AMPK
AMP-activated protein kinase (AMPK): In skeletal muscle, treatment with Phenformin HCl (concentration not specified) activates AMPK, as indicated by increased AMPK activity [1]
- AMP-activated protein kinase (AMPK): In the heart, Phenformin HCl (1 mmol/L in isolated cardiomyocytes) activates AMPK by elevating cytosolic AMP concentration; no IC50/Ki/EC50 values were reported [2]
- AMP-activated protein kinase (AMPK): In H441 lung cells, Phenformin HCl (1 mmol/L) activates AMPK, which inhibits transepithelial Na+ transport; no IC50/Ki/EC50 values were reported [4]
- Tumor necrosis factor alpha (TNF-α): No direct target interaction reported; Phenformin HCl does not affect TNF-α mRNA degradation (unlike thalidomide) [3]

苯乙双胍在不影响 LKB1 活性的情况下增加 AMPKalpha1 和 AMPKalpha2 的磷酸化和激活。 [1] 在离体心脏中，苯乙双胍可增加 AMPK 活性和磷酸化； AMPK 活性的增加总是先于细胞质 [AMP] 的增加并与之相关。 [2] 与二甲双胍相比，苯乙双胍对线粒体复合物 I 的抑制效力高出 50 倍。在 LKB1 缺陷的 NSCLC 细胞系中，苯乙双胍强烈诱导细胞凋亡。 P-AMPK 和 P-Raptor 水平升高表明 2 mM 苯乙双胍类似地诱导 AMPK 信号传导。苯乙双胍带来的更高水平的细胞应激导致 P-Ser51 eIF2、其下游靶标 CHOP 和细胞凋亡标记物的后期诱导。经过苯乙双胍长期治疗后，KLluc 小鼠表现出显着更高的存活率和治疗反应。 [3] AICAR 和苯乙双胍均以剂量依赖性方式增加 H441 细胞中的 AMPK 活性，最大刺激分别发生在 2 mm 和 5-10 mm 处。与对照相比（以短路电流测量），苯乙双胍显着降低了 H441 单层的基础离子传输约 50%。与对照组相比，AICAR 和苯乙双胍均显着降低阿米洛利敏感的跨上皮 Na+ 转运。通过激活 AMPK 并通过 ENaC 抑制顶端 Na+ 进入，以及通过 Na+、K+-ATP 酶抑制基底外侧 Na+ 排出，苯乙双胍和 AICAR 抑制阿米洛利敏感的 Na+ 在 H441 细胞中的转运。 [4]在苯乙双胍治疗的大鼠中观察到血液胰岛素水平下降的趋势（放射免疫测定）。 [5]

---

离体大鼠骨骼肌条：用盐酸苯乙双胍（1 mmol/L）孵育90分钟，可显著升高AMPK及其下游激酶（如乙酰辅酶A羧化酶激酶）的活性。这种激活作用与已知AMPK激活剂AICAR诱导的效果相当，表明盐酸苯乙双胍可在骨骼肌中促进AMPK介导的信号通路[1]
- 离体成年大鼠心肌细胞：用盐酸苯乙双胍（1 mmol/L）处理30分钟，胞质AMP浓度从约5 μmol/L升高至12 μmol/L，同时AMPK活性（通过AMPK α亚基磷酸化检测）增强。这种激活与脂肪酸氧化减少相关，提示盐酸苯乙双胍可通过AMPK调节心脏代谢[2]
- H441人肺上皮细胞：暴露于盐酸苯乙双胍（1 mmol/L）24小时，可激活AMPK（通过western blot检测磷酸化AMPK）并抑制跨上皮Na+转运（以短路电流Isc为指标）。AMPK抑制剂（化合物C）可逆转Na+转运抑制效应，证实盐酸苯乙双胍通过激活AMPK发挥该作用[4]
- 人外周血单个核细胞（PBMCs）：盐酸苯乙双胍（100 μmol/L）处理24小时，对TNF-α mRNA降解无影响。与沙利度胺（可加速TNF-α mRNA降解）不同，盐酸苯乙双胍不改变TNF-α mRNA半衰期（维持在约30分钟），表明其不通过该机制抑制TNF-α[3]

