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36167-63-2
  • names:

    Halofantrine hydrochloride

  • CAS號:

    36167-63-2

    MDL Number: MFCD00879136
  • MF(分子式): C26H31Cl3F3NO MW(分子量): 536.88
  • EINECS:252-895-4 Reaxys Number:
  • Pubchem ID:37392 Brand:BIOFOUNT
鹽酸鹵泛群
鹽酸鹵泛群(36167-63-2,Halofantrine hydrochloride)是一種通過抑制人ERG通道來延遲整流鉀電流的阻滯劑,是一種有效的抗瘧疾產(chǎn)品。
貨品編碼 規(guī)格 純度 價格 (¥) 現(xiàn)價(¥) 特價(¥) 庫存描述 數(shù)量 總計 (¥)
YZM000818-10mg 10mg >98.0% ¥ 2328.00 ¥ 2328.00 2-3天
- +
0.00
YZM000818-5mg 5mg >98.0% ¥ 1268.00 ¥ 1268.00 2-3天
- +
0.00
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中文別名 鹽酸鹵泛群(36167-63-2,Halofantrine hydrochloride);鹵泛群鹽酸鹽
英文別名 Halofantrine hydrochloride(36167-63-2)
CAS號 36167-63-2
Inchi InChI=1S/C26H30Cl2F3NO.ClH/c1-3-5-10-32(11-6-4-2)12-9-25(33)23-16-22-21(14-18(27)15-24(22)28)20-13-17(26(29,30)31)7-8-19(20)23;/h7-8,13-16,25,33H,3-6,9-12H2,1-2H3;1H
InchiKey WANGFTDWOFGECH-UHFFFAOYSA-N
分子式 Formula C26H31Cl3F3NO
分子量 Molecular Weight 536.88
溶解度Solubility 生物體外In Vitro:DMSO溶解度30 mg/mL(55.88 mM;Need ultrasonic)
性狀 白色至灰白色固體粉末
儲藏條件 Storage conditions -20°C 3 years年 4°C 2 years年 /溶液中:-80°C 6 months月 -20°C 1 month月

鹽酸鹵泛群(36167-63-2,Halofantrine hydrochloride)毒性測試:
生物 測試類型 路線 報告劑量(標(biāo)準(zhǔn)化劑量) 影響 參考
man TDLo oral 7143ug/kg (7.143mg/kg) LIVER: LIVER FUNCTION TESTS IMPAIRED

KIDNEY, URETER, AND BLADDER: URINE VOLUME DECREASED

KIDNEY, URETER, AND BLADDER: HEMATURIA
Lancet. Vol. 340, Pg. 909, 1992.
man TDLo oral 7143ug/kg (7.143mg/kg) LIVER: "JAUNDICE, OTHER OR UNCLASSIFIED"

BLOOD: OTHER HEMOLYSIS WITH OR WITHOUT ANEMIA

KIDNEY, URETER, AND BLADDER: URINE VOLUME DECREASED
Lancet. Vol. 340, Pg. 909, 1992.
man TDLo oral 18mg/kg/D (18mg/kg) GASTROINTESTINAL: OTHER CHANGES

GASTROINTESTINAL: NAUSEA OR VOMITING
Drugs of the Future. Vol. 5, Pg. 547, 1980.
rat LD50 intraperitoneal 2050mg/kg (2050mg/kg)   Acta Tropica. Vol. 37, Pg. 232, 1980.
rat LD50 intraperitoneal 2050mg/kg (2050mg/kg) GASTROINTESTINAL: NAUSEA OR VOMITING Acta Tropica. Vol. 37, Pg. 232, 1980.
rat LD50 oral 3400mg/kg (3400mg/kg)   Acta Tropica. Vol. 37, Pg. 232, 1980.
rat LD50 oral 3400mg/kg (3400mg/kg) GASTROINTESTINAL: NAUSEA OR VOMITING Acta Tropica. Vol. 37, Pg. 232, 1980.
women LDLo oral 72mg/kg/3D-I (72mg/kg) CARDIAC: CARDIOMYOPATHY INCLUDING INFARCTION Lancet. Vol. 341, Pg. 1054, 1993.

鹽酸鹵泛群(36167-63-2,Halofantrine hydrochloride)實驗注意事項:
1.實驗前需戴好防護(hù)眼鏡,穿戴防護(hù)服和口罩,佩戴手套,避免與皮膚接觸。
2.實驗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,必要時實驗操作需要手套箱內(nèi)完成以免對實驗人員造成傷害
3.實驗后產(chǎn)生的廢棄物需分類存儲,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

Halofantrine hydrochloride(36167-63-2) 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.

