購物車 
-
PFK-158
- names：
PFK-158
- CAS號(hào)：
1462249-75-7
MDL Number： MFCD28386154 - MF(分子式)： C18H11F3N2O MW(分子量)： 328.29
- EINECS: Reaxys Number:
- Pubchem ID:71730058 Brand:BIOFOUNT
PFK-158(1462249-75-7,ACT-PFK-158)是一種有效的，選擇性的PFKFB3抑制劑，IC50 PFK-158具有廣泛的抗腫瘤活性。PFK-158還可以增強(qiáng)。大約137nM。PFK-158可減少葡萄糖中葡萄糖的攝取，ATP的產(chǎn)生，乳酸的釋放，并誘導(dǎo)細(xì)胞分解和自噬。 Colistin對(duì)細(xì)菌的抵抗力。
| 貨品編碼 | 規(guī)格 | 純度 | 價(jià)格 (￥) | 現(xiàn)價(jià)(￥) | 特價(jià)(￥) | 庫存描述 | 數(shù)量 | 總計(jì) (￥) |
|---|---|---|---|---|---|---|---|---|
| YZM001265-10mg | 10mg | 98.85% | ￥ 1215.00 | ￥ 1215.00 | 2-3天 | ￥ 0.00 | ||
| YZM001265-5mg | 5mg | 98.85% | ￥ 780.00 | ￥ 780.00 | 2-3天 | ￥ 0.00 |
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| 中文別名 | PFK-158(1462249-75-7); PFK158；PFK 158；PFK158；ACTPFK158;(2E)-1-(4-吡啶基)-3-[7-(三氟甲基)-2-喹啉基]-2-丙烯-1-酮;PFKFB3抑制劑(PFK-158); |
| 英文別名 | PFK-158(1462249-75-7);PFK158; PFK 158; PFK158; ACTPFK158;:PFK-158;PFK-158, ACT-PFK-158;(2E)-1-(4-Pyridinyl)-3-[7-(trifluoromethyl)-2-quinolinyl]-2-propen-1-one;PFK-158;PFK 158;PFK-158 free base; |
| CAS號(hào) | 1462249-75-7 |
| Inchi | InChI=1S/C18H11F3N2O/c19-18(20,21)14-3-1-12-2-4-15(23-16(12)11-14)5-6-17(24)13-7-9-22-10-8-13/h1-11H/b6-5+ |
| InchiKey | IAJOMYABKVAZCN-AATRIKPKSA-N |
| 分子式 Formula | C18H11F3N2O |
| 分子量 Molecular Weight | 328.29 |
| 溶解度Solubility | 生物體外In Vitro:DMSO溶解度≥ 30 mg/mL(91.38 mM)H2O< 0.1 mg/mL(insoluble)*"≥" means soluble可溶, but saturation unknown溶解度未知. |
| 性狀 | 固體粉末,Power |
| 儲(chǔ)藏條件 Storage conditions | -20°C 3 years年 4°C 2 years年 / In solvent溶液中:-80°C 6 months月 -20°C 1 month月 |
PFK-158(1462249-75-7,ACT-PFK-158)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:PFK-158試劑,PFK-158雜質(zhì),PFK-158中間體,PFK-158密度,PFK-158溶解度,PFK-158旋光度,PFK-158合成,PFK-158閃點(diǎn),PFK-158熔點(diǎn),PFK-158購買,
| 產(chǎn)品說明 | PFK-158(1462249-75-7,ACT-PFK-158)是一種有效且選擇性的PFKFB3抑制劑,目前正在I期研究中對(duì)晚期實(shí)體惡性腫瘤患者進(jìn)行研究. |
| Introduction | PFK-158(1462249-75-7,ACT-PFK-158)is a potent and selective inhibitor of PFKFB3 that is currently being investigated in a phase I study in patients with advanced solid malignancies. |
| Application1 | |
| Application2 | |
| Application3 |
PFK-158(1462249-75-7,ACT-PFK-158)藥理學(xué)：
