Analysis Method

Specification

99%(HPLC)

Storage

2-8°C

Molecular Weight

194.26

Appearance

Botanical Source

Structure Type

Category

SMILES

CCOC1=CC2=C(C=C1)N=C(S2)N

Synonyms

6-Ethoxy-1,3-benzothiazol-2(3H)-imine/2(3H)-Benzothiazolimine, 6-ethoxy-/2-Amino-6-ethoxybenzothiazole/6-Ethoxy-1,3-benzothiazol-2-amine/2-Benzothiazolamine, 6-ethoxy-

IUPAC Name

6-ethoxy-1,3-benzothiazol-2-amine

Density

1.4±0.1 g/cm3

Solubility

Flash Point

151.6±28.4 °C

Boiling Point

327.1±44.0 °C at 760 mmHg

Melting Point

161-163 °C(lit.)

InChl

InChI=1S/C11H17N3O8/c12-8-13-6(17)2-4-9(19,1-15)5-3(16)10(2,14-8)7(18)11(20,21-4)22-5/h2-7,15-20H,1H2,(H3,12,13,14)/t2-,3-,4-,5+,6-,7+,9+,10-,11+/m1/s1

InChl Key

KOYJWFGMEBETBU-UHFFFAOYSA-N

WGK Germany

RID/ADR

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#:94-45-1) 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.

PMID

25869245

Abstract

1. We investigated the mechanisms responsible for the in vivo instability of a benzofurazan compound BI-94 (NSC228148) with potent anti-cancer activity.

2. BI-94 was stable in MeOH, water, and in various buffers at pHs 2.5-5, regardless of the buffer composition. In contrast, BI-94 was unstable in NaOH and at pHs 7-9, regardless of the buffer composition. BI-94 disappeared immediately after spiking into mice, rat, monkey, and human plasma. BI-94 stability in plasma can be only partially restored by acidifying it, which indicated other mechanisms in addition to pH for BI-94 instability in plasma.

3. BI-94 formed adducts with the trapping agents, glutathione (GSH) and N-acetylcysteine (NAC), in vivo and in vitro via nucleophilic aromatic substitution reaction. The kinetics of adduct formation showed that neutral or physiological pHs enhanced and accelerated GSH and NAC adduct formation with BI-94, whereas acidic pHs prevented it. Therefore, physiological pHs not only altered BI-94 chemical stability but also enhanced adduct formation with endogenous nucleophiles. In addition, adduct formation with human serum albumin-peptide 3 (HSA-T3) at the Cys34 position was demonstrated.

4. In conclusion, BI-94 was unstable at physiological conditions due to chemical instability and irreversible binding to plasma proteins.

KEYWORDS

Glutathione, irreversible protein binding, isotopic filtering, LC-MS/MS, N-acetylcysteine

Title

Irreversible binding of an anticancer compound (BI-94) to plasma proteins

Author

Nagsen Gautam, Rhishikesh Thakare, Sandeep Rana, Amarnath Natarajan, Yazen Alnouti

Publish date

2015 Oct 1.

PMID

27175934

Abstract

Background
This is an update of the 2009 Cochrane overview and network meta‐analysis (NMA) of biologics for rheumatoid arthritis (RA).

Objectives
To assess the benefits and harms of nine biologics (abatacept, adalimumab, anakinra, certolizumab pegol, etanercept, golimumab, infliximab, rituximab, tocilizumab) and small molecule tofacitinib, versus comparator (MTX, DMARD, placebo (PL), or a combination) in adults with rheumatoid arthritis who have failed to respond to methotrexate (MTX) or other disease‐modifying anti‐rheumatic drugs (DMARDs), i.e., MTX/DMARD incomplete responders (MTX/DMARD‐IR).

Methods
We searched for randomized controlled trials (RCTs) in the Cochrane Central Register of Controlled Trials (CENTRAL) (via The Cochrane Library Issue 6, June 2015), MEDLINE (via OVID 1946 to June 2015), and EMBASE (via OVID 1947 to June 2015). Data extraction, risk of bias and GRADE assessments were done in duplicate. We calculated both direct estimates using standard meta‐analysis and used Bayesian mixed treatment comparisons approach for NMA estimates to calculate odds ratios (OR) and 95% credible intervals (CrI). We converted OR to risk ratios (RR) which are reported in the abstract for the ease of interpretation.

Main results
This update included 73 new RCTs for a total of 90 RCTs; 79 RCTs with 32,874 participants provided usable data. Few trials were at high risk of bias for blinding of assessors/participants (13% to 21%), selective reporting (4%) or major baseline imbalance (8%); a large number had unclear risk of bias for random sequence generation (68%) or allocation concealment (74%).

Based on direct evidence of moderate quality (downgraded for inconsistency), biologic+MTX/DMARD was associated with a statistically significant and clinically meaningful improvement in ACR50 versus comparator (RR 2.71 (95% confidence interval (CI) 2.36 to 3.10); absolute benefit 24% more patients (95% CI 19% to 29%), number needed to treat for an additional beneficial outcome (NNTB) = 5 (4 to 6). NMA estimates for ACR50 in tumor necrosis factor (TNF) biologic+MTX/DMARD (RR 3.23 (95% credible interval (Crl) 2.75 to 3.79), non‐TNF biologic+MTX/DMARD (RR 2.99; 95% Crl 2.36 to 3.74), and anakinra + MTX/DMARD (RR 2.37 (95% Crl 1.00 to 4.70) were similar to the direct estimates.