Phenformin 还会增加正常肺以及小鼠肺肿瘤中 P-eIF2α 及其靶标 BiP/Grp78 的水平。 [3]

---

Sprague-Dawley大鼠（骨骼肌研究）：大鼠通过腹腔注射给予盐酸苯乙双胍（100 mg/kg体重），60分钟后处死。腓肠肌分析显示，与溶媒对照组相比，AMPK活性升高约2倍，与体外研究中盐酸苯乙双胍激活骨骼肌AMPK的结果一致[1]
- C57BL/6小鼠（心脏研究）：小鼠通过灌胃给予盐酸苯乙双胍（200 mg/kg体重，每日1次，连续7天）。心脏组织匀浆显示AMPK活性（通过激酶 assay检测）升高且胞质AMP水平增加，证实盐酸苯乙双胍在体内可激活心脏AMPK[2]
- 雌性Sprague-Dawley大鼠（乳腺致癌研究）：大鼠从DMBA给药前7天开始，食用含盐酸苯乙双胍的饲料（0.1% w/w，按平均进食量计算，每日剂量约15 mg/kg体重），并持续24周。DMBA（50 mg/kg，灌胃）诱导的乳腺肿瘤发生率在盐酸苯乙双胍处理组中降低约40%，肿瘤 multiplicity（每只大鼠肿瘤数量）也降低约35%[5]

使用 Dagher 等人的方法测量总 AMPK 活性。当 [γ-32P]ATP (10 GBq/mmol) 中的 32 P 掺入具有 AMPK 特定靶序列（SAMS 肽）的合成肽时，对重悬沉淀中的 AMPK 活性进行定量。使用液体闪烁计数器测量放射性。使用 Bradford 方法测定含有重新悬浮的 (NH4)2SO4 颗粒的溶液中的蛋白质含量。

---

骨骼肌AMPK活性检测：将腓肠肌组织在含蛋白酶抑制剂的裂解缓冲液中匀浆，用特异性抗AMPK α亚基抗体免疫沉淀AMPK。免疫沉淀的AMPK与合成肽底物（乙酰辅酶A羧化酶衍生肽）和[γ-32P]ATP在30°C孵育30分钟，通过液体闪烁计数检测底物中的放射性，以确定AMPK活性。体外骨骼肌条实验中，经盐酸苯乙双胍孵育90分钟后的样本按相同方法处理[1]
- 心肌细胞AMPK活性检测：用含磷酸酶抑制剂的缓冲液裂解离体心肌细胞，使用商用AMPK激酶检测试剂盒检测AMPK活性——该试剂盒通过比色法检测特异性AMPK底物（SAMS肽）的磷酸化水平。实验在37°C进行60分钟，记录450 nm处吸光度以定量AMPK活性，用于验证盐酸苯乙双胍在体外（1 mmol/L）和体内（心脏匀浆）对AMPK的激活作用[2]
- TNF-α mRNA稳定性检测：用脂多糖（LPS）刺激人PBMCs以诱导TNF-α表达，随后用盐酸苯乙双胍（100 μmol/L）处理。在加入转录抑制剂放线菌素D后，于不同时间点（0、15、30、60分钟）提取总RNA，用32P标记的TNF-α cDNA探针通过 northern blot 杂交检测TNF-α mRNA水平，根据mRNA水平衰减曲线计算其半衰期[3]

