Cat. No.: HY-P1107

Antisauvagine-30

Name: Antisauvagine-30
Brand: MedChemExpress
SKU: HY-P1107
Price: 320.00 USD
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(Synonyms: aSvg-30)

4 Cited Publications

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Based on 4 publication(s) in Google Scholar

Antisauvagine-30 (aSvg-30) is a selective peptide antagonist of the CRF₂ receptor, with an IC₅₀ of 1.1 nM for mouse CRF₂. Antisauvagine-30 modulates cAMP signaling, gastric emptying, food intake, fear conditioning, anxiety-like behavior, stress responses, corticosterone levels, c-Fos expression, and CRF expression. Antisauvagine-30 is used in studies of anxiety-related disorders.

For research use only. We do not sell to patients.

Purity : 99.74%
CAS No.: 220673-95-0
Formula: C₁₆₁H₂₇₄N₄₈O₄₆S
Molecular Weight:3650.26

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)

Antisauvagine-30 Chemical Structure

CAS No.: 220673-95-0

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Fluorescent Dye

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

Biological Activity
- Description
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Publications (4)
Solvent & Solubility
- In Vitro
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target

^[1]^[2]^[3]^[4]^[5]^[6]^[7]

CRFR2

1.1 nM nM (IC₅₀)

All CRFR Isoforms :

CRFR1
CRFR2

In Vitro

Antisauvagine-30 (aSvg-30) (90 min) is a CRF₂-selective competitive antagonist with an IC₅₀ of 1.1 nM at mouse CRF₂β receptors and an IC₅₀ of 400 nM at human CRF₁ receptors in stably transfected CHO cell membranes^[1].
Antisauvagine-30 binds with high affinity to CRF2 receptor subtypes (K_i = 0.41-0.8 nM; K_d = 1.4 nM for mouse CRF2b) and with lower affinity to CRF1 receptor subtypes (K_i = 66-170 nM) in transfected HEK293 cell membrane preparations^[2].
Antisauvagine-30 functionally antagonizes CRF₁-mediated cAMP signaling in HEK293-rat CRF₁ cells and Y79 retinoblastoma cells with IC₅₀ values of 1-2 μM^[2].
Antisauvagine-30 (0-1 µM; 60 min) binds with high affinity and strong selectivity to mCRFR2b over rCRFR1 in membrane preparations from transfected HEK 293 cells, with a K_d of 1.4 nM for mCRFR2b^[4].
Antisauvagine-30 (0.01-1 µM; 30 min) is a potent antagonist of Svg-stimulated cAMP production in HEK-mCRFR2b cells with low intrinsic activity, while displaying much weaker antagonist activity in HEK-rCRFR1 cells, consistent with CRFR2b selectivity^[4].
Antisauvagine-30 is a highly selective CRF-R2 ligand with nanomolar affinity for murine CRF-R2b and human CRF-R2α, and negligible affinity for CRF-R1 in recombinant HEK293 cell membrane preparations^[5].
Antisauvagine-30 binds with high affinity to recombinant CRF₂ receptor splice variants (K_d of 0.125 nM for CRF₂(a), K_i of 1.4 nM for CRF₂(b)) and exhibits substantially lower affinity for CRF₁ receptors (K_i of 154 nM at rat CRF₁, no detectable specific binding at human CRF₁), confirming its selectivity as a CRF₂ receptor ligand^[7].

