購(gòu)物車 
-
PAC-1
- names：
PAC-1
- CAS號(hào)：
315183-21-2
MDL Number： MFCD02051977 - MF(分子式)： C23H28N4O2 MW(分子量)： 392.494
- EINECS: Reaxys Number:
- Pubchem ID:135421197 Brand:BIOFOUNT
PAC-1(315183-21-2,procaspase activating compound-1)是一種 procaspase-3 激活劑，誘導(dǎo)癌細(xì)胞凋亡，EC50 為 2.08 μM。PAC-1已用于研究淋巴瘤，黑素瘤，實(shí)體瘤，乳腺癌和胸癌等的治療研究中。
| 貨品編碼 | 規(guī)格 | 純度 | 價(jià)格 (￥) | 現(xiàn)價(jià)(￥) | 特價(jià)(￥) | 庫(kù)存描述 | 數(shù)量 | 總計(jì) (￥) |
|---|---|---|---|---|---|---|---|---|
| HCC340301-5mg | 5mg | 97% | ￥ 731.50 | ￥ 731.50 | 4-7周 | ￥ 0.00 |
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| 中文別名 | PAC-1(315183-21-2);PAC1; PAC 1；PAC1; VO-100; VO100; VO 100; procaspase激活化合物1; |
| 英文別名 | PAC-1(315183-21-2);PAC1; PAC 1; PAC1; VO-100; VO100; VO 100; procaspase activating compound-1; |
| CAS號(hào) | 315183-21-2 |
| Inchi | InChI=1S/C23H28N4O2/c1-2-7-20-10-6-11-21(23(20)29)16-24-25-22(28)18-27-14-12-26(13-15-27)17-19-8-4-3-5-9-19/h2-6,8-11,16,29H,1,7,12-15,17-18H2,(H,25,28)/b24-16- |
| InchiKey | YQNRVGJCPCNMKT-JLPGSUDCSA-N |
| 分子式 Formula | C23H28N4O2 |
| 分子量 Molecular Weight | 392.494 |
| 溶解度Solubility | 生物體外In Vitro:DMSO溶解度50 mg/mL(127.39 mM;Need ultrasonic)H2O< 0.1 mg/mL(insoluble) |
| 性狀 | 白色固體 |
| 儲(chǔ)藏條件 Storage conditions | Store at +4°C，storage at -4℃ (1-2weeks), longer storage period at -20℃ (1-2years) |
PAC-1(315183-21-2,procaspase activating compound-1)實(shí)驗(yàn)注意事項(xiàng)：
1.實(shí)驗(yàn)前需戴好防護(hù)眼鏡，穿戴防護(hù)服和口罩，佩戴手套，避免與皮膚接觸。
2.實(shí)驗(yàn)過(guò)程中如遇到有毒或者刺激性物質(zhì)及有害物質(zhì)產(chǎn)生，必要時(shí)實(shí)驗(yàn)操作需要手套箱內(nèi)完成以免對(duì)實(shí)驗(yàn)人員造成傷害
3.實(shí)驗(yàn)后產(chǎn)生的廢棄物需分類存儲(chǔ)，并交于專業(yè)生物廢氣物處理公司處理，以免造成環(huán)境污染Experimental considerations:
1. Wear protective glasses, protective clothing and masks, gloves, and avoid contact with the skin during the experiment.
2. The waste generated after the experiment needs to be stored separately, and handed over to a professional biological waste gas treatment company to avoid environmental pollution.
