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BDS I

* Please kindly note that our products are not to be used for therapeutic purposes and cannot be sold to patients.

BDS I is a reversible Kv3.4 potassium channel blocker (IC50 = 47 nM) and Nav1.7 channel agonist. BDS I potentiates TTX-sensitive sodium currents in rat small dorsal root ganglion neurons. BDS I has potential therapeutic effect on major CNS disorders, such as Alzheimer and Parkinson diseases.

Category

Peptide Inhibitors

Catalog number

BAT-010275

Molecular Formula

C210H297N57O56S6

Molecular Weight

4708.37

Specification
Reference Reading

IUPAC Name

2-[[1-[2-[[2a,21-bis(4-aminobutyl)-14a,93-bis(2-amino-2-oxoethyl)-6-[[1-[2-(2-aminopropanoylamino)propanoyl]pyrrolidine-2-carbonyl]amino]-9-benzyl-17a,48-di(butan-2-yl)-33,54-bis(3-carbamimidamidopropyl)-39-(carboxymethyl)-60,87-bis(1-hydroxyethyl)-15,90-bis(hydroxymethyl)-78,84,99-tris[(4-hydroxyphenyl)methyl]-5a,45-bis(1H-indol-3-ylmethyl)-42,51-bis(2-methylpropyl)-a,3a,6a,7,10,12a,13,15a,16,18a,19,20a,22,28,31,34,37,40,43,46,49,52,55,58,61,64,70,73,76,79,82,85,88,91,94,97-hexatriacontaoxo-3,4,24a,25a,28a,29a-hexathia-1a,4a,7a,8,11,13a,14,16a,17,19a,20,21a,23,29,32,35,38,41,44,47,50,53,56,59,62,65,71,74,77,80,83,86,89,92,95,98-hexatriacontazahexacyclo[61.56.7.412,96.023,27.065,69.0107,111]triacontahectane-22a-carbonyl]amino]-3-(4-hydroxyphenyl)propanoyl]pyrrolidine-2-carbonyl]amino]-3-(1H-imidazol-4-yl)propanoic acid

Synonyms

Blood depressing substance 1

Appearance

White Lyophilized Solid

Purity

>95%

Sequence

AAPC(1)FC(2)SGKPGRGDLWILRGTC(3)PGGYGYTSNC(2)YKWPNIC(1)C(3)YPH

Storage

Store at -20°C

Application

potential treatment of major CNS disorders

InChI

InChI=1S/C210H297N57O56S6/c1-13-107(7)169-199(313)247-134(74-106(5)6)179(293)239-130(42-27-67-222-210(218)219)175(289)227-95-167(284)259-171(111(11)270)201(315)258-153-103-329-328-99-149(191(305)248-143(79-117-54-62-124(275)63-55-117)205(319)266-71-32-47-158(266)197(311)250-145(208(322)323)82-120-88-220-104-232-120)255-193(307)152-102-327-326-101-151(256-198(312)156-45-30-68-263(156)203(317)110(10)233-173(287)109(9)213)190(304)242-137(75-113-33-16-15-17-34-113)182(296)253-150(192(306)251-146(96-268)177(291)229-91-164(281)235-132(40-23-25-65-212)204(318)264-69-28-43-154(264)195(309)231-94-163(280)234-129(41-26-66-221-209(216)217)174(288)226-92-166(283)238-142(85-168(285)286)184(298)241-133(73-105(3)4)180(294)244-139(186(300)260-169)80-118-86-223-127-37-20-18-35-125(118)127)100-325-324-98-148(189(303)243-138(78-116-52-60-123(274)61-53-116)181(295)240-131(39-22-24-64-211)178(292)249-144(81-119-87-224-128-38-21-19-36-126(119)128)206(320)267-72-31-46-157(267)196(310)246-141(84-160(215)277)187(301)261-170(108(8)14-2)200(314)257-152)254-183(297)140(83-159(214)276)245-188(302)147(97-269)252-202(316)172(112(12)271)262-185(299)136(77-115-50-58-122(273)59-51-115)237-165(282)93-228-176(290)135(76-114-48-56-121(272)57-49-114)236-162(279)90-225-161(278)89-230-194(308)155-44-29-70-265(155)207(153)321/h15-21,33-38,48-63,86-88,104-112,129-158,169-172,223-224,268-275H,13-14,22-32,39-47,64-85,89-103,211-213H2,1-12H3,(H2,214,276)(H2,215,277)(H,220,232)(H,225,278)(H,226,288)(H,227,289)(H,228,290)(H,229,291)(H,230,308)(H,231,309)(H,233,287)(H,234,280)(H,235,281)(H,236,279)(H,237,282)(H,238,283)(H,239,293)(H,240,295)(H,241,298)(H,242,304)(H,243,303)(H,244,294)(H,245,302)(H,246,310)(H,247,313)(H,248,305)(H,249,292)(H,250,311)(H,251,306)(H,252,316)(H,253,296)(H,254,297)(H,255,307)(H,256,312)(H,257,314)(H,258,315)(H,259,284)(H,260,300)(H,261,301)(H,262,299)(H,285,286)(H,322,323)(H4,216,217,221)(H4,218,219,222)

