製品番号: HY-126562

Piperlonguminine

Name: Piperlonguminine
Brand: MedChemExpress
SKU: HY-126562
Price: 120.00 USD
Availability: InStock
Rating: 5 (1 reviews)

1 Cited Publications

カスタマーレビュー

Based on 1 publication(s) in Google Scholar

Piperlonguminine is a cytochrome P450 (CYP450) inhibitor. Piperlonguminine also inhibits the growth of epimastigotes and intracellular amastigotes of Trypanosoma cruzi, with IC₅₀ values of 53.8 and 33.9 μM, respectively. Piperlonguminine regulates HMGB1/TLR4-NF-κB/MAPK-related inflammatory responses, endothelial protein C receptor (EPCR) shedding, melanogenesis, glycolipid metabolism, ischemic brain injury and tumor growth. Piperlonguminine can be used in research on hyperlipidemia, sepsis, Chagas disease, ischemic stroke, sarcoma and severe acute pancreatitis-associated lung injury.

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研究用途以外に使用した場合、当社は一切の責任を負いかねます。

純度 : 99.81%
CAS 番号: 5950-12-9
分子式: C₁₆H₁₉NO₃
分子量:273.33

保管条件:

4°C, sealed storage, away from moisture and light

* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)

Piperlonguminine 構造式

CAS 番号: 5950-12-9

容量

価格（税別）

在庫状況

数量

Amount: USD 0.00

* アイテムを追加する前、数量をご選択ください

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Use of MCE Products

Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

HY-126562R
Piperlonguminine (Standard)

Reference Standard

生物活性
- 製品説明
- IC₅₀ & Target
- Cellular Effect
- 体外実験
- Parmacokinetics
- 体内実験
化学情報
Publications (1)
溶剤 & 溶解度
- 体外
- 体内
純度とドキュメンテーション
参考文献
Help & FAQs
関連分類
Bioz

生物活性

製品説明

Piperlonguminine is a cytochrome P450 (CYP450) inhibitor. Piperlonguminine also inhibits the growth of epimastigotes and intracellular amastigotes of Trypanosoma cruzi, with IC₅₀ values of 53.8 and 33.9 μM, respectively^[10]. Piperlonguminine regulates HMGB1/TLR4-NF-κB/MAPK-related inflammatory responses, endothelial protein C receptor (EPCR) shedding, melanogenesis, glycolipid metabolism, ischemic brain injury and tumor growth. Piperlonguminine can be used in research on hyperlipidemia, sepsis, Chagas disease, ischemic stroke, sarcoma and severe acute pancreatitis-associated lung injury^[1]^[2]^[3]^[4]^[5]^[6]^[7]^[8]^[9]^[10]^[11]^[12].

IC₅₀ & Target

^[6]

CYP3A

23.2 μM (IC₅₀)

CYP2C9

69 μM (IC₅₀)

CYP2E1

140.9 μM (IC₅₀)

CYP2C8

251.5 μM (IC₅₀)

CYP2D6

359.2 μM (IC₅₀)

Parasite アイソフォーム固有の製品をすべて表示 :

p38 MAPK アイソフォーム固有の製品をすべて表示 :

NF-κB アイソフォーム固有の製品をすべて表示 :

Cytochrome P450 アイソフォーム固有の製品をすべて表示 :

Cellular Effect

Cell Line	Type	Value	Description	References
HCT-116	IC₅₀	>20 μM Compound: 1a	Cytotoxicity against human HCT116 cells after 24 hrs by MTT assay Cytotoxicity against human HCT116 cells after 24 hrs by MTT assay	[PMID: 21745740]
HepG2 2.2.15	CC₅₀	0.32 mM Compound: 11	Cytotoxicity against human HepG2(2.2.15) cells Cytotoxicity against human HepG2(2.2.15) cells	[PMID: 23434420]
HepG2 2.2.15	IC₅₀	>4.51 mM Compound: 11	Antiviral activity against Hepatitis B virus-infected human HepG2(2.2.15) cells assessed as inhibition of HBeAg secretion Antiviral activity against Hepatitis B virus-infected human HepG2(2.2.15) cells assessed as inhibition of HBeAg secretion	[PMID: 23434420]
HepG2 2.2.15	IC₅₀	>4.51 mM Compound: 11	Antiviral activity against Hepatitis B virus-infected human HepG2(2.2.15) cells assessed as inhibition of HBsAg secretion Antiviral activity against Hepatitis B virus-infected human HepG2(2.2.15) cells assessed as inhibition of HBsAg secretion	[PMID: 23434420]