Tag:鹽酸鹵泛群(36167-63-2,Halofantrine hydrochloride),鹽酸鹵泛群試劑,鹽酸鹵泛群抑制劑,鹵泛群鹽酸鹽,鹵泛群游離態(tài),鹽酸鹵泛群的純度,鹽酸鹵泛群的作用,鹽酸鹵泛群的合成,鹽酸鹵泛群的生產(chǎn),鹽酸鹵泛群的廠家,鹽酸鹵泛群的MSDS
產(chǎn)品說明 鹽酸鹵泛群(36167-63-2,Halofantrine hydrochloride)是一種通過抑制人ERG通道來延遲整流鉀電流的阻滯劑,是一種有效的抗瘧疾產(chǎn)品。
IntroductionHalofantrine hydrochloride (36167-63-2,鹽酸鹵泛群) is a blocker that delays rectifying potassium current by inhibiting human ERG channels and is an effective anti-malarial product.
Application1
Application2
Application3
Some haematological parameters of albino mice experimentally inoculated with Trypanosoma brucei brucei after administration of Halofantrine hydrochloride, chloroquine and diaminazine aceturate
Plasma concentrations of the enantiomers of halofantrine and its main metabolite in malaria patients(European Journal of Clinical Pharmacology,1994)
Effect of kolanut on the pharmacokinetics of the antimalarial drug halofantrine(European Journal of Clinical Pharmacology,2007)
Pharmacokinetics of halofantrine and n-desbutylhalofantrine in patients with falciparum malaria following a multiple dose regimen of halofantrine
Drug Solubilization Behavior During in Vitro Digestion of Suspension Formulations of Poorly Water-Soluble Drugs in Triglyceride Lipids

High-level artemisinin-resistance with quinine co-resistance emerges in P. falciparum malaria under in vivo artesunate pressure
Background:
Humanity has become largely dependent on artemisinin derivatives for both the treatment and control of malaria, with few alternatives available. A Plasmodium falciparum phenotype with delayed parasite clearance during artemisinin-based combination therapy has established in Southeast Asia, and is emerging elsewhere. Therefore, we must know how fast, and by how much, artemisinin-resistance can strengthen.
Methods:P. falciparum was subjected to discontinuous in vivo artemisinin drug pressure by capitalizing on a novel model that allows for long-lasting, high-parasite loads. Intravenous artesunate was administered, using either single flash-doses or a 2-day regimen, to P. falciparum-infected humanized NOD/SCID IL-2Rγ−/−immunocompromised mice, with progressive dose increments as parasites recovered. The parasite’s response to artemisinins and other available anti-malarial compounds was characterized in vivo and in vitro.
Results:Artemisinin resistance evolved very rapidly up to extreme, near-lethal doses of artesunate (240 mg/kg), an increase of > 3000-fold in the effective in vivo dose, far above resistance levels reported from the field. Artemisinin resistance selection was reproducible, occurring in 80% and 41% of mice treated with flash-dose and 2-day regimens, respectively, and the resistance phenotype was stable. Measuring in vitro sensitivity proved inappropriate as an early marker of resistance, as IC50 remained stable despite in vivo resistance up to 30 mg/kg (ART-S: 10.7 nM (95% CI 10.2–11.2) vs. ART-R30: 11.5 nM (6.6–16.9), F = 0.525, p = 0.47). However, when in vivo resistance strengthened further, IC50 increased 10-fold (ART-R240 100.3 nM (92.9–118.4), F = 304.8, p < 0.0001), reaching a level much higher than ever seen in clinical samples. Artemisinin resistance in this African P. falciparum strain was not associated with mutations in kelch-13, casting doubt over the universality of this genetic marker for resistance screening. Remarkably, despite exclusive exposure to artesunate, full resistance to quinine, the only other drug sufficiently fast-acting to deal with severe malaria, evolved independently in two parasite lines exposed to different artesunate regimens in vivo, and was confirmed in vitro.
Conclusion:P. falciparum has the potential to evolve extreme artemisinin resistance and more complex patterns of multidrug resistance than anticipated. If resistance in the field continues to advance along this trajectory, we will be left with a limited choice of suboptimal treatments for acute malaria, and no satisfactory option for severe malaria.

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