Tags:PAC-1試劑,PAC-1雜質(zhì),PAC-1中間體,PAC-1密度,PAC-1溶解度,PAC-1合成,PAC-1旋光度,PAC-1閃點(diǎn),PAC-1購(gòu)買,
| 產(chǎn)品說(shuō)明 | PAC-1(315183-21-2,procaspase activating compound-1)可以作為藥物雜質(zhì)對(duì)照品以及生物醫(yī)藥類試劑。 |
| Introduction | PAC-1(315183-21-2,procaspase activating compound-1)can be used as a reference substance for drug impurities and reagents，only for research. |
| Application1 | |
| Application2 | |
| Application3 |
PAC-1(315183-21-2,procaspase activating compound-1)藥理學(xué)：
1、PAC-1被稱為首個(gè)激活蛋白酶的化合物，可選擇性誘導(dǎo)癌細(xì)胞中的細(xì)胞凋亡或細(xì)胞自殺。PAC-1在小鼠模型中顯示出良好的效果，并且正在進(jìn)一步評(píng)估其在人類中的使用。2010年，一項(xiàng)發(fā)表的研究表明PAC-1對(duì)研究犬是安全的，同年晚些時(shí)候發(fā)表的第二項(xiàng)研究報(bào)告說(shuō)，在一項(xiàng)小型的I期臨床試驗(yàn)中，PAC-1衍生物（稱為S-PAC-1）具有良好的耐受性。淋巴瘤的寵物狗。即使在低劑量的S-PAC-1中，腫瘤也會(huì)在1/6只狗中消退，并且在3/6只狗中疾病得以穩(wěn)定（沒(méi)有額外的腫瘤生長(zhǎng)）。
2、PAC-1是caspase 3激活劑。Caspase激活是癌癥治療中的關(guān)鍵策略。半胱天冬酶3是關(guān)鍵的執(zhí)行者半胱天冬酶和凋亡的直接效應(yīng)子。許多癌癥的標(biāo)志是規(guī)避of子手胱天蛋白酶激活和凋亡反應(yīng)喪失的信號(hào)。半胱天冬酶3激活的EC 50 = 0.33μM，半胱天冬酶7 = 4.5μM。凋亡誘導(dǎo)的IC 50 = 0.92μM。癌細(xì)胞系和組織中caspase 3的水平升高使PAC-1選擇性地誘導(dǎo)組織中的細(xì)胞凋亡。
3、脯氨酸蛋白酶激活化合物1（PAC-1）是鄰羥基N-酰基肼化合物。對(duì)多種癌細(xì)胞具有細(xì)胞毒性，例如淋巴瘤，白血病，乳腺癌和成膠質(zhì)細(xì)胞瘤。高劑量的PAC-1可以促進(jìn)神經(jīng)興奮。PAC-1有助于原酶蛋白酶的體外自激活，PAC-1可作為其他蛋白酶激活化合物的原型。 procaspase-3的PAC-1依賴性激活與鋅的螯合有關(guān)。
1、PAC-1被稱為首個(gè)激活蛋白酶的化合物，可選擇性誘導(dǎo)癌細(xì)胞中的細(xì)胞凋亡或細(xì)胞自殺。PAC-1在小鼠模型中顯示出良好的效果，并且正在進(jìn)一步評(píng)估其在人類中的使用。2010年，一項(xiàng)發(fā)表的研究表明PAC-1對(duì)研究犬是安全的，同年晚些時(shí)候發(fā)表的第二項(xiàng)研究報(bào)告說(shuō)，在一項(xiàng)小型的I期臨床試驗(yàn)中，PAC-1衍生物（稱為S-PAC-1）具有良好的耐受性。淋巴瘤的寵物狗。即使在低劑量的S-PAC-1中，腫瘤也會(huì)在1/6只狗中消退，并且在3/6只狗中疾病得以穩(wěn)定（沒(méi)有額外的腫瘤生長(zhǎng)）。
2、PAC-1是caspase 3激活劑。Caspase激活是癌癥治療中的關(guān)鍵策略。半胱天冬酶3是關(guān)鍵的執(zhí)行者半胱天冬酶和凋亡的直接效應(yīng)子。許多癌癥的標(biāo)志是規(guī)避of子手胱天蛋白酶激活和凋亡反應(yīng)喪失的信號(hào)。半胱天冬酶3激活的EC 50 = 0.33μM，半胱天冬酶7 = 4.5μM。凋亡誘導(dǎo)的IC 50 = 0.92μM。癌細(xì)胞系和組織中caspase 3的水平升高使PAC-1選擇性地誘導(dǎo)組織中的細(xì)胞凋亡。
3、脯氨酸蛋白酶激活化合物1（PAC-1）是鄰羥基N-酰基肼化合物。對(duì)多種癌細(xì)胞具有細(xì)胞毒性，例如淋巴瘤，白血病，乳腺癌和成膠質(zhì)細(xì)胞瘤。高劑量的PAC-1可以促進(jìn)神經(jīng)興奮。PAC-1有助于原酶蛋白酶的體外自激活，PAC-1可作為其他蛋白酶激活化合物的原型。 procaspase-3的PAC-1依賴性激活與鋅的螯合有關(guān)。
| 警示圖 | |
| 危險(xiǎn)性 | warning |
| 危險(xiǎn)性警示 | Not available |
| 安全聲明 | H303+H313+H333 |
| 安全防護(hù) | P264+P280+P305+P351+P338+P337+P313 |
| 備注 | 實(shí)驗(yàn)過(guò)程中防止吸入、食入，做好安全防護(hù) |
PAC-1(315183-21-2,procaspase activating compound-1)危害標(biāo)識(shí)：