1、PFK-158是一種有效且選擇性的PFKFB3抑制劑，目前正在I期研究中對(duì)晚期實(shí)體惡性腫瘤患者進(jìn)行研究。；目標(biāo)：PFKFB3；體外：PFK-158是第一種在癌癥患者中進(jìn)行臨床試驗(yàn)的6-磷酸果糖-2-激酶/果糖-2,6-雙磷酸酶3（PFKFB3）抑制劑。PFK-158是一種小分子治療性候選藥物，可在人類臨床試驗(yàn)中從未檢測(cè)到的可滅活新型癌癥代謝靶標(biāo)的物質(zhì)。PFK-158不僅是一流的抗癌藥物，而且還是第一個(gè)通過抑制PFKFB3靶向葡萄糖代謝的藥物。PFK-158是重組PFKFB3的納摩爾抑制劑。PFK-158在癌細(xì)胞中抑制PFKFB3活性和糖酵解。體內(nèi)：PFK158在大鼠和狗中具有良好的耐受性，可產(chǎn)生可接受的臨床前治療指數(shù)。PFK158在人源性腫瘤的多個(gè)臨床前小鼠模型和同系小鼠模型中非常有效。
2、PFK-158也稱為ACT-PFK-158，是6-磷酸果糖-2-激酶/果糖-2,6-雙磷酸酶（PFK-2 / FBPase）同工型3（PFKFB3）和3-（ 3-吡啶基）-1- [4-吡啶基] -2-丙烯-1-酮（3PO），具有潛在的抗腫瘤活性。給藥后，PFKFB3抑制劑PFK-158結(jié)合并抑制PFKFB3的活性，從而抑制癌細(xì)胞中的糖酵解途徑和葡萄糖攝取。與正常的健康細(xì)胞相比，這可以防止大分子的產(chǎn)生和能量的產(chǎn)生，從而導(dǎo)致癌細(xì)胞中細(xì)胞增殖的增強(qiáng)。剝奪癌細(xì)胞的營養(yǎng)和能量會(huì)導(dǎo)致癌細(xì)胞生長受到抑制。PFKFB3，一種催化果糖6-磷酸轉(zhuǎn)化為果糖2,6-雙磷酸的酶，在人類癌細(xì)胞中高表達(dá)和活躍；它在增加癌細(xì)胞的糖酵解通量和增殖中起關(guān)鍵作用。
1、PFK-158是一種有效且選擇性的PFKFB3抑制劑，目前正在I期研究中對(duì)晚期實(shí)體惡性腫瘤患者進(jìn)行研究。；目標(biāo)：PFKFB3；體外：PFK-158是第一種在癌癥患者中進(jìn)行臨床試驗(yàn)的6-磷酸果糖-2-激酶/果糖-2,6-雙磷酸酶3（PFKFB3）抑制劑。PFK-158是一種小分子治療性候選藥物，可在人類臨床試驗(yàn)中從未檢測(cè)到的可滅活新型癌癥代謝靶標(biāo)的物質(zhì)。PFK-158不僅是一流的抗癌藥物，而且還是第一個(gè)通過抑制PFKFB3靶向葡萄糖代謝的藥物。PFK-158是重組PFKFB3的納摩爾抑制劑。PFK-158在癌細(xì)胞中抑制PFKFB3活性和糖酵解。體內(nèi)：PFK158在大鼠和狗中具有良好的耐受性，可產(chǎn)生可接受的臨床前治療指數(shù)。PFK158在人源性腫瘤的多個(gè)臨床前小鼠模型和同系小鼠模型中非常有效。
2、PFK-158也稱為ACT-PFK-158，是6-磷酸果糖-2-激酶/果糖-2,6-雙磷酸酶（PFK-2 / FBPase）同工型3（PFKFB3）和3-（ 3-吡啶基）-1- [4-吡啶基] -2-丙烯-1-酮（3PO），具有潛在的抗腫瘤活性。給藥后，PFKFB3抑制劑PFK-158結(jié)合并抑制PFKFB3的活性，從而抑制癌細(xì)胞中的糖酵解途徑和葡萄糖攝取。與正常的健康細(xì)胞相比，這可以防止大分子的產(chǎn)生和能量的產(chǎn)生，從而導(dǎo)致癌細(xì)胞中細(xì)胞增殖的增強(qiáng)。剝奪癌細(xì)胞的營養(yǎng)和能量會(huì)導(dǎo)致癌細(xì)胞生長受到抑制。PFKFB3，一種催化果糖6-磷酸轉(zhuǎn)化為果糖2,6-雙磷酸的酶，在人類癌細(xì)胞中高表達(dá)和活躍；它在增加癌細(xì)胞的糖酵解通量和增殖中起關(guān)鍵作用。
| 警示圖 | |
| 危險(xiǎn)性 | warning |
| 危險(xiǎn)性警示 | Not available |
| 安全聲明 | H303吞入可能有害+H313皮膚接觸可能有害+H2413吸入可能對(duì)身體有害 |
| 安全防護(hù) | P264處理后徹底清洗+P280戴防護(hù)手套/穿防護(hù)服/戴防護(hù)眼罩/戴防護(hù)面具+P305如果進(jìn)入眼睛+P351用水小心沖洗幾分鐘+P338取出隱形眼鏡（如果有）并且易于操作,繼續(xù)沖洗+P337如果眼睛刺激持續(xù)+P2393獲得醫(yī)療建議/護(hù)理 |
| 備注 | 實(shí)驗(yàn)過程中防止吸入、食入，做好安全防護(hù) |
| Mondal S, et al. Therapeutic targeting of PFKFB3 with a novel glycolytic inhibitor PFK158 promotes lipophagy and chemosensitivity in gynecologic cancers. Int J Cancer. 2019 Jan 1;144(1):178-189. |
| Zhang Y, et al. Synergistic Effect of Colistin Combined with PFK-158 against Colistin-Resistant Enterobacteriaceae. Antimicrob Agents Chemother. 2019 Jun 24;63(7). pii: e00271-19. |