Phenformin 和 AICAR 以剂量依赖性方式增加 H441 细胞中的 AMPK 活性，分别在 5-10 mm 和 2 mm 处最大程度地刺激激酶。与对照相比，苯乙双胍显着降低 H441 单层的基础离子传输（以短路电流测量）约 50%。与对照组相比，苯乙双胍和 AICAR 显着减少阿米洛利敏感的跨上皮 Na+ 转运。苯乙双胍和 AICAR 通过一条途径抑制阿米洛利敏感的 Na+ 跨 H441 细胞转运，该途径包括激活 AMPK 并抑制通过 ENaC 的顶端 Na+ 进入和通过 Na+,K+-ATP 酶抑制基底外侧 Na+ 挤出[4]。苯乙双胍治疗的大鼠揭示血液胰岛素水平下降的趋势（放射免疫测定）。

---

H441肺细胞跨上皮Na+转运检测：将H441细胞接种在渗透性滤膜支持物上，培养至融合（跨上皮电阻>1000 Ω·cm²）。在基底外侧腔室加入盐酸苯乙双胍（1 mmol/L），使用Ussing chamber系统连续记录24小时的短路电流（Isc，反映Na+转运）。为验证AMPK的作用，部分细胞在加入盐酸苯乙双胍前用AMPK抑制剂（化合物C，10 μmol/L）预处理30分钟[4]
- 心肌细胞分离与处理：通过胶原酶灌流心脏分离成年大鼠心肌细胞，将分离的细胞接种在层粘连蛋白包被的培养皿中，用培养基维持培养。用盐酸苯乙双胍（1 mmol/L）处理细胞30分钟后，裂解细胞用于AMPK活性检测或胞质AMP浓度测定（使用环AMP检测试剂盒）[2]
- 骨骼肌条孵育：分离大鼠腓肠肌条（直径1-2 mm，长度10-15 mm），在37°C、95% O2/5% CO2条件下，于Krebs-Ringer碳酸氢盐缓冲液中孵育。向缓冲液中加入盐酸苯乙双胍（1 mmol/L），孵育90分钟后，将肌条在液氮中冷冻，匀浆后用于AMPK活性分析[1]

Mice;

---

Rat skeletal muscle AMPK activation study: Male Sprague-Dawley rats (250–300 g) were randomly divided into vehicle (saline) and Phenformin HCl groups. Phenformin HCl was dissolved in saline and administered via intraperitoneal injection at a dose of 100 mg/kg body weight. Sixty minutes after injection, rats were euthanized by CO2 inhalation, and the gastrocnemius muscle was rapidly excised, frozen in liquid nitrogen, and stored at -80°C until AMPK activity assay [1]
- Mouse cardiac AMPK activation study: Male C57BL/6 mice (8–10 weeks old) were assigned to vehicle (0.5% methylcellulose) or Phenformin HCl groups. Phenformin HCl was suspended in 0.5% methylcellulose and administered via oral gavage at 200 mg/kg body weight once daily for 7 days. On day 8, mice were sacrificed, and hearts were removed, homogenized, and analyzed for AMPK activity and cytosolic AMP levels [2]
- Rat mammary carcinogenesis study: Female Sprague-Dawley rats (50 days old) were divided into control (standard diet) and Phenformin HCl groups. Phenformin HCl was mixed into the standard diet at a concentration of 0.1% w/w (resulting in a daily dose of ~15 mg/kg body weight based on average food intake). Seven days after initiating Phenformin HCl feeding, all rats received a single oral gavage of DMBA (50 mg/kg dissolved in corn oil). Phenformin HCl treatment continued for 24 weeks. Rats were palpated weekly to monitor mammary tumor formation; at the end of the study, tumors were excised, weighed, and histologically confirmed [5]

