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鹽酸鹵泛群

NMR下載 COA and HPLC MSDS下載
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(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品。

貨品編碼	規格	純度	價格 (￥)	現價(￥)	特價(￥)	庫存描述	數量	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（標準化劑量）	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.實驗前需戴好防護眼鏡，穿戴防護服和口罩，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及有害物質產生，必要時實驗操作需要手套箱內完成以免對實驗人員造成傷害
3.實驗后產生的廢棄物需分類存儲，并交于專業生物廢氣物處理公司處理，以免造成環境污染

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.

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產品說明	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品。
Introduction	Halofantrine 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

警示圖
危險性	warning
危險性警示	Not available
安全聲明	H303吞入可能有害+H313皮膚接觸可能有害+H2413吸入可能對身體有害
安全防護	P264處理后徹底清洗+P280戴防護手套/穿防護服/戴防護眼罩/戴防護面具+P305如果進入眼睛+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,繼續沖洗+P337如果眼睛刺激持續+P2393獲得醫療建議/護理
備注	實驗過程中防止吸入、食入，做好安全防護

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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