| Pooran Chand, et al. Pfkfb3 inhibitor and methods of use as an anti-cancer therapeutic. WO2013148228A1. |
PFK-158(1462249-75-7,ACT-PFK-158)參考文獻(xiàn)：
1、Therapeutic targeting of PFKFB3 with a novel glycolytic inhibitor PFK158 promotes lipophagy and chemosensitivity in gynecologic cancers
Susmita Mondal 1 2, Debarshi Roy 1, Sayantani Sarkar Bhattacharya 1, Ling Jin 1, Deokbeom Jung 1, Song Zhang 3, Eleftheria Kalogera 4, Julie Staub 1, Yaxian Wang 1, Wen Xuyang 1, Ashwani Khurana 1, Jeremey Chien 5, Sucheta Telang 6, Jason Chesney 6, Gilles Tapolsky 7, Dzeja Petras 3, Viji Shridhar
Abstract Metabolic alterations are increasingly recognized as important novel anti-cancer targets. Among several regulators of metabolic alterations, fructose 2,6 bisphosphate (F2,6BP) is a critical glycolytic regulator. Inhibition of the active form of PFKFB3ser461 using a novel inhibitor, PFK158 resulted in reduced glucose uptake, ATP production, lactate release as well as induction of apoptosis in gynecologic cancer cells. Moreover, we found that PFK158 synergizes with carboplatin (CBPt) and paclitaxel (PTX) in the chemoresistant cell lines, C13 and HeyA8MDR but not in their chemosensitive counterparts, OV2008 and HeyA8, respectively. We determined that PFK158-induced autophagic flux leads to lipophagy resulting in the downregulation of cPLA2, a lipid droplet (LD) associated protein. Immunofluorescence and co-immunoprecipitation revealed colocalization of p62/SQSTM1 with cPLA2 in HeyA8MDR cells uncovering a novel pathway for the breakdown of LDs promoted by PFK158. Interestingly, treating the cells with the autophagic inhibitor bafilomycin A reversed the PFK158-mediated synergy and lipophagy in chemoresistant cells. Finally, in a highly metastatic PTX-resistant in vivo ovarian mouse model, a combination of PFK158 with CBPt significantly reduced tumor weight and ascites and reduced LDs in tumor tissue as seen by immunofluorescence and transmission electron microscopy compared to untreated mice. Since the majority of cancer patients will eventually recur and develop chemoresistance, our results suggest that PFK158 in combination with standard chemotherapy may have a direct clinical role in the treatment of recurrent cancer.