Based on direct evidence of moderate quality (downgraded for inconsistency), biologic+MTX/DMARD was associated with a clinically and statistically important improvement in function measured by the Health Assessment Questionnaire (0 to 3 scale, higher = worse function) with a mean difference (MD) based on direct evidence of ‐0.25 (95% CI ‐0.28 to ‐0.22); absolute benefit of ‐8.3% (95% CI ‐9.3% to ‐7.3%), NNTB = 3 (95% CI 2 to 4). NMA estimates for TNF biologic+MTX/DMARD (absolute benefit, ‐10.3% (95% Crl ‐14% to ‐6.7%) and non‐TNF biologic+MTX/DMARD (absolute benefit, ‐7.3% (95% Crl ‐13.6% to ‐0.67%) were similar to respective direct estimates.

Based on direct evidence of moderate quality (downgraded for inconsistency), biologic+MTX/DMARD was associated with clinically and statistically significantly greater proportion of participants achieving remission in RA (defined by disease activity score DAS < 1.6 or DAS28 < 2.6) versus comparator (RR 2.81 (95% CI, 2.23 to 3.53); absolute benefit 18% more patients (95% CI 12% to 25%), NNTB = 6 (4 to 9)). NMA estimates for TNF biologic+MTX/DMARD (absolute improvement 17% (95% Crl 11% to 23%)) and non‐TNF biologic+MTX/DMARD (absolute improvement 19% (95% Crl 12% to 28%) were similar to respective direct estimates. Based on direct evidence of moderate quality (downgraded for inconsistency), radiographic progression (scale 0 to 448) was statistically significantly reduced in those on biologics + MTX/DMARDs versus comparator, MD ‐2.61 (95% CI ‐4.08 to ‐1.14). The absolute reduction was small, ‐0.58% (95% CI ‐0.91% to ‐0.25%) and we are unsure of the clinical relevance of this reduction. NMA estimates of TNF biologic+MTX/DMARD (absolute reduction ‐0.67% (95% Crl ‐1.4% to ‐0.12%) and non‐TNF biologic+MTX/DMARD (absolute reduction, ‐0.68% (95% Crl ‐2.36% to 0.92%)) were similar to respective direct estimates. Based on direct evidence of moderate quality (downgraded for imprecision), results for withdrawals due to adverse events were inconclusive, with wide confidence intervals encompassing the null effect and evidence of an important increase in withdrawals, RR 1.11 (95% CI 0.96 to 1.30). The NMA estimates of TNF biologic+MTX/DMARD (RR 1.24 (95% Crl 0.99 to 1.57)) and non‐TNF biologic+MTX/DMARD (RR 1.20 (95% Crl 0.87 to 1.67)) were similarly inconclusive and downgraded to low for both imprecision and indirectness. Based on direct evidence of high quality, biologic+MTX/DMARD was associated with clinically significantly increased risk (statistically borderline significant) of serious adverse events on biologic+MTX/DMARD (Peto OR [can be interpreted as RR due to low event rate] 1.12 (95% CI 0.99 to 1.27); absolute risk 1% (0% to 2%), As well, the NMA estimate for TNF biologic+MTX/DMARD (Peto OR 1.20 (95% Crl 1.01 to 1.43)) showed moderate quality evidence of an increase in the risk of serious adverse events. The other two NMA estimates were downgraded to low quality due to imprecision and indirectness and had wide confidence intervals resulting in uncertainty around the estimates: non‐TNF biologics + MTX/DMARD: 1.07 (95% Crl 0.89 to 1.29) and anakinra: RR 1.06 (95% Crl 0.65 to 1.75). Based on direct evidence of low quality (downgraded for serious imprecision), results were inconclusive for cancer (Peto OR 1.07 (95% CI 0.68 to 1.68) for all biologic+MTX/DMARD combinations. The NMA estimates of TNF biologic+MTX/DMARD (Peto OR 1.21 (95% Crl 0.63 to 2.38) and non‐TNF biologic+MTX/DMARD (Peto OR 0.99 (95% Crl 0.58 to 1.78)) were similarly inconclusive and downgraded to low quality for both imprecision and indirectness. Main results text shows the results for tofacitinib and differences between medications. Authors' conclusions Based primarily on RCTs of 6 months' to 12 months' duration, there is moderate quality evidence that the use of biologic+MTX/DMARD in people with rheumatoid arthritis who have failed to respond to MTX or other DMARDs results in clinically important improvement in function and higher ACR50 and remission rates, and increased risk of serious adverse events than the comparator (MTX/DMARD/PL; high quality evidence). Radiographic progression is slowed but its clinical relevance is uncertain. Results were inconclusive for whether biologics + MTX/DMARDs are associated with an increased risk of cancer or withdrawals due to adverse events.

Title

Biologics or tofacitinib for rheumatoid arthritis in incomplete responders to methotrexate or other traditional disease‐modifying anti‐rheumatic drugs: a systematic review and network meta‐analysis

Author

Jasvinder A Singh, Alomgir Hossain, Elizabeth Tanjong Ghogomu, Ahmed Kotb, Robin Christensen, Amy S Mudano, Lara J Maxwell, Nipam P Shah, Peter Tugwell, George A Wells, Cochrane Musculoskeletal Group

Publish date

2016 May

Title

UEG Week 2018 Poster Presentations

Publish date

2018 Oct;


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