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

In Vivo

Antisauvagine-30 (3-30 µg/kg; i.p.; single dose; 10 min before Urocortin) dose-dependently antagonizes Urocortin-induced delay of gastric emptying in mice, with partial reversal at 30 µg/kg^[1].
Antisauvagine-30 (100 µg/kg; s.c.; single dose; 3 or 6 h prior to Urocortin) at 100 µg/kg does not significantly antagonize Urocortin-induced delayed gastric emptying when administered 3 or 6 h prior to Urocortin in mice^[1].
Antisauvagine-30 (3 nmol; i.c.v.; single bolus) reduces shock-induced freezing in mice independently of CRF₂ receptor status, with no effect on marble burying or elevated plus-maze measures of anxiety-like behavior^[2].
Antisauvagine-30 (2.70-5.40 nmol/rat; i.c.v.; single dose 15 min before the conditioned fear test) dose-dependently enhances conditioned fear responses, elevates plasma corticosterone, and increases c-Fos and CRF expression in corticolimbic and hypothalamic brain regions of fear-conditioned Wistar rats^[3].
Antisauvagine-30 (30-200 μg/kg; i.p.; single dose 10 min before Urocortin) at 100 μg/kg completely blocks Urocortin-induced inhibition of gastric emptying in mice, while the 30 μg/kg dose produces 54% antagonism^[5].
Antisauvagine-30 (30-200 μg/kg; i.p.; single dose 10 min before Urocortin) only partially reverses Urocortin-induced hypophagia in fasted mice, with ~35% reduction of the inhibitory effect at 100 μg/kg^[5].
Antisauvagine-30 (100 μg/kg; i.p.; single dose 10 min before Urocortin) combined with the CRF-R1 antagonist CP 154526 (HY-12130) does not show enhanced partial reversal of Urocortin-induced hypophagia compared to Antisauvagine-30 alone^[5].
Antisauvagine-30 (400 ng per mouse; bilateral injection into dorsal hippocampus or lateral intermediate septum; 15 min before training alone or 10 min before h/rCRF for combined treatment), a CRFR2-preferring antagonist, blocks septal CRFR2-mediated impairment of fear conditioning and enhances fear conditioning when administered alone into the lateral intermediate septum, while having no effect on hippocampal CRFR1-mediated enhancement of fear conditioning^[6].
Antisauvagine-30 (100 pmol per mouse; bilateral injection into lateral intermediate septum; 10 min before h/rCRF for combined treatment or 30 min before plus-maze test alone) completely blocks CRF-induced anxiety mediated by septal CRFR2 without affecting baseline anxiety levels in mice^[6].
Antisauvagine-30 (bilateral injection into lateral intermediate septum; before immobilization stress) fully prevents stress-induced anxiety when administered into the lateral intermediate septum, confirming the role of septal CRFR2 in mediating stress-generated anxiety^[6].
Antisauvagine-30 (0.03-10 mg/kg; i.v. bolus), a selective CRF₂ receptor antagonist, completely blocks Urocortin 2-induced hypotension in conscious rats at doses of 1-10 mg/kg i.v., but has no effect on basal mean arterial blood pressure or heart rate when administered alone^[7].

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

Animal Model:

C57BL/6 (male; 8-12 weeks old; 20-25 g)^[1]
Dosage:

3 µg/kg; 10 µg/kg; 30 µg/kg
Administration:

i.p.; single dose; 10 min before Urocortin
Result:

Showed no significant antagonist effect on Urocortin-induced inhibition of gastric emptying at 3 µg/kg.
Increased gastric emptying to 38.0% at 10 µg/kg.
Increased gastric emptying to 44.0% at 30 µg/kg.
Did not alter basal gastric emptying when injected alone at 30 µg/kg.

Animal Model:

C57BL/6 (male; 8-12 weeks old; 20-25 g)^[1]
Dosage:

100 µg/kg (3 h before Urocortin); 100 µg/kg (6 h before Urocortin)
Administration:

s.c.; single dose (3 h before Urocortin); single dose (6 h before Urocortin)
Result:

Had no significant antagonist effect on Urocortin-induced inhibition of gastric emptying when administered 3 h before Urocortin at 100 µg/kg.
Had no significant antagonist effect on Urocortin-induced inhibition of gastric emptying when administered 6 h before Urocortin at 100 µg/kg.
Did not influence basal gastric emptying when injected alone at 100 µg/kg.
Did not significantly alter food intake measured at 2 h or 5 h after injection at 100 µg/kg.

Animal Model:

C57BL/6J (adult male; ≥12 generations backcrossed; CRF₂ receptor knockout and wildtype littermates; 26.5-32.3 g at study onset; cannulated)^[2]
Dosage:

3 nmol (10.7 µg)
Administration:

i.c.v.; single bolus infusion of 2 µL delivered by gravity over 30 sec; pretreatment 15 min before marble burying test, 30 min before elevated plus-maze and shock-induced freezing tests
Result:

Reduced the duration of shock-induced freezing in both wildtype and CRF₂ knockout mice, with treated mice freezing less than vehicle-pretreated mice.
Showed no significant effects on % open arm time, raw open arm time, total number of arm entries in the elevated plus-maze, or number of marbles buried in the marble burying test.

Animal Model:

Wistar rats (male; adult; 200 g)^[3]
Dosage:

2.70 nmol/rat (10 μg/rat); 5.40 nmol/rat (20 μg/rat)
Administration:

i.c.v.; single dose 15 min before the conditioned fear test
Result:

Increased total freezing duration relative to vehicle-treated fear-conditioned rats at both tested doses.
Elevated plasma corticosterone levels in fear-conditioned rats compared to vehicle-treated fear-conditioned controls at both tested doses.
Increased c-Fos expression at 115 min after administration in the cingulate cortex areas 1 and 2 (Cg1: 56.83 cells per 0.1 mm²; Cg2: 86.58 cells per 0.1 mm²), secondary motor cortex (M2: 78.67 cells per 0.1 mm²), central amygdala (CeA: 78.00 cells per 0.1 mm²), medial amygdala (MeA: 67.58 cells per 0.1 mm²), and parvocellular paraventricular hypothalamic nucleus (pPVN: 60.00 cells per 0.1 mm²) in fear-conditioned rats relative to vehicle-treated fear-conditioned rats at the 5.40 nmol/rat dose.
Increased CRF expression at 35 min after administration in the Cg1 (57.17 cells per 0.1 mm²), M2 (64.67 cells per 0.1 mm²), and pPVN (36.00 cells per 0.1 mm²) in fear-conditioned rats compared to vehicle-treated fear-conditioned rats at the 5.40 nmol/rat dose.
Increased CRF expression in the CeA (44.83 cells per 0.1 mm²) reflecting a significant fear×reagent interaction at the 5.40 nmol/rat dose.