体外実験

Piperlonguminine (5-40 μM; 6 h; HUVECs) inhibits LPS (HY-D1056)/HMGB1-induced HMGB1 release and RAGE expression, and reduces the increased endothelial barrier permeability induced by HMGB1^[2].
Piperlonguminine (5-40 μM; 6 h; HUVECs) inhibits HMGB1-induced expression of VCAM-1, ICAM-1 and E-selectin, as well as THP-1 cell adhesion and transendothelial migration, and reduces TNF-α, IL-6, and signaling associated with NF-κB, ERK1/2 and p38^[2].
Piperlonguminine (5-40 μM; 6 h; HUVECs) inhibits LPS-induced production of TNF-α and IL-6, activation of NF-κB p65 and ERK1/2, reduces the expression of VCAM-1, ICAM-1 and E-selectin, and suppresses monocyte adhesion and migration^[5].
Piperlonguminine (0.39-25 μg/mL; 72 h) exhibits no significant cytotoxicity in HL-60, HCT-8, SF-295, and MDA-MB-435 cells, with an IC₅₀ >25 μg/mL for all four cell lines^[4].
Piperlonguminine (5-40 μM; 6 h; HUVECs) dose-dependently attenuates LPS (100 ng/mL)-induced endothelial barrier disruption, and inhibits TLR4 expression and p38 MAPK phosphorylation; piperlonguminine does not significantly reduce HUVEC viability at concentrations up to 100 μM^[5].
Piperlonguminine (10-40 μM; 6 h; HUVECs) inhibits PMA (HY-18739) (1 μM; 1 h)-induced EPCR shedding and TACE/ADAM17 expression, and reduces the phosphorylation of p38, ERK1/2 and JNK; piperlonguminine also inhibits TNF-α- or IL-1β-induced EPCR shedding^[7].
Piperlonguminine (0.1-1000 μM; 30 min preincubation; human liver microsomes) exhibits time-dependent inhibition of CYP3A4, CYP2C9, CYP2E1, CYP2C8, and CYP2D6 in the presence of NADPH, with the IC₅₀ values of CYP3A4 and CYP2C9 decreasing to 23.2 μM and 69.0 μM, respectively^[6].
Piperlonguminine (100 μM; rat/human liver microsomes; NADPH) forms O-dealkylation metabolite M1 and hydroxylation metabolite M2, as well as four N-acetylcysteine-trapped conjugates M3-M6 derived from O-quinone; CYP3A4 is the major CYP450 enzyme mediating the metabolic activation of Piperlonguminine^[6].
Piperlonguminine (6-25 μM; 72 h; B16 cells) dose-dependently inhibits melanogenesis induced by α-MSH (HY-P0252), IBMX (HY-12318) and protoporphyrin IX (HY-B1247), with IC₅₀ values of 9.6, 9.2 and 9.1 μM, respectively, but does not significantly suppress OAG/PKC-mediated melanogenesis^[9].
Piperlonguminine (3-25 μM; B16 cells) dose-dependently reduces α-MSH-induced CREB phosphorylation and MITF expression, and downregulates Tyrosinase transcription/expression, but does not directly inhibit the L-DOPA oxidizing activity of cell-free Tyrosinase^[9].
Piperlonguminine (1-30 μM; during 3T3-L1 differentiation) promotes triglyceride accumulation and increases 2-deoxyglucose uptake in a concentration-dependent manner, enhances adiponectin release at 10 and 30 μM, and upregulates the mRNA levels of adiponectin, PPARγ2, GLUT4 and aP2; piperlonguminine does not exhibit significant direct PPARγ agonistic activity in assays without nuclear receptor cofactors^[8].
Piperlonguminine (3.6-361 μM; 96 h) inhibits the growth of T. cruzi Y strain epimastigotes with an IC₅₀ of 53.8 μM; it inhibits intracellular amastigotes in LLCMK2 cells at 18-361 μM with an IC₅₀ of 33.9 μM. The CC₅₀ of piperlonguminine against LLCMK2 cells is 303.1 μM, with a selectivity index (SI) of 8.9^[10].
Piperlonguminine (34 μM; 24 h; *T. cruzi* extracellular amastigotes) increases MDC-labeled autophagic vacuoles, and this change is partially inhibited by wortmannin; ultrastructural and mitochondrial analyses also show that piperlonguminine induces mitochondrial abnormalities, cytoplasmic vacuolization, and alterations in membrane structures^[10].
Piperlonguminine (2.5-40 μM; 12 h; SH-SY5Y) concentration-dependently enhances cell viability and reduces apoptosis after 3 h of oxygen-glucose deprivation (OGD)^[11].
Piperlonguminine (20 μM; 12 h; SH-SY5Y) inhibits TNF-α (20 ng/mL; 30 min)-induced phosphorylation of p38 MAPK and NF-κB p65^[11].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay^[11]