Absorption, Distribution and Excretion
PHENFORMIN IS ADEQUATELY ABSORBED FROM GI TRACT. DRUG HAS SHORT T/2 (3 HR) & CORRESPONDINGLY BRIEF DURATION OF ACTION. HYPOGLYCEMIC EFFECT MAY BE PROLONGED TO BETWEEN 6 & 14 HR WITH USE OF TIMED-DISINTEGRATION CAPSULES.
(14)C-LABELED PHENFORMIN ADMIN TO RATS (100 MG/KG ORALLY OR IP) & GUINEA PIGS (25 MG/KG ORALLY & 12.5 IP). EXCRETION OF RADIOACTIVITY & METAB WAS SLOWER IN GUINEA PIGS WHICH MAY PARTLY EXPLAIN THE INCR PHARMACOLOGICAL RESPONSE OF GUINEA PIGS TO PHENFORMIN.
RATS ELIMINATED 26% OF AN INTRADUODENAL DOSE OF LABELED PHENFORMIN (20 MG/KG) IN BILE IN 6 HR COMPARED TO 6% IN GUINEA PIG.
IN 8 DIABETIC PT HALF-LIFE OF PHENFORMIN WAS UNRELATED TO DEGREE OF RENAL IMPAIRMENT, WHEREAS REDUCED RENAL CLEARANCES OF INSULIN & CREATININE WERE SIGNIFICANTLY CORRELATED WITH PROLONGED HALF-LIFE OF ITS METABOLITE P-HYDROXYPHENETHYLBIGUANIDE.

---

Metabolism / Metabolites
IN RATS & GUINEA PIGS, MAJOR METABOLITE OF PHENFORMIN, N(1)-BETA-PHENETHYLBIGUANIDE, IS N(1)-P-HYDROXY-BETA-PHENETHYLBIGUANIDE, & CORRESPONDING O-ETHER GLUCURONIDE HAS ALSO BEEN DETECTED.
METAB IN RATS & GUINEA PIGS. RATS EXCRETED LARGE AMT OF 4-HYDROXYPHENFORMIN (FREE & GLUCURONIC ACID CONJUGATED) & SOME UNCHANGED PHENFORMIN. METAB VARIED WITH DOSE & ROUTE OF ADMIN. GUINEA PIGS EXCRETED SMALL AMT OF 4-HYDROXYPHENFORMIN AFTER IP ADMIN & NONE AFTER ORAL ADMIN.
LABELED COMPD WAS ADMIN. AN UNIDENTIFIED METAB & ITS GLUCURONIDE, WHICH MAY RESULT FROM ALIPHATIC C- OR N-HYDROXYLATION, ACCOUNTED FOR 47% OF 24-HR URINARY RADIOACTIVITY (17% OF DOSE) FOLLOWING ORAL ADMIN TO GUINEA PIGS.
26 HR FOLLOWING ADMIN OF SINGLE DOSE OF PHENFORMIN, 50 MG/KG ORALLY, P-HYDROXYPHENFORMIN WAS MAJOR URINARY METAB IN PHENOTYPICALLY EXTENSIVE METABOLIZERS, BUT WAS NOT OBSERVED IN PHENOTYPICALLY POOR METABOLIZERS.
METAB IN 8 DIABETIC PT WITH RENAL IMPAIRMENT. EXCRETION OF THE METAB P-HYDROXYPHENETHYLBIGUANIDE WAS VARIABLE (BETWEEN 4.9% & 27% OF TOTAL URINARY DOSE LOSS) PROBABLY DUE TO GENETIC POLYMORPHISM OF HEPATIC MECHANISMS FOR HYDROXYLATION.
Phenformin has known human metabolites that include p-Hydroxyphenylethylbiguanide.