| 象形圖 |  |
| 信號(hào) | Warning |
| GHS危險(xiǎn)說(shuō)明 | Aggregated GHS information provided by 38 companies from 1 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies. |
| H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral] | |
| H315 (100%): Causes skin irritation [Warning Skin corrosion/irritation] | |
| H319 (100%): Causes serious eye irritation [Warning Serious eye damage/eye irritation] | |
| H335 (100%): May cause respiratory irritation [Warning Specific target organ toxicity, single exposure; Respiratory tract irritation] | |
| H400 (100%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard] | |
| Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. | |
| 防范說(shuō)明代碼 | P261, P264, P270, P271, P273, P280, P301+P312, P302+P352, P304+P340, P305+P351+P338, P312, P321, P330, P332+P313, P337+P313, P362, P391, P403+P233, P405, and P501 |
| (The corresponding statement to each P-code can be found at the GHS Classification page.) |
| Wang F, et al. A novel small-molecule activator of procaspase-3 induces apoptosis in cancer cells and reduces tumor growth in human breast, liver and gallbladder cancer xenografts. Mol Oncol. 2014 Dec |
| Seervi M, et al. ERO1α-dependent endoplasmic reticulum-mitochondrial calcium flux contributes to ER stress and mitochondrial permeabilization by procaspase-activating compound-1 (PAC-1). Cell Death Di |
| Putt KS, et al. Small-molecule activation of procaspase-3 to caspase-3 as a personalized anticancer strategy. Nat Chem Biol. 2006 Oct;2(10):543-50. |
| Parallel signaling pathways of pituitary adenylate cyclase activating polypeptide (PACAP) regulate several intrinsic ion channels PMID 31162688; Annals of the New York Academy of Sciences 2019 11; 145 |
| Protamine stimulates platelet aggregation in vitro with activation of the fibrinogen receptor and alpha-granule release, but impairs secondary activation via ADP and thrombin receptors PMID 31992110; |
PAC-1(315183-21-2,procaspase activating compound-1)參考文獻(xiàn)：
1.The Effect of Regular Intake of Dry-Cured Ham Rich in Bioactive Peptides on Inflammation, Platelet and Monocyte Activation Markers in Humans.
Martínez-Sánchez SM;Minguela A;Prieto-Merino D;Zafrilla-Rentero MP;Abellán-Alemán J;Montoro-García S Nutrients. 2017 Mar 23;9(4). pii: E321. doi: 10.3390/nu9040321.
