Bundlin B
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| Category | Antibiotics |
| Catalog number | BBF-00189 |
| CAS | 23477-98-7 |
| Molecular Weight | 501.57 |
| Molecular Formula | C27H35NO8 |
| Purity | 95% |
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Description
Bundlin B is a macrolide antibiotic produced by Streptomyces greseofuscus and has only weak anti-Staphylococcus aureus effect.
Specification
| Synonyms | Sedecamycin; Lankacidin A |
| IUPAC Name | [(1S,2R,3E,5E,7S,9E,11E,13S,15R,19R)-7-hydroxy-1,4,10,19-tetramethyl-17,18-dioxo-2-(2-oxopropanoylamino)-16-oxabicyclo[13.2.2]nonadeca-3,5,9,11-tetraen-13-yl] acetate |
| Canonical SMILES | CC1C2CC(C=CC(=CCC(C=CC(=CC(C(C1=O)(C(=O)O2)C)NC(=O)C(=O)C)C)O)C)OC(=O)C |
| InChI | InChI=1S/C27H35NO8/c1-15-7-10-20(31)11-8-16(2)13-23(28-25(33)18(4)29)27(6)24(32)17(3)22(36-26(27)34)14-21(12-9-15)35-19(5)30/h7-9,11-13,17,20-23,31H,10,14H2,1-6H3,(H,28,33)/b11-8+,12-9+,15-7+,16-13+/t17-,20+,21-,22-,23-,27+/m1/s1 |
| InChI Key | LSNBAGMWJRMBEO-VGBMZARNSA-N |
Properties
| Appearance | Needle Crystal |
| Antibiotic Activity Spectrum | Gram-positive bacteria |
| Melting Point | 213-215°C |
| Density | 1.22 g/cm3 |
| Solubility | Soluble in Chloroform, Methanol, Methyl ether, benzene, water |
Reference Reading
1. Neuroimaging and biomarker evidence of neurodegeneration in asthma
Melissa A Rosenkranz, Douglas C Dean rd, Barbara B Bendlin, Nizar N Jarjour, Stephane Esnault, Henrik Zetterberg, Amanda Heslegrave, Michael D Evans, Richard J Davidson, William W Busse J Allergy Clin Immunol. 2022 Feb;149(2):589-598.e6. doi: 10.1016/j.jaci.2021.09.010. Epub 2021 Sep 15.
Background: Epidemiologic studies have shown that Alzheimer's disease (AD) and related dementias (ADRD) are seen more frequently with asthma, especially with greater asthma severity or exacerbation frequency. Objective: To examine the changes in brain structure that may underlie this phenomenon, we examined diffusion-weighted magnetic resonance imaging (dMRI) and blood-based biomarkers of AD (phosphorylated tau 181, p-Tau181), neurodegeneration (neurofilament light chain, NfL), and glial activation (glial fibrillary acidic protein, GFAP). Methods: dMRI data were obtained in 111 individuals with asthma, ranging in disease severity from mild to severe, and 135 healthy controls. Regression analyses were used to test the relationships between asthma severity and neuroimaging measures, as well as AD pathology, neurodegeneration, and glial activation, indexed by plasma p-Tau181, NfL, and GFAP, respectively. Additional relationships were tested with cognitive function. Results: Asthma participants had widespread and large-magnitude differences in several dMRI metrics, which were indicative of neuroinflammation and neurodegeneration, and which were robustly associated with GFAP and, to a lesser extent, NfL. The AD biomarker p-Tau181 was only minimally associated with neuroimaging outcomes. Further, asthma severity was associated with deleterious changes in neuroimaging outcomes, which in turn were associated with slower processing speed, a test of cognitive performance. Conclusions: Asthma, particularly when severe, is associated with characteristics of neuroinflammation and neurodegeneration, and may be a potential risk factor for neural injury and cognitive dysfunction. There is a need to determine how asthma may affect brain health and whether treatment directed toward characteristics of asthma associated with these risks can mitigate these effects.
2. An examination of a novel multipanel of CSF biomarkers in the Alzheimer's disease clinical and pathological continuum
Carol Van Hulle, Erin M Jonaitis, Tobey J Betthauser, Richard Batrla, Norbert Wild, Gwendlyn Kollmorgen, Ulf Andreasson, Ozioma Okonkwo, Barbara B Bendlin, Sanjay Asthana, Cynthia M Carlsson, Sterling C Johnson, Henrik Zetterberg, Kaj Blennow Alzheimers Dement. 2021 Mar;17(3):431-445. doi: 10.1002/alz.12204. Epub 2020 Dec 18.
Introduction: This study examines the utility of a multipanel of cerebrospinal fluid (CSF) biomarkers complementing Alzheimer's disease (AD) biomarkers in a clinical research sample. We compared biomarkers across groups defined by clinical diagnosis and pTau181 /Aβ42 status (+/-) and explored their value in predicting cognition. Methods: CSF biomarkers amyloid beta (Aβ)42 , pTau181 , tTau, Aβ40 , neurogranin, neurofilament light (NfL), α-synuclein, glial fibrillary acidic protein (GFAP), chitinase-3-like protein 1 (YKL-40), soluble triggering receptor expressed on myeloid cells 2 (sTREM2), S100 calcium binding protein B (S100B), and interleukin 6 (IL6), were measured with the NeuroToolKit (NTK) for 720 adults ages 40 to 93 years (mean age = 63.9 years, standard deviation [SD] = 9.0; 50 with dementia; 54 with mild cognitive impairment [MCI], 616 unimpaired). Results: Neurodegeneration and glial activation biomarkers were elevated in pTau181 /Aβ42 + MCI/dementia participants relative to all pTau181 /Aβ42 - participants. Neurodegeneration biomarkers increased with clinical severity among pTau181 /Aβ42 + participants and predicted worse cognitive performance. Glial activation biomarkers were unrelated to cognitive performance. Discussion: The NTK contains promising markers that improve the pathophysiological characterization of AD. Neurodegeneration biomarkers beyond tTau improved statistical prediction of cognition and disease stages.
3. Alzheimer's disease biomarkers in Black and non-Hispanic White cohorts: A contextualized review of the evidence
Carey E Gleason, Megan Zuelsdorff, Diane C Gooding, Amy J H Kind, Adrienne L Johnson, Taryn T James, Nickolas H Lambrou, Mary F Wyman, Fred B Ketchum, Alexander Gee, Sterling C Johnson, Barbara B Bendlin, Henrik Zetterberg Alzheimers Dement. 2022 Aug;18(8):1545-1564. doi: 10.1002/alz.12511. Epub 2021 Dec 6.
Black Americans are disproportionately affected by dementia. To expand our understanding of mechanisms of this disparity, we look to Alzheimer's disease (AD) biomarkers. In this review, we summarize current data, comparing the few studies presenting these findings. Further, we contextualize the data using two influential frameworks: the National Institute on Aging-Alzheimer's Association (NIA-AA) Research Framework and NIA's Health Disparities Research Framework. The NIA-AA Research Framework provides a biological definition of AD that can be measured in vivo. However, current cut-points for determining pathological versus non-pathological status were developed using predominantly White cohorts-a serious limitation. The NIA's Health Disparities Research Framework is used to contextualize findings from studies identifying racial differences in biomarker levels, because studying biomakers in isolation cannot explain or reduce inequities. We offer recommendations to expand study beyond initial reports of racial differences. Specifically, life course experiences associated with racialization and commonly used study enrollment practices may better account for observations than exclusively biological explanations.
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