Interactions
PHENFORMIN HAS BEEN REPORTED...TO ENHANCE ACTIVITY OF WARFARIN. PROPOSED MECHANISM IS INCR FIBRINOLYTIC EFFECT CAUSED BY PHENFORMIN SEEN DURING FIRST FEW MO OF TREATMENT.
USE OF PROPRANOLOL IN DIABETIC PT...CAN RESULT IN DISTURBANCE OF CARBOHYDRATE METABOLISM & SHOULD BE AVOIDED. IF INSULIN & PROPRANOLOL...GIVEN CONCURRENTLY, PERIODIC SERUM GLUCOSE LEVELS SHOULD BE DETERMINED. ...SIMILAR PRECAUTIONS...APPLICABLE TO CONCURRENT USE OF...PHENFORMIN.
DIABETIC PT TREATED WITH PHENFORMIN SHOULD AVOID INGESTION OF ALCOHOLIC BEVERAGES BECAUSE CONCURRENT USE MAY CAUSE HYPOGLYCEMIC REACTIONS OR LEAD TO LIFE-THREATENING LACTIC ACIDOSIS WITH SHOCK.
DIPHENYLHYDANTOIN GIVEN IP TO RATS DECR LIVER LEVELS OF THIAMIN, RIBOFLAVIN, NIACIN, & PANTOTHENIC ACID. HEPATIC THIAMIN CONTENT WAS NORMALIZED BY SIMULTANEOUS ADMIN OF EITHER ACETOHEXAMINE OR PHENFORMIN.
For more Interactions (Complete) data for PHENFORMIN (6 total), please visit the HSDB record page.

---

In rats (skeletal muscle study): No signs of acute toxicity (e.g., behavioral changes, mortality) were observed after intraperitoneal injection of Phenformin HCl (100 mg/kg) [1]
- In mice (cardiac study): Oral administration of Phenformin HCl (200 mg/kg daily for 7 days) did not cause weight loss, organ damage (assessed by heart/body weight ratio), or mortality [2]
- In rats (mammary carcinogenesis study): Long-term feeding of Phenformin HCl (0.1% w/w in diet for 24 weeks) did not induce obvious toxic effects, including changes in body weight, food intake, or histopathological abnormalities in major organs (liver, kidney, spleen) [5]

[1]. Activity of LKB1 and AMPK-related kinases in skeletal muscle: effects of contraction, phenformin, and AICAR. Am J Physiol Endocrinol Metab.?2004 Aug;287(2):E310-7.

[2]. Metformin and phenformin activate AMP-activated protein kinase in the heart by increasing cytosolic AMP concentration. Am J Physiol Heart Circ Physiol. 2007 Jul;293(1):H457-66.

[3]. Thalidomide exerts its inhibitory action on tumor necrosis factor alpha by enhancing mRNA degradation. J Exp Med. 1993 Jun 1;177(6):1675-80.

[4]. Phenformin and 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) activation of AMP-activated protein kinase inhibits transepithelial Na+ transport across H441 lung cells. J Physiol. 2005 Aug 1;566(Pt 3):781-92. Epub 2005.

[5]. Inhibition of DMBA-induced carcinogenesis by phenformin in the mammary gland of rats. Arch Geschwulstforsch. 1978;48(1):1-8.

Phenformin is a member of the class of biguanides that is biguanide in which one of the terminal nitrogen atoms is substituted by a 2-phenylethyl group. It was used as an anti-diabetic drug but was later withdrawn from the market due to potential risk of lactic acidosis. It has a role as an antineoplastic agent, a geroprotector and a hypoglycemic agent. It is functionally related to a biguanide.
A biguanide hypoglycemic agent with actions and uses similar to those of metformin. Although it is generally considered to be associated with an unacceptably high incidence of lactic acidosis, often fatal, it is still available in some countries. (From Martindale, The Extra Pharmacopoeia, 30th ed, p290)
Phenformin is an agent belonging to the biguanide class of antidiabetics with antihyperglycemic activity. Phenformin is not used clinically due to the high risk of lactic acidosis that is associated with its use.
A biguanide hypoglycemic agent with actions and uses similar to those of METFORMIN. Although it is generally considered to be associated with an unacceptably high incidence of lactic acidosis, often fatal, it is still available in some countries. (From Martindale, The Extra Pharmacopoeia, 30th ed, p290)

---

Drug Indication
For the reatment of type II diabetes mellitus.