Background and aims;: Dietary studies have shown that active biopeptides provide protective health benefits, although the mediating pathways are somewhat uncertain. To throw light on this situation, we studied the effects of consuming Spanish dry-cured ham on platelet function, monocyte activation markers and the inflammatory status of healthy humans with pre-hypertension. ;Methods;: Thirty-eight healthy volunteers with systolic blood pressure of >125 mmHg were enrolled in a two-arm crossover randomized controlled trial. Participants received 80 g/day dry-cured pork ham of >11 months proteolysis or 100 g/day cooked ham (control product) for 4 weeks followed by a 2-week washout before "crossing over" to the other treatment for 4 more weeks. Soluble markers and cytokines were analyzed by ELISA. Platelet function was assessed by measuring P-selectin expression and PAC-1 binding after ADP (adenosine diphosphate) stimulation using whole blood flow cytometry. Monocyte markers of the pathological status (adhesion, inflammatory and scavenging receptors) were also measured by flow cytometry in the three monocyte subsets after the interventional period. ;Results;: The mean differences between dry-cured ham and cooked ham followed by a time period adjustment for plasmatic P-selectin and interleukin 6 proteins slightly failed (;p =; 0.
2.Localization of the pituitary adenylate cyclase-activating polypeptide receptor and its mRNA in the rat adrenal medulla.
Shioda S;Shimoda Y;Hori T;Mizushima H;Ajiri T;Funahashi H;Ohtaki K;Ryushi T Neurosci Lett. 2000 Dec 8;295(3):81-4.
We examined the localization of the pituitary adenylate cyclase-activating peptide (PACAP) receptor (PAC1-R) and its mRNA with immunocytochemistry and in situ hybridization, respectively. PAC1-R immunoreactivity and its transcript were detected in both chromaffin cells and ganglion cells but not detected in the adrenal cortex. In addition, strong PAC1-R immunoreactivity was found beneath the plasma membrane of the immunoreactive medullary cells. Electron microscopic immunocytochemistry revealed that PAC1-R was predominantly expressed in adrenaline-containing cells. This report supports the notion that PACAP is an activator and modulator of catecholamine secretion as well as synthesis in the adrenal medulla.
3.Magnitude and time course of platelet inhibition with Aggrenox and Aspirin in patients after ischemic stroke: the AGgrenox versus Aspirin Therapy Evaluation (AGATE) trial.
Serebruany VL;Malinin AI;Sane DC;Jilma B;Takserman A;Atar D;Hennekens CH Eur J Pharmacol. 2004 Sep 24;499(3):315-24.
The European Stroke Prevention Study showed greater stroke prevention for Aggrenox than either for aspirin or dipyridamole alone. To test whether Aggrenox has superior antiplatelet properties to aspirin alone we conducted the AGgrenox versus Aspirin Therapy Evaluation (AGATE) trial. Forty patients with prior ischemic stroke not taking aspirin for at least 30 days were randomized to Aggrenox (2 pills/daily) or aspirin (81 mg plus matching placebo/daily) for 30 days. Platelet function was assessed at baseline, 24 h, and days 3, 7, 15, and 30 by aggregometry, flow cytometry and cartridge-based analyzers. Both Aggrenox and aspirin provided fast and sustained platelet inhibition. Aggrenox(R), however, especially after 15 days, showed significant prolongation of the closure time (P=0.04), diminished expression of platelet/endothelial cell adhesion molecule-1 (PECAM-1) (P=0.01), glycoprotein IIb (GPIIb) antigen (P=0.02), and GPIIb/IIIa activity (P=0.01) by PAC-1 C antibody, CD63 (P=0.03), as well as inhibition of Protease Activated Receptors (PAR-1) associated with intact (SPAN12, P=0.01) and cleaved (WEDE15, P=0.01) thrombin receptors as compared with aspirin. Surprisingly, GPIb expression increased, especially after aspirin.
1.The Effect of Regular Intake of Dry-Cured Ham Rich in Bioactive Peptides on Inflammation, Platelet and Monocyte Activation Markers in Humans.
Martínez-Sánchez SM;Minguela A;Prieto-Merino D;Zafrilla-Rentero MP;Abellán-Alemán J;Montoro-García S Nutrients. 2017 Mar 23;9(4). pii: E321. doi: 10.3390/nu9040321.