2、PFKFB3 inhibition reprograms malignant pleural mesothelioma to nutrient stress-induced macropinocytosis and ER stress as independent binary adaptive responses
Sayantani Sarkar Bhattacharya 1 2, Prabhu Thirusangu 1, Ling Jin 1, Debarshi Roy 1, Deokbeom Jung 1, Yinan Xiao 1, Julie Staub 1, Bhaskar Roy 3, Julian R Molina 4, Viji Shridhar
Abstract The metabolic signatures of cancer cells are often associated with elevated glycolysis. Pharmacological (PFK158 treatment) and genetic inhibition of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), a critical control point in the glycolytic pathway, decreases glucose uptake, ATP production, and lactate dehydrogenase activity and arrests malignant pleural mesothelioma (MPM) cells in the G0/G1 phase to induce cell death. To overcome this nutrient stress, inhibition of PFKFB3 activity led to an escalation in endoplasmic reticulum (ER) activity and aggravated ER stress mostly by upregulating BiP and GADD153 expression and activation of the endocytic Rac1-Rab5-Rab7 pathway resulting in a unique form of cell death called "methuosis" in both the sarcomatoid (H28) and epithelioid (EMMeso) cells. Transmission electron microscopy (TEM) analysis showed the formation of nascent macropinocytotic vesicles, which rapidly coalesced to form large vacuoles with compromised lysosomal function. Both immunofluorescence microscopy and co-immunoprecipitation analyses revealed that upon PFKFB3 inhibition, two crucial biomolecules of each pathway, Rac1 and Calnexin interact with each other. Finally, PFK158 alone and in combination with carboplatin-inhibited tumorigenesis of EMMeso xenografts in vivo. Since most cancer cells exhibit an increased glycolytic rate, these results provide evidence for PFK158, in combination with standard chemotherapy, may have a potential in the treatment of MPM.
3、Synergistic Effect of Colistin Combined with PFK-158 against Colistin-Resistant Enterobacteriaceae
Youwen Zhang 1, Xiukun Wang 1, Xue Li 1, Limin Dong 1, Xinxin Hu 1, Tongying Nie 1, Yun Lu 1, Xi Lu 1, Jing Pang 1, Guoqing Li 1, Xinyi Yang 1, Congran Li 1, Xuefu You
Abstract As increasing numbers of colistin-resistant bacteria emerge, new therapies are urgently needed to treat infections caused by these pathogens. The discovery of new combination therapies is one important way to solve such problems. Here, we report that the antitumor drug PFK-158 and its analogs PFK-015 and 3PO can exert synergistic effects with colistin against colistin-resistant Enterobacteriaceae, including mcr-1-positive or high-level-colistin-resistant (HLCR) isolates, as shown by a checkerboard assay. The results of a time-kill assay revealed that colistin combined with PFK-158 continuously eliminated colistin-resistant Escherichia coli 13-43, Klebsiella pneumoniae H04, and Enterobacter cloacae D01 in 24 h. Images from scanning electron microscopy (SEM) at 5 h postinoculation confirmed the killing effect of the combination. Finally, in vivo treatment showed that PFK-158 had a better synergistic effect than its analogs. Compared to the corresponding rates after colistin monotherapy, the survival rates of systemically infected mice were significantly increased 30% or 60% when the mice received an intravenous injection of colistin in combination with 15 mg/kg of body weight PFK-158. These results have important implications for repurposing PFK-158 to combat colistin resistance.
1、Therapeutic targeting of PFKFB3 with a novel glycolytic inhibitor PFK158 promotes lipophagy and chemosensitivity in gynecologic cancers
Susmita Mondal 1 2, Debarshi Roy 1, Sayantani Sarkar Bhattacharya 1, Ling Jin 1, Deokbeom Jung 1, Song Zhang 3, Eleftheria Kalogera 4, Julie Staub 1, Yaxian Wang 1, Wen Xuyang 1, Ashwani Khurana 1, Jeremey Chien 5, Sucheta Telang 6, Jason Chesney 6, Gilles Tapolsky 7, Dzeja Petras 3, Viji Shridhar
Abstract Metabolic alterations are increasingly recognized as important novel anti-cancer targets. Among several regulators of metabolic alterations, fructose 2,6 bisphosphate (F2,6BP) is a critical glycolytic regulator. Inhibition of the active form of PFKFB3ser461 using a novel inhibitor, PFK158 resulted in reduced glucose uptake, ATP production, lactate release as well as induction of apoptosis in gynecologic cancer cells. Moreover, we found that PFK158 synergizes with carboplatin (CBPt) and paclitaxel (PTX) in the chemoresistant cell lines, C13 and HeyA8MDR but not in their chemosensitive counterparts, OV2008 and HeyA8, respectively. We determined that PFK158-induced autophagic flux leads to lipophagy resulting in the downregulation of cPLA2, a lipid droplet (LD) associated protein. Immunofluorescence and co-immunoprecipitation revealed colocalization of p62/SQSTM1 with cPLA2 in HeyA8MDR cells uncovering a novel pathway for the breakdown of LDs promoted by PFK158. Interestingly, treating the cells with the autophagic inhibitor bafilomycin A reversed the PFK158-mediated synergy and lipophagy in chemoresistant cells. Finally, in a highly metastatic PTX-resistant in vivo ovarian mouse model, a combination of PFK158 with CBPt significantly reduced tumor weight and ascites and reduced LDs in tumor tissue as seen by immunofluorescence and transmission electron microscopy compared to untreated mice. Since the majority of cancer patients will eventually recur and develop chemoresistance, our results suggest that PFK158 in combination with standard chemotherapy may have a direct clinical role in the treatment of recurrent cancer.