Animal Model:

C57BL/6 (male; 8-12 weeks old; 20-25 g; 18-20 h fasted with solid nutrient meal challenge)^[5]
Dosage:

30 μg/kg (54% antagonism); 100 μg/kg (complete antagonism); 200 μg/kg
Administration:

i.p.; single dose 10 min before Urocortin
Result:

Dose-dependently antagonized Urocortin-induced inhibition of gastric emptying by 54% at 30 μg/kg and 100% at 100 μg/kg.
Resulted in gastric emptying values of 40.9% at 30 μg/kg and 71.2% at 100 μg/kg.
Showed a tendency to increase basal gastric emptying to 78.3% at 100 μg/kg alone.

Animal Model:

C57BL/6 (male; 8-12 weeks old; 20-25 g; 18-20 h fasted with food intake measurement after refeeding)^[5]
Dosage:

30 μg/kg (no effect); 100 μg/kg (35% reversal); 200 μg/kg (31% reversal)
Administration:

i.p.; single dose 10 min before Urocortin
Result:

Partially reversed Urocortin-induced decrease in 2-h cumulative food intake by 35% at 100 μg/kg and 31% at 200 μg/kg.
Showed no effect on Urocortin-induced hypophagia at 30 mg/kg.
Resulted in 2-h cumulative food intake values of 0.36 g at 100 μg/kg, 0.34 g at 200 μg/kg, and 0.26 g at 30 μg/kg.
Did not influence basal food intake at 30, 100, or 200 μg/kg alone, with values of 0.54 g, 0.53 g, and 0.57 g, respectively.

Animal Model:

C57BL/6 (male; 8-12 weeks old; 20-25 g; 18-20 h fasted with Urocortin challenge and food intake measurement)^[5]
Dosage:

100 μg/kg (co-administered with CP-154,526 10 μg/kg)
Administration:

i.p.; single dose 10 min before Urocortin
Result:

Resulted in 32% inhibition of 2-h cumulative food intake by Urocortin when co-administered with CP-154,526, similar to the antagonism observed when administered alone.

Animal Model:

BALB/c mice (9-week-old male)^[6]
Dosage:

400 ng (100 pmol) per mouse
Administration:

bilateral injection into dorsal hippocampus or lateral intermediate septum (0.25 μl per side); 15 min before training (alone); 10 min before h/rCRF (combined treatment)
Result:

Did not affect context- or tone-dependent fear conditioning when injected alone into the dorsal hippocampus.
Significantly enhanced both context-dependent and tone-dependent fear conditioning when injected alone into the lateral intermediate septum.
Did not block h/rCRF-induced enhancement of fear conditioning when co-administered before intrahippocampal h/rCRF injection.
Completely blocked h/rCRF-induced impairment of both context-dependent and tone-dependent fear conditioning when co-administered before intraseptal h/rCRF injection.

Animal Model:

BALB/c mice (9-week-old male)^[6]
Dosage:

100 pmol per mouse
Administration:

bilateral injection into lateral intermediate septum (0.25 μl per side); 10 min before h/rCRF (combined treatment); 30 min before plus-maze test (alone)
Result:

Did not affect baseline anxiety levels as measured by time spent and number of entries on the open arms of the elevated plus-maze when injected alone into the lateral intermediate septum.
Completely antagonized h/rCRF-induced reduction in time spent on the open arms and reduction in the number of open arm entries when co-administered with h/rCRF via intraseptal injection.

Animal Model:

Sprague-Dawley rats (male; adult; 220-240 g upon arrival; conscious freely moving with indwelling carotid artery and jugular vein cannulae)^[7]
Dosage:

0.03, 0.1, 0.3, 1, 3, 10 mg/kg (assessment of effects alone); 1, 3, 10 mg/kg (antagonist pretreatment assessment)
Administration:

i.v. bolus (cumulative dosing every 20 min, for assessment of effects alone); i.v. bolus (administered 30 min prior to Urocortin 2 challenge, for antagonist pretreatment assessment)
Result:

Produced no significant effects on mean arterial blood pressure or heart rate at doses up to 10 mg/kg in the cumulative dose-response study.
Blocked Urocortin 2 (0.1 mg/kg, i.v.)-induced reduction in mean arterial blood pressure at 1, 3, and 10 mg/kg in the pretreatment experiment.
Had no significant effect on mean arterial blood pressure at any tested dose when administered alone.
Produced no statistically significant effects on heart rate in the pretreatment experiment.