InChI Key

NHDQBZJQNKDJOQ-UHFFFAOYSA-N

Canonical SMILES

CCC(C)C1C(=O)NC(C(=O)NC(C(=O)NCC(=O)NC(C(=O)NC2CSSCC(NC(=O)C3CSSCC(C(=O)NC(C(=O)NC(CSSCC(C(=O)NC(C(=O)NC(C(=O)NC(C(=O)N4CCCC4C(=O)NC(C(=O)NC(C(=O)N3)C(C)CC)CC(=O)N)CC5=CNC6=CC=CC=C65)CCCCN)CC7=CC=C(C=C7)O)NC(=O)C(NC(=O)C(NC(=O)C(NC(=O)C(NC(=O)CNC(=O)C(NC(=O)CNC(=O)CNC(=O)C8CCCN8C2=O)CC9=CC=C(C=C9)O)CC2=CC=C(C=C2)O)C(C)O)CO)CC(=O)N)C(=O)NC(C(=O)NCC(=O)NC(C(=O)N2CCCC2C(=O)NCC(=O)NC(C(=O)NCC(=O)NC(C(=O)NC(C(=O)NC(C(=O)N1)CC1=CNC2=CC=CC=C21)CC(C)C)CC(=O)O)CCCNC(=N)N)CCCCN)CO)CC1=CC=CC=C1)NC(=O)C1CCCN1C(=O)C(C)NC(=O)C(C)N)C(=O)NC(CC1=CC=C(C=C1)O)C(=O)N1CCCC1C(=O)NC(CC1=CNC=N1)C(=O)O)C(C)O)CCCNC(=N)N)CC(C)C

1. The Anemonia sulcata Toxin BDS-I Protects Astrocytes Exposed to Aβ1-42 Oligomers by Restoring [Ca2+]i Transients and ER Ca2+ Signaling

Agnese Secondo, Francesca Boscia, Anna Pannaccione, Valeria de Rosa, Paolo Grieco, Ilaria Piccialli, Roselia Ciccone, Valentina Tedeschi, Antonella Casamassa Toxins (Basel) . 2020 Dec 31;13(1):20. doi: 10.3390/toxins13010020.

Intracellular calcium concentration ([Ca2+]i) transients in astrocytes represent a highly plastic signaling pathway underlying the communication between neurons and glial cells. However, how this important phenomenon may be compromised in Alzheimer's disease (AD) remains unexplored. Moreover, the involvement of several K+channels, including KV3.4 underlying the fast-inactivating currents, has been demonstrated in several AD models. Here, the effect of KV3.4 modulation by the marine toxin blood depressing substance-I (BDS-I) extracted fromAnemonia sulcatahas been studied on [Ca2+]itransients in rat primary cortical astrocytes exposed to Aβ1-42oligomers. We showed that: (1) primary cortical astrocytes expressing KV3.4 channels displayed [Ca2+]itransients depending on the occurrence of membrane potential spikes, (2) BDS-I restored, in a dose-dependent way, [Ca2+]itransients in astrocytes exposed to Aβ1-42oligomers (5 µM/48 h) by inhibiting hyperfunctional KV3.4 channels, (3) BDS-I counteracted Ca2+overload into the endoplasmic reticulum (ER) induced by Aβ1-42oligomers, (4) BDS-I prevented the expression of the ER stress markers including active caspase 12 and GRP78/BiP in astrocytes treated with Aβ1-42oligomers, and (5) BDS-I prevented Aβ1-42-induced reactive oxygen species (ROS) production and cell suffering measured as mitochondrial activity and lactate dehydrogenase (LDH) release. Collectively, we proposed that the marine toxin BDS-I, by inhibiting the hyperfunctional KV3.4 channels and restoring [Ca2+]ioscillation frequency, prevented Aβ1-42-induced ER stress and cell suffering in astrocytes.