Background and aims;: Dietary studies have shown that active biopeptides provide protective health benefits, although the mediating pathways are somewhat uncertain. To throw light on this situation, we studied the effects of consuming Spanish dry-cured ham on platelet function, monocyte activation markers and the inflammatory status of healthy humans with pre-hypertension. ;Methods;: Thirty-eight healthy volunteers with systolic blood pressure of >125 mmHg were enrolled in a two-arm crossover randomized controlled trial. Participants received 80 g/day dry-cured pork ham of >11 months proteolysis or 100 g/day cooked ham (control product) for 4 weeks followed by a 2-week washout before "crossing over" to the other treatment for 4 more weeks. Soluble markers and cytokines were analyzed by ELISA. Platelet function was assessed by measuring P-selectin expression and PAC-1 binding after ADP (adenosine diphosphate) stimulation using whole blood flow cytometry. Monocyte markers of the pathological status (adhesion, inflammatory and scavenging receptors) were also measured by flow cytometry in the three monocyte subsets after the interventional period. ;Results;: The mean differences between dry-cured ham and cooked ham followed by a time period adjustment for plasmatic P-selectin and interleukin 6 proteins slightly failed (;p =; 0.
2.Localization of the pituitary adenylate cyclase-activating polypeptide receptor and its mRNA in the rat adrenal medulla.
Shioda S;Shimoda Y;Hori T;Mizushima H;Ajiri T;Funahashi H;Ohtaki K;Ryushi T Neurosci Lett. 2000 Dec 8;295(3):81-4.
We examined the localization of the pituitary adenylate cyclase-activating peptide (PACAP) receptor (PAC1-R) and its mRNA with immunocytochemistry and in situ hybridization, respectively. PAC1-R immunoreactivity and its transcript were detected in both chromaffin cells and ganglion cells but not detected in the adrenal cortex. In addition, strong PAC1-R immunoreactivity was found beneath the plasma membrane of the immunoreactive medullary cells. Electron microscopic immunocytochemistry revealed that PAC1-R was predominantly expressed in adrenaline-containing cells. This report supports the notion that PACAP is an activator and modulator of catecholamine secretion as well as synthesis in the adrenal medulla.
3.Magnitude and time course of platelet inhibition with Aggrenox and Aspirin in patients after ischemic stroke: the AGgrenox versus Aspirin Therapy Evaluation (AGATE) trial.
Serebruany VL;Malinin AI;Sane DC;Jilma B;Takserman A;Atar D;Hennekens CH Eur J Pharmacol. 2004 Sep 24;499(3):315-24.
The European Stroke Prevention Study showed greater stroke prevention for Aggrenox than either for aspirin or dipyridamole alone. To test whether Aggrenox has superior antiplatelet properties to aspirin alone we conducted the AGgrenox versus Aspirin Therapy Evaluation (AGATE) trial. Forty patients with prior ischemic stroke not taking aspirin for at least 30 days were randomized to Aggrenox (2 pills/daily) or aspirin (81 mg plus matching placebo/daily) for 30 days. Platelet function was assessed at baseline, 24 h, and days 3, 7, 15, and 30 by aggregometry, flow cytometry and cartridge-based analyzers. Both Aggrenox and aspirin provided fast and sustained platelet inhibition. Aggrenox(R), however, especially after 15 days, showed significant prolongation of the closure time (P=0.04), diminished expression of platelet/endothelial cell adhesion molecule-1 (PECAM-1) (P=0.01), glycoprotein IIb (GPIIb) antigen (P=0.02), and GPIIb/IIIa activity (P=0.01) by PAC-1 C antibody, CD63 (P=0.03), as well as inhibition of Protease Activated Receptors (PAR-1) associated with intact (SPAN12, P=0.01) and cleaved (WEDE15, P=0.01) thrombin receptors as compared with aspirin. Surprisingly, GPIb expression increased, especially after aspirin.
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微流控鍵合解決方案：微流控芯片制造的一個(gè)重要環(huán)節(jié)，也是最容易被忽視的--芯片鍵合。其中一個(gè)重要因素是：微流控...
2023/7/27 12:44:28
