IUB0271 hydrochloride
Based on 1 Customer Validation
IUB0271 hydrochloride (acyl-GIP hydrochloride) is a glucose-dependent insulinotropic polypeptide receptor (GIPR) agonist with blood-brain barrier permeability. IUB0271 hydrochloride activates the GIPR signaling pathway, inhibits food intake and weight gain, and induces cFos neuron activation in the area postrema. IUB0271 hydrochloride enhances lipid clearance and induces systemic fatty acid oxidation. IUB0271 hydrochloride improves dyslipidemia, reduces atherosclerotic plaque formation and decreases adipocyte volume. IUB0271 hydrochloride can be used in studies related to obesity, dyslipidemia and atherosclerosis.
For research use only. We do not sell to patients.
- Purity: 98.67%
- Formula: C264H403N65O77S·xHCl
- Molecular Weight:5751.48 (free base)
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Storage:
Sealed storage, away from moisture.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Biological Activity
IUB0271 (1 nmol/kg; subcutaneous injection; 30 min prior to tolerance testing) hydrochloride increases lipid tolerance by approximately 38% and improves glucose tolerance in obese male C57BL/6J mice[2].
IUB0271 (150 nmol/kg; subcutaneous injection; single bolus) hydrochloride activates cFos expression in specific brain regions of male C57BL/6J wild-type mice fed a normal diet, but does not induce cFos activation in key brain regions of male C57BL/6J Vgat-Gipr knockout mice fed a normal diet[1].
IUB0271 (1 nmol/kg; subcutaneous injection; single administration 30 min prior to gavage) hydrochloride enhances the clearance of plasma lipids into brown adipose tissue (BAT) by increasing lipoprotein lipase activity in BAT of obese male C57BL/6J mice by approximately 21%[2].
IUB0271 (1 nmol/kg; subcutaneous injection; single administration 30 min before gavage; single administration at 11:00 a.m. for metabolic evaluation) hydrochloride increases lipid tolerance by approximately 28% and elevates systemic fatty acid oxidation levels by approximately 11% in obese male GiprBAT+/+ mice[2].
IUB0271 (10 nmol/kg; subcutaneous injection; once daily for 28 consecutive days) hydrochloride improves dyslipidemia and reduces atherosclerotic plaque formation in male LDLR-/- mice[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J wild-type mice
(male, diet-induced obese via high-fat diet for ~20 weeks)
(Vgat-cre+/−Giprflx/flx, male, diet-induced obese via high-fat diet for ~20 weeks)[1] -
Dosage:100 nmol/kg (acute food intake testing)
100 nmol/kg (chronic metabolic effects) -
Administration:s.c.; single bolus (acute food intake testing)
s.c.; daily; 26 days (chronic metabolic effects) -
Result:Reduced 18-hour cumulative food intake with single subcutaneous injection, and lowered body weight, food intake and fat mass after 26 days of daily dosing in wild-type obese mice; lean mass, glycemic indicators and plasma triglycerides remained unaffected.
Showed no changes in acute food intake, body weight or tissue mass under either single or chronic subcutaneous dosing in Vgat-Gip knockout obese mice; it decreased fasting insulin and improved insulin sensitivity without altering blood glucose, glucose tolerance or triglyceride levels.
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Animal Model:C57BL/6J wild-type mice (male, normal chow-fed)
C57BL/6J Vgat-Gipr knockout mice (Vgat-cre+/−Giprflx/flx, male, normal chow-fed)[1] -
Dosage:150 nmol/kg
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Administration:s.c.; single bolus
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Result:Accumulated within the area postrema and hypothalamic median eminence in both wild-type and Vgat-Gip knockout chow-fed male mice.
Triggered obvious cFos activation in the area postrema, arcuate nucleus and paraventricular nucleus only in wild-type mice, while no notable cFos induction occurred in these three brain regions in Vgat-Gip knockout mice.
Produced no cFos signal in the nucleus tractus solitarius, ventromedial hypothalamus, dorsomedial hypothalamus and lateral parabrachial nucleus of wild-type mice.
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Animal Model:C57BL/6J (male, 20-26 weeks old, high-fat diet-induced obesity and insulin resistance)[2]
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Dosage:1 nmol/kg
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Administration:s.c.; single dose 30 minutes prior to tolerance tests
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Result:Lowered plasma triglyceride excursions by ~38% during lipid tolerance tests.
Significantly lowered blood glucose during intraperitoneal glucose tolerance tests.
Abolished effects observed with pharmacological GIPR inhibition or whole-body GIPR knockout.