Cell Line:

human neuroblastoma SH-SY5Y cells
Concentration:

2.5 μM (12 h post-OGD); 5 μM (12 h post-OGD); 10 μM (12 h post-OGD); 20 μM (12 h post-OGD, also without OGD); 40 μM (12 h post-OGD)
Incubation Time:

12 h (post-OGD incubation)
Result:

Attenuated OGD-induced cytotoxicity in a concentration-dependent manner, increasing cell viability relative to the OGD-only control.
Reduced OGD-induced apoptosis in a concentration-dependent manner, lowering the percentage of apoptotic cells relative to the OGD-only control.

Western Blot Analysis^[11]

Cell Line:

human neuroblastoma SH-SY5Y cells
Concentration:

20 μM (pre-incubation before TNF-α stimulation)
Incubation Time:

12 h (pre-incubation before TNF-α stimulation)
Result:

Blocked the TNF-α-induced phosphorylation of p38MAPK, reducing its relative protein expression level.
Inhibited the TNF-α-induced activation of NF-κBp65, reducing its relative protein expression level.

ELISA Assay^[2]

Cell Line:

primary human umbilical vein endothelial cells (HUVECs)
Concentration:

5-40 μM
Incubation Time:

6 h
Result:

Inhibited HMGB1-mediated upregulation of VCAM-1, ICAM-1, and E-selectin in a concentration-dependent manner.\nSignificantly reduced HMGB1-mediated activation of phosphorylated NF-κB p65 and phosphorylated ERK1/2 in a concentration-dependent manner.

Cell Migration Assay ^[2]

Cell Line:

primary human umbilical vein endothelial cells (HUVECs), THP-1 monocyte cells
Concentration:

5-40 μM (pre-treatment; post-treatment)
Incubation Time:

6 h (pre-treatment; post-treatment)
Result:

Reduced HMGB1-mediated THP-1 monocyte migration across HUVEC monolayers in a concentration-dependent manner when administered as a pre-treatment or post-treatment.

ELISA Assay^[5]

Cell Line:

primary human umbilical vein endothelial cells (HUVECs)
Concentration:

5-40 μM (6 h pre-incubation before LPS treatment); 40 μM (6 h incubation alone, no LPS)
Incubation Time:

6 h (pre-incubation before LPS treatment); 6 h (incubation alone, no LPS)
Result:

Did not alter baseline TNF-α and IL-6 secretion at 40 μM alone.
Dose-dependently inhibited LPS-induced production of both cytokines.

ELISA Assay^[7]

Cell Line:

primary human umbilical vein endothelial cells (HUVECs)
Concentration:

10-40 μM
Incubation Time:

6 h (piperlonguminine pretreatment); 1 h (phorbol 12-myristate 13-acetate stimulation)
Result:

Reduced EPCR shedding and TACE/ADAM17 expression.

Cell Cytotoxicity Assay^[4]

Cell Line:

HL-60 (human leukemia), MDA-MB-435 (human melanoma), SF-295 (human brain cancer), HCT-8 (human colon cancer)
Concentration:

0.39, 1.56, 3.12, 6.25, 12.5, 25 μg/mL
Incubation Time:

72 h
Result:

Showed no cytotoxic activity against all four tested human tumor cell lines, with IC₅₀ values greater than 25 μg/mL.

Real Time qPCR^[8]

Cell Line:

differentiated 3T3-L1 adipocytes
Concentration:

3, 10, 30 μM
Incubation Time:

8 days
Result:

Increased mRNA levels of adiponectin (significantly at 30 μM), PPARγ2 (significantly at 10 and 30 μM), GLUT4 (significantly at all tested concentrations), and aP2 (significantly at 30 μM) relative to vehicle control.