2. Performance of BDS-3: Measurement Quality Analysis, Precise Orbit and Clock Determination

Jingnan Liu, Tao Geng, Xin Xie, Bin Wang, Qile Zhao Sensors (Basel) . 2017 May 28;17(6):1233. doi: 10.3390/s17061233.

Since 2015, China has successfully launched five experimental BeiDou global navigation system (BDS-3) satellites for expanding the regional system to global coverage. An initial performance assessment and characterization analysis of the BDS-3 is presented. Twenty days of tracking data have been collected from eleven monitoring stations. The tracking characteristics and measurement quality are analyzed and compared with the regional BDS (BDS-2) in terms of observed carrier-to-noise density ratio, pseudo-range multipath, and noise. The preliminary results suggest that the measurement quality of BDS-3 outperforms the BDS-2 for the same type of satellites. In addition, the analysis of multipath combinations reveals that the problem of satellite-induced code biases found in BDS-2 seems to have been solved for BDS-3. Precise orbit and clock determination are carried out and evaluated. The orbit overlap comparison show a precision of 2-6 dm in 3D root mean square (RMS) and 6-14 cm in the radial component for experimental BDS-3 satellites. External validations with satellite laser ranging (SLR) show residual RMS on the level of 1-3 dm. Finally, the performance of the new-generation onboard atomic clocks is evaluated and results confirm an increased stability compared to BDS-2 satellite clocks.

3. Synthesis and Pharmacological Evaluation of a Novel Peptide Based on Anemonia sulcata BDS-I Toxin as a New KV3.4 Inhibitor Exerting a Neuroprotective Effect Against Amyloid-β Peptide

Anna Pannaccione, Paolo Grieco, Francesco Merlino, Ilaria Piccialli, Roselia Ciccone, Lucio Annunziato Front Chem . 2019 Jul 9;7:479. doi: 10.3389/fchem.2019.00479.

There is increasing evidence that the fast-inactivating potassium current IA, encoded by KV3. 4 channels, plays an important role in Alzheimer's Disease (AD), since the neurotoxic β-amyloid peptide1-42 (Aβ1-42) increases the IAcurrent triggering apoptotic processes. The specific inhibition of KV3.4 by the marine toxin extracted fromAnemonia sulcata, named blood depressing substance-I (BDS-I), reverts the Aβ peptide-induced cell death. The aim of the present study was to identify the smallest fragments of BDS-I, obtained by peptide synthesis, able to inhibit KV3.4 currents. For this purpose, whole-cell patch clamp technique was used to evaluate the effects of BDS-I fragments on KV3.4 currents in CHO cells heterologously expressing KV3.4. We found that BDS-I[1-8] fragment, containing the N-terminal octapeptide sequence of full length BDS-I, was able to inhibit KV3.4 currents in a concentration dependent manner, whereas the scrambled sequence of BDS-I[1-8] and all the other fragments obtained from BDS-I full length were ineffective. As we demonstrated in a previous study, BDS-I full length is able to counteract Aβ1-42-induced enhancement of KV3.4 activity, preventing Aβ1-42-induced caspase-3 activation and the abnormal nuclear morphology in NGF-differentiated PC-12 cells. Similarly to BDS-I, we found that BDS-I[1-8] blocking KV3.4 currents prevented Aβ1-42-induced caspase-3 activation and apoptotic processes. Collectively, these results suggest that BDS-I[1-8] could represent a lead compound to be developed as a new drug targeting KV3.4 channels.