2、PFKFB3 inhibition reprograms malignant pleural mesothelioma to nutrient stress-induced macropinocytosis and ER stress as independent binary adaptive responses
Sayantani Sarkar Bhattacharya 1 2, Prabhu Thirusangu 1, Ling Jin 1, Debarshi Roy 1, Deokbeom Jung 1, Yinan Xiao 1, Julie Staub 1, Bhaskar Roy 3, Julian R Molina 4, Viji Shridhar
Abstract The metabolic signatures of cancer cells are often associated with elevated glycolysis. Pharmacological (PFK158 treatment) and genetic inhibition of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), a critical control point in the glycolytic pathway, decreases glucose uptake, ATP production, and lactate dehydrogenase activity and arrests malignant pleural mesothelioma (MPM) cells in the G0/G1 phase to induce cell death. To overcome this nutrient stress, inhibition of PFKFB3 activity led to an escalation in endoplasmic reticulum (ER) activity and aggravated ER stress mostly by upregulating BiP and GADD153 expression and activation of the endocytic Rac1-Rab5-Rab7 pathway resulting in a unique form of cell death called "methuosis" in both the sarcomatoid (H28) and epithelioid (EMMeso) cells. Transmission electron microscopy (TEM) analysis showed the formation of nascent macropinocytotic vesicles, which rapidly coalesced to form large vacuoles with compromised lysosomal function. Both immunofluorescence microscopy and co-immunoprecipitation analyses revealed that upon PFKFB3 inhibition, two crucial biomolecules of each pathway, Rac1 and Calnexin interact with each other. Finally, PFK158 alone and in combination with carboplatin-inhibited tumorigenesis of EMMeso xenografts in vivo. Since most cancer cells exhibit an increased glycolytic rate, these results provide evidence for PFK158, in combination with standard chemotherapy, may have a potential in the treatment of MPM.
3、Synergistic Effect of Colistin Combined with PFK-158 against Colistin-Resistant Enterobacteriaceae
Youwen Zhang 1, Xiukun Wang 1, Xue Li 1, Limin Dong 1, Xinxin Hu 1, Tongying Nie 1, Yun Lu 1, Xi Lu 1, Jing Pang 1, Guoqing Li 1, Xinyi Yang 1, Congran Li 1, Xuefu You
Abstract As increasing numbers of colistin-resistant bacteria emerge, new therapies are urgently needed to treat infections caused by these pathogens. The discovery of new combination therapies is one important way to solve such problems. Here, we report that the antitumor drug PFK-158 and its analogs PFK-015 and 3PO can exert synergistic effects with colistin against colistin-resistant Enterobacteriaceae, including mcr-1-positive or high-level-colistin-resistant (HLCR) isolates, as shown by a checkerboard assay. The results of a time-kill assay revealed that colistin combined with PFK-158 continuously eliminated colistin-resistant Escherichia coli 13-43, Klebsiella pneumoniae H04, and Enterobacter cloacae D01 in 24 h. Images from scanning electron microscopy (SEM) at 5 h postinoculation confirmed the killing effect of the combination. Finally, in vivo treatment showed that PFK-158 had a better synergistic effect than its analogs. Compared to the corresponding rates after colistin monotherapy, the survival rates of systemically infected mice were significantly increased 30% or 60% when the mice received an intravenous injection of colistin in combination with 15 mg/kg of body weight PFK-158. These results have important implications for repurposing PFK-158 to combat colistin resistance.
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