Western Blot Analysis^[9]

Cell Line:

α-MSH-stimulated melanoma B16 cells
Concentration:

3-25 μM
Incubation Time:

2 h preincubation; 48 h incubation with α-MSH
Result:

Reduced CREB phosphorylation, MITF expression, and tyrosinase expression.

Western Blot Analysis^[9]

Cell Line:

α-MSH-stimulated melanoma B16 cells
Concentration:

6-25 μM
Incubation Time:

72 h
Result:

Inhibited α-MSH-, IBMX-, and protoporphyrin IX-induced melanogenesis with IC₅₀ values of 9.6, 9.2, and 9.1 μM, respectively.

Cell Cytotoxicity Assay^[10]

Cell Line:

LLCMK2 monkey kidney epithelial cells
Concentration:

3.6-360.0 μM
Incubation Time:

96 h
Result:

Showed low toxicity to LLCMK2 cells, with a CC₅₀ of 303.1 μM.
Resulted in a selective index of 8.9, calculated as the ratio of CC₅₀ against LLCMK2 cells to IC₅₀ against intracellular amastigotes.

Parmacokinetics

Species	Dose	Route	C_max	T_max	AUC_0-24
Mice^[8]	5 mg/kg	p.o.	0.316 μg/mL	0.9 h	0.914 μg·h/mL
Mice^[8]	10 mg/kg	p.o.	0.708 μg/mL	1.2 h	2.51 μg·h/mL
Mice^[8]	20 mg/kg	p.o.	1.97 μg/mL	1 h	9.06 μg·h/mL

体内実験

Piperlonguminine (5.5 or 11.0 μg/mouse; i.v.) reduces HMGB1-induced increases in vascular permeability and peritoneal leukocyte migration when administered either before or after HMGB1 stimulation^[2].
Piperlonguminine (5.5 or 11.0 μg/mouse; i.v.) reduces LPS-induced increases in vascular permeability and peritoneal leukocyte migration in mice^[5].
Piperlonguminine (11 μg/mouse; administered 12 h after CLP or at 12 and 50 h after CLP) reduces CLP-induced serum soluble EPCR (sEPCR) levels^[7].
Piperlonguminine (11.0 μg/mouse; i.v.; at 12 and 50 h post-CLP) increases the survival rate from 0% to 40% in CLP-induced septic mice^[2].
Piperlonguminine (11.0 μg/mouse; i.v.; 12 and 50 h after LPS) increases the survival rate from 0% to 40% in LPS (15 mg/kg; i.p.)-induced septic mice^[5].
Piperlonguminine (10 mg/kg; p.o.; once daily for 14 days) reduces total cholesterol (TC), triglycerides (TG) and low-density lipoprotein cholesterol (LDL-C), while increases high-density lipoprotein cholesterol (HDL-C) in high-fat diet-fed Wistar rats; the levels of TC, TG, LDL-C and HDL-C are 9.67, 1.47, 3.57 and 1.31 mmol/L, respectively, compared with 22.26, 2.86, 5.44 and 0.68 mmol/L in the high-fat diet control group^[3].
Piperlonguminine (25 or 50 mg/kg; i.p.; once daily for 7 days) reduces tumor weight in Sarcoma 180 tumor-bearing mice, with tumor growth inhibition rates of 38.71% and 40.68%, respectively^[4].
Piperlonguminine (2.4 mg/kg; i.p.; immediately after reperfusion) reduces neurological deficit scores, cerebral infarction volume and brain water content, and alleviates increased blood-brain barrier (BBB) permeability in a rat model of focal cerebral ischemia; the cerebral infarction volume decreases from 22.9% in the vehicle group to 14.7%^[11].
Piperlonguminine (5, 10, or 15 mg/kg; i.p.; 24 h) dose-dependently alleviates pancreatic and pulmonary tissue injury, alveolar thickening, and edema in rats with severe acute pancreatitis induced by 4% sodium taurocholate (HY-N0545). A dose of 10 mg/kg achieves the main experimental effect, so 10 mg/kg is used in subsequent mechanism experiments^[12].
Piperlonguminine (10 mg/kg; i.p.; 24 h) reduces serum TNF-α, IL-1β and IL-6 by 27.57%, 44.91% and 51.29%, respectively, in rats with severe acute pancreatitis. It also downregulates NOX2, NOX4, ROS, MPO, IL-1β, TLR4 and NF-κB signaling in lung tissues, while decreasing the phosphorylation of IκB-α and p65^[12].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

Sprague-Dawley (male, 240-270 g, intraluminal middle cerebral artery occlusion for 1 h followed by 23 h reperfusion)^[11]
Dosage:

2.4 mg/kg
Administration:

i.p.; single dose
Result:

Reduced neurological deficit scores to 2.4.
Reduced cerebral infarct volume to 14.7%.
Reduced brain water content to 76.1%.
Attenuated Evans blue extravasation.
Decreased phosphorylated levels of NF-κB p65 and p38MAPK.