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Animal Model:C57BL/6J (male, 24-32 weeks old, high-fat diet-induced obesity and insulin resistance)[2]
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Dosage:1 nmol/kg
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Administration:s.c.; single dose 30 minutes prior to oral gavage
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Result:Lowered active GLP-1 plasma concentrations during the first 30 minutes post-oral lipid gavage.
Increased brown adipose tissue (BAT) fatty acid uptake by ~8% compared to PBS-treated mice.
Increased BAT lipoprotein lipase activity by ~21% compared to PBS-treated mice.
Did not affect gastric emptying, plasma triglyceride appearance, or levels of insulin, glucagon, or c-peptide.
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Animal Model:GiprBAT+/+ (BAT GIPR-expressing) and GiprBAT-/- (BAT-specific GIPR knockout) on C57BL/6J background (male, 24 weeks old, high-fat diet-induced obesity and insulin resistance)[2]
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Dosage:1 nmol/kg
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Administration:s.c.; single dose 30 minutes prior to oral gavage; single dose at 11:00 AM for metabolic assessments
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Result:Lowered plasma triglyceride excursions by ~28% in GiprBAT+/+ mice.
Reduced RER for 6 hours post-treatment in GiprBAT+/+ mice.
Increased whole-body fatty acid oxidation by ~11% in GiprBAT+/+ mice.
No effects observed in GiprBAT-/- mice.
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Animal Model:LDL receptor knockout (LDLR-/-) (male, 8-week-old, western diet-induced atherogenic dyslipidemia)[3]
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Dosage:10 nmol/kg
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Administration:s.c.; daily; 28 days
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Result:Lowered plasma triglyceride levels.
Lowered plasma cholesterol levels.
Dropped VLDL and LDL fractions without altering HDL levels.
Shrank atherosclerotic plaque area in aortic arches, aortic valves and descending aorta.
Reduced adipocyte size within subcutaneous inguinal white adipose tissue (iWAT).
Suppressed complement/coagulation cascades, fibrinolysis, cholesterol metabolism, fat digestion and absorption, and triglyceride catabolism pathways in iWAT.
Triggered minimal gene expression shifts and preserved adipocyte size in visceral gonadal white adipose tissue (gWAT).
Chemical Information
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Appearance Solid
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Molecular Weight 5751.48 (free base)
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Formula C264H403N65O77S·xHCl
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Color White to off-white
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Synonyms
acyl-GIP hydrochloride
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Sequence
Tyr-{Aib}-Glu-Gly-Thr-Phe-Ile-Ser-Asp-Tyr-Ser-Ile-Ala-Met-Asp-Lys-Ile-His-Gln-Gln-Asp-Phe-Val-Asn-Trp-Leu-Leu-Ala-Gln-Lys-Gly-Lys-Lys-Asn-Asp-Trp-Lys-His-Asn-Ile-Thr-Gln-Lys(γGlu-γGlu-γGlu-C16)
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Sequence Shortening
Y-{Aib}-EGTFISDYSIAMDKIHQQDFVNWLLAQKGKKNDWKHNITQ-Lys(γGlu-γGlu-γGlu-C16)
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Sealed storage, away from moisture
Powder -80°C 2 years -20°C 1 year * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Solvent & Solubility
DMSO : ≥ 100 mg/mL
H2O : ≥ 25 mg/mL
* "≥" means soluble, but saturation unknown.
Purity & Documentation
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Data Sheet (303 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
[1]. Liskiewicz A, et al. Glucose-dependent insulinotropic polypeptide regulates body weight and food intake via GABAergic neurons in mice. Nature metabolism. 2023 Dec;5(12):2075-2085. [Content Brief]
[2]. Lyons SA, et al. Acute exogenous acyl-GIP treatment enhances lipid handling and fatty acid oxidation by involving brown fat. EMBO reports. 2025 Nov;26(21):5154-5171. [Content Brief]
[3]. Sachs S, et al. GIP receptor agonism improves dyslipidemia and atherosclerosis independently of body weight loss in preclinical mouse model for cardio-metabolic disease. Cardiovascular diabetology. 2023 Aug 17;22(1):217. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
- IUB0271
- acyl-GIP
- IUB 0271
- IUB-0271
- GLP Receptor
- hypothalamic median eminence
- cardiometabolic disease
- Vgat-expressing inhibitory GABAergic neurons
- glucose-dependent insulinotropic polypeptide receptor
- subcutaneous adipose tissue
- brown adipose tissue
- diet-induced obesity
- dyslipidemia
- area postrema
- atherosclerosis
- Inhibitor
- inhibitor
- inhibit