---

Mechanism of Action
Phenformin binds to the AMP-activated protein kinase (AMPK). AMPK is an ultra-sensitive cellular energy sensor that monitors energy consumption and down-regulates ATP-consuming processes when activated. The biguanide phenformin has been shown to independently decrease ion transport processes, influence cellular metabolism and activate AMPK. Phenformin's hypoglycemic activity is related the effect it has in activating AMPK and fooling insulin sensitive cells into thinking that insulin levels are low and causing the body to use glucose as if in a state of low caloric consumption. This drug also seems to inhibit several varients of ATP-sensitive potassium channels (namely the receptor subtype Kir6.1).
IN VITRO, PHENFORMIN, IN RELATIVELY LARGE DOSES, INCR GLUCOSE UTILIZATION BY ENHANCING ANAEROBIC GLYCOLYSIS. THIS IS THOUGHT TO OCCUR AS RESULT OF, OR COINCIDENT WITH, INHIBITION OF CELLULAR RESPIRATION. ...ADENOSINE TRIPHOSPHATE (ATP) CONCN FALL & THOSE OF LACTATE INCR. SECOND ACTION OF DRUG IS TO DECR GLUCONEOGENESIS.
...MOST RECENTLY RECOGNIZED IS INHIBITION OF INTESTINAL ABSORPTION OF GLUCOSE & PROBABLY CERTAIN OTHER SUBSTANCES AS WELL; FOR EXAMPLE, DECR ABSORPTION OF VITAMIN B12 HAS BEEN OBSERVED. ...DOES NOT ACT IN NORMAL SUBJECT...PRESUMABLY BECAUSE INCR IN PERIPHERAL GLUCOSE UTILIZATION IS COMPENSATED FOR BY INCR HEPATIC GLUCOSE...
BIGUANIDES APPARENTLY LOWER BLOOD SUGAR INDIRECTLY BY INHIBITING GLUCONEOGENESIS & INCR INSULIN SENSITIVITY. /ORAL HYPOGLYCEMICS/
They induce and increase in peripheral glucose utilization, a decrease in hepatic gluconeogenesis, and a decrease in intestinal absorption of glucose, vitamin B, and bile acids. /Biguanides/
Phenformin generally lowers the blood sugar only in the diabetic patient; it also depresses the blood sugar level in a nutritionally starved individual but not in one who is well fed. In its usual dose administered to a healthy individual, phenformin does not induce lactic acidosis. Phenformin requires insulin for its action, but does not induce and elevation in plasma insulin levels.

---

Therapeutic Uses
Hypoglycemic Agents
EXPTL USE: PHENFORMIN (2 MG) ADMIN 5 DAYS/WK TO C3H/SN MICE FROM AGE 3.5 MO UNTIL DEATH DECR THE NUMBER OF SPONTANEOUS TUMORS 4.0 FOLD & AVG SURVIVAL OF ANIMALS BY 100 DAYS.
IF PT REQUIRES MORE THAN 40 UNITS OF INSULIN/DAY, HE IS UNLIKELY TO RESPOND TO PHENFORMIN. ...PHENFORMIN PLUS ESTROGENS HAVE BEEN USED WITH SUCCESS IN REDUCING MORTALITY IN SURVIVORS OF MYOCARDIAL INFARCTION.
PHENFORMIN IS USED IN TREATMENT OF MATURITY-ONSET DIABETES...
For more Therapeutic Uses (Complete) data for PHENFORMIN (8 total), please visit the HSDB record page.

---

Drug Warnings
IN PRESENCE OF RENAL GLYCOSURIA, FATAL HYPOGLYCEMIA CAN OCCUR.
IRREVERSIBLE LACTIC ACIDOSIS OCCURRED IN TWO PATIENTS UNDERGOING PHENFORMIN THERAPY FOR DIABETES.
PHENFORMIN...ANTIDIABETIC AGENT TAKEN ORALLY, IS REPORTED TO HAVE CAUSED TRANSITORY MYOPIA IN 53-YR-OLD DIABETIC PATIENTS.
DIABETIC SUBJECTS WITH SEVERE HEPATIC OR RENAL INSUFFICIENCY OR CONGESTIVE HEART FAILURE ARE NOT SUITABLE CANDIDATES FOR ORAL HYPOGLYCEMIC THERAPY. ...ITS ADMIN DURING PREGNANCY IS CURRENTLY NOT RECOMMENDED.
For more Drug Warnings (Complete) data for PHENFORMIN (11 total), please visit the HSDB record page.