Animal Model:

C57BL/6 (male, 6-7-weeks-old, 18-20 g, CLP-induced sepsis model)^[2]
Dosage:

11.0 µg/mouse
Administration:

i.v.; single dose (12 h before CLP); two doses (12 h and 50 h after CLP)
Result:

Increased CLP-induced sepsis survival rate from 0 to 40%.
Prolonged survival of CLP-induced septic mice compared to untreated mice.

Animal Model:

C57BL/6 (male, 6-7-weeks-old, 18-20 g, HMGB1-induced vascular permeability model)^[2]
Dosage:

5.5-11.0 µg/mouse
Administration:

i.v.; single dose; pre- or post-HMGB1 injection
Result:

Significantly inhibited HMGB1-induced peritoneal Evans blue dye leakage.
Significantly reduced HMGB1-induced leukocyte migration into the peritoneal cavity.

Animal Model:

C57BL/6 (male, 6-7-weeks-old, 18-20 g, CLP-induced sepsis model)^[2]
Dosage:

5.5-11.0 µg/mouse
Administration:

i.v.; single dose; pre- or post-CLP
Result:

Significantly inhibited CLP-induced serum HMGB1 release.

Animal Model:

C57BL/6 (male, 6-7 weeks old, 18-20 g)^[5]
Dosage:

5.5 μg/mouse; 11.0 μg/mouse
Administration:

i.v.
Result:

Markedly inhibited LPS-induced peritoneal leakage of Evans blue dye.\nSignificantly reduced LPS-induced leukocyte migration into mouse peritoneal cavities, lowering total leukocyte counts.

Animal Model:

C57BL/6 (male, 6-7 weeks old, 18-20 g)^[5]
Dosage:

11.0 μg/mouse
Administration:

i.v.; twice at 12 h and 50 h post-LPS injection
Result:

Increased the survival rate of LPS-injected mice from 0% to 40%.

Animal Model:

C57BL/6 (male, 6-7 weeks old, 18-20 g, CLP-induced sepsis model)^[7]
Dosage:

11 μg per mouse
Administration:

single dose at 12 hours post-CLP; two doses at 12 hours and 50 hours post-CLP
Result:

Inhibited CLP-induced sEPCR shedding on days 1 and 2 post-CLP with single dose.
Inhibited CLP-induced sEPCR shedding on days 1, 2, 3, and 4 post-CLP with two doses.

Animal Model:

Wistar (male, initial body weight 182.3 g, high-fat diet-induced hyperlipidaemia)^[3]
Dosage:

10 mg/kg
Administration:

p.o.; daily; 14 days
Result:

Reduced rat body weight gain to 66.3 g over 15 days.
Decreased serum total cholesterol to 9.67 mmol/L.
Decreased serum triglyceride to 1.47 mmol/L.
Decreased serum low-density lipoprotein cholesterol to 3.57 mmol/L.
Increased serum high-density lipoprotein cholesterol to 1.31 mmol/L.

Animal Model:

Swiss mice (male, 25-30 g, subcutaneous implantation of sarcoma 180 ascites tumor cells)^[4]
Dosage:

25 mg/kg; 50 mg/kg
Administration:

i.p.; daily; 7 days
Result:

Inhibited tumor growth by 38.71% and 40.68%, respectively.

化学情報

CAS 番号 5950-12-9
性状 Solid
分子量 273.33
分子式 C₁₆H₁₉NO₃
Color White to off-white
SMILES

O=C(NCC(C)C)/C=C/C=C/C1=CC=C(OCO2)C2=C1
Structure Classification
- Alkaloids
- Other Alkaloids
Initial Source
輸送条件

Room temperature in continental US; may vary elsewhere.
保管条件

4°C, sealed storage, away from moisture and light

* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)

Publications (1)

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Journal Impact Factor

Chin Med

Identification of anti-fibrotic compounds from Piper longum L via hollow fiber cell fishing and high-performance liquid chromatography with in vivo and in vitro validation. [Abstract]

2025 Aug 19;20(1):127. PMID: 40830877

溶剤 & 溶解度

体外:

DMSO : ≥ 50 mg/mL (182.93 mM; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

* "≥" means soluble, but saturation unknown.

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

3.6586 mL

18.2929 mL

36.5858 mL

5 mM

0.7317 mL

3.6586 mL

7.3172 mL

10 mM

0.3659 mL

1.8293 mL

3.6586 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

モル濃度計算機

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

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分子量分子量

希釈計算機

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体内:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 1.25 mg/mL (4.57 mM); Clear solution

This protocol yields a clear solution of ≥ 1.25 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (12.5 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

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The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).

Working solution concentration: 0.22 mg/mL

純度とドキュメンテーション

バッチを選択:

純度: 99.98%

Assay: 99.98%

ee.: 99.98%

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参考文献

[1]. Wang H, et al. Protection effect of piperine and piperlonguminine from Piper longum L. alkaloids against rotenone-induced neuronal injury. Brain research. 2016 May 15;1639:214-27.

[2]. Ku SK, et al. Vascular barrier protective effects of piperlonguminine in vitro and in vivo. Inflammation research : official journal of the European Histamine Research Society ... [et al.]. 2014 May;63(5):369-79.

[3]. Sarnaizul E, et al. The preparation and antihyperlipidaemic assay of piperlonguminine in vivo. Phytochemistry Letters. 2012, article in press.

[4]. Bezerra DP, et al. In vivo growth inhibition of sarcoma 180 by piperlonguminine, an alkaloid amide from the Piper species. Journal of applied toxicology : JAT. 2008 Jul;28(5):599-607. [Content Brief]

[5]. Lee W, et al. Barrier protective effects of piperlonguminine in LPS-induced inflammation in vitro and in vivo. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association. 2013 Aug;58:149-57.

[6]. Chi Y, et al. Metabolic activation and cytochrome P450 inhibition of piperlonguminine mediated by CYP3A4. International journal of biological macromolecules. 2024 May;268(Pt 2):131502.

[7]. Ku SK, et al. Piperlonguminine downregulates endothelial protein C receptor shedding in vitro and in vivo. Inflammation. 2014 Apr;37(2):435-42.

[8]. Yamaguchi I, et al. Adipogenic effects of piperlonguminine in 3T3-L1 cells and plasma concentrations of several amide constituents from Piper chaba extracts after treatment of mice. Journal of Natural Medicines. 2013.

[9]. Kim KS, et al. Inhibitory effect of piperlonguminine on melanin production in melanoma B16 cell line by downregulation of tyrosinase expression. Pigment cell research. 2006 Feb;19(1):90-8.

[10]. Veiga-Santos P, et al. The natural compounds piperovatine and piperlonguminine induce autophagic cell death on Trypanosoma cruzi. Acta tropica. 2013 Mar;125(3):349-56.

[11]. Yang T, et al. Piperlonguminine is neuroprotective in experimental rat stroke. International immunopharmacology. 2014 Dec;23(2):447-51. [Content Brief]

[12]. Hu Q, et al. Effects of piperlonguminine on lung injury in severe acute pancreatitis via the TLR4/NF-κB pathway. European journal of histochemistry : EJH. 2023 Mar 20;67(2):3639. [Content Brief]

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	3.6586 mL	18.2929 mL	36.5858 mL	91.4645 mL
	5 mM	0.7317 mL	3.6586 mL	7.3172 mL	18.2929 mL
	10 mM	0.3659 mL	1.8293 mL	3.6586 mL	9.1465 mL
	15 mM	0.2439 mL	1.2195 mL	2.4391 mL	6.0976 mL
	20 mM	0.1829 mL	0.9146 mL	1.8293 mL	4.5732 mL
	25 mM	0.1463 mL	0.7317 mL	1.4634 mL	3.6586 mL
	30 mM	0.1220 mL	0.6098 mL	1.2195 mL	3.0488 mL
	40 mM	0.0915 mL	0.4573 mL	0.9146 mL	2.2866 mL
	50 mM	0.0732 mL	0.3659 mL	0.7317 mL	1.8293 mL
	60 mM	0.0610 mL	0.3049 mL	0.6098 mL	1.5244 mL
	80 mM	0.0457 mL	0.2287 mL	0.4573 mL	1.1433 mL
	100 mM	0.0366 mL	0.1829 mL	0.3659 mL	0.9146 mL

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Piperlonguminine

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Piperlonguminine

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