Chemical Information

CAS No. 220673-95-0
Appearance Solid
Molecular Weight 3650.26
Formula C₁₆₁H₂₇₄N₄₈O₄₆S
Color White to off-white
SMILES

O=C(N[C@@H](CC1=CNC=N1)C(N[C@@H](CC(C)C)C(N[C@@H](CC(C)C)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCCCN)C(N[C@@H](CCSC)C(N[C@@H]([C@@H](C)CC)C(N[C@@H](CCC(O)=O)C(N[C@@H]([C@@H](C)CC)C(N[C@@H](CCC(O)=O)C(N[C@@H](CCCCN)C(N[C@@H](CCC(N)=O)C(N[C@@H](CCC(O)=O)C(N[C@@H](CCCCN)C(N[C@@H](CCC(O)=O)C(N[C@@H](CCCCN)C(N[C@@H](CCC(N)=O)C(N[C@@H](CCC(N)=O)C(N[C@@H](C)C(N[C@@H](C)C(N[C@@H](CC(N)=O)C(N[C@@H](CC(N)=O)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CC(C)C)C(N[C@@H](CC(C)C)C(N[C@@H](CC(C)C)C(N[C@@H](CC(O)=O)C(N[C@@H]([C@H](O)C)C(N[C@@H]([C@@H](C)CC)C(N)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)[C@@H](CC2=CC=CC=C2)N
Synonyms

aSvg-30
Sequence

{DPhe}-His-Leu-Leu-Arg-Lys-Met-Ile-Glu-Ile-Glu-Lys-Gln-Glu-Lys-Glu-Lys-Gln-Gln-Ala-Ala-Asn-Asn-Arg-Leu-Leu-Leu-Asp-Thr-Ile-NH2
Sequence Shortening

(DPhe)-HLLRKMIEIEKQEKEKQQAANNRLLLDTI-NH2
Shipping

Room temperature in continental US; may vary elsewhere.

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)

Publications (4)

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Journal Impact Factor

Adv Sci (Weinh)

PVNCRF Neurons Regulate Migraine-Like Allodynia by Activating CRFR2 on Spinal Trigeminal Caudalis Glutamatergic Neurons. [Abstract]

2026 Feb 28:e20530. PMID: 41762709
Pain

Mast cell corticotropin-releasing factor receptor 1 contributes to pancreatic cancer pain via mitogen-activated protein kinase/sphingosine kinases type 1 signaling. [Abstract]

2026 Apr 1;167(4):962-975. PMID: 41615309
Ann Med

Corticotropin-releasing hormone inhibits autophagy by suppressing PTEN to promote apoptosis in dermal papilla cells. [Abstract]

2025 Dec;57(1):2490823. PMID: 40219757
Sci Rep

Spinal CRH facilitates the micturition reflex via the CRH2 receptor in rats with normal bladder and bladder outlet obstruction. [Abstract]

2025 Jan 29;15(1):3604. PMID: 39875474

Solvent & Solubility

In Vitro:

DMSO : 4 mg/mL (1.10 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

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Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

0.2740 mL

1.3698 mL

2.7395 mL

5 mM

---

10 mM

---

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). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

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Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (316 KB)
SDS (254 KB)
- English - EN (254 KB)
- Français - FR (254 KB)
- Deutsch - DE (254 KB)
- Norwegian - NO (254 KB)
- Español - ES (254 KB)
- Swedish - SV (254 KB)
- Italian - IT (254 KB)
- Korean - KR (254 KB)
- Portuguese - PT (254 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
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SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Rivier J, et al. Potent and long-acting corticotropin releasing factor (CRF) receptor 2 selective peptide competitive antagonists. Journal of medicinal chemistry. 2002 Oct 10;45(21):4737-47. [Content Brief]

[2]. Zorrilla EP, et al. Anxiolytic-like effects of antisauvagine-30 in mice are not mediated by CRF2 receptors. PloS one. 2013;8(8):e63942.

[3]. Skórzewska A, et al. The effect of CRF2 receptor antagonists on rat conditioned fear responses and c-Fos and CRF expression in the brain limbic structures. Behavioural brain research. 2011 Aug 01;221(1):155-65.

[4]. Rühmann A, et al. Structural requirements for peptidic antagonists of the corticotropin-releasing factor receptor (CRFR): development of CRFR2beta-selective antisauvagine-30. Proc Natl Acad Sci U S A. 1998 Dec 22;95(26):15264-9.

[5]. Wang L, et al. Peripheral urocortin inhibits gastric emptying and food intake in mice: differential role of CRF receptor 2. American journal of physiology. Regulatory, integrative and comparative physiology. 2001 Nov