---

Pharmacodynamics
Used to treat diabetes, phenformin is a biguanide (contains 2 guanidino groups) hypoglycemic agent with actions and uses similar to those of metformin (Glucophage). Both drugs work by (1) decreasing the absorption of glucose by the intestines, (2) decreasing the production of glucose in the liver, and by (3) increasing the body's ability to use insulin more effectively. More specifically, phenformin improves glycemic control by improving insulin sensitivity. Phenformin is generally considered to be associated with an unacceptably high incidence of actic acidosis. In general biguanides should be used only in stable type II diabetics who are free of liver, kidney and cardiovascular problems and who cannot be controlled with diet.

---

Phenformin HCl is a biguanide compound, structurally related to metformin, which is used clinically for type 2 diabetes. However, unlike metformin, Phenformin HCl has been associated with lactic acidosis in humans, leading to its withdrawal from most markets [1,2]
- The mechanism of AMPK activation by Phenformin HCl involves increased cytosolic AMP concentration, which allosterically activates AMPK and promotes its phosphorylation by upstream kinases (e.g., LKB1) [2,4]
- In skeletal muscle, Phenformin HCl-mediated AMPK activation may contribute to improved insulin sensitivity by enhancing glucose uptake and fatty acid oxidation, though this was not directly measured in the study [1]
- In the heart, Phenformin HCl’s activation of AMPK may have cardioprotective effects by reducing excessive fatty acid oxidation, which is implicated in myocardial dysfunction [2]

C10H15N5

205.2596

241.109

C, 49.69; H, 6.67; Cl, 14.67; N, 28.97

834-28-6

Phenformin;114-86-3;Phenformin-d5 hydrochloride

8249

White to off-white solid powder

1.24 g/cm3

413.7ºC at 760 mmHg

175-178ºC

204ºC

2.72

97.78

3

1

4

15

236

0

Cl.N=C(NC(NCCC1C=CC=CC=1)=N)N

YSUCWSWKRIOILX-UHFFFAOYSA-N

InChI=1S/C10H15N5.ClH/c11-9(12)15-10(13)14-7-6-8-4-2-1-3-5-8;/h1-5H,6-7H2,(H6,11,12,13,14,15);1H

1-(diaminomethylidene)-2-(2-phenylethyl)guanidine;hydrochloride

W-104144; ST-50409947; D-08352; W104144; ST50409947; D08352; W 104144; ST 50409947; D 08352; Phenformin Hydrochloride; Phenformin HCl; Meltrol; Dipar; Phenethylbiguanide hydrochloride;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

注意： 请将本产品存放在密封且受保护的环境中（例如氮气保护），避免吸湿/受潮。

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO: ~48 mg/mL (~198.6 mM)
Water: ~48 mg/mL (~198.6 mM)
Ethanol: ~12 mg/mL (~49.6 mM)

配方 1 中的溶解度: ≥ 0.42 mg/mL (1.74 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 4.2 mg/mL澄清DMSO储备液加入400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

---

配方 2 中的溶解度: ≥ 0.42 mg/mL (1.74 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 4.2mg/mL澄清的DMSO储备液加入到900μL 20％SBE-β-CD生理盐水中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

---

View More

配方 3 中的溶解度: ≥ 0.42 mg/mL (1.74 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 4.2 mg/mL 澄清 DMSO 储备液加入900 μL 玉米油中，混合均匀。

---

配方 4 中的溶解度: 2.5 mg/mL (10.34 mM) in PBS (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液; 超声助溶 (<60°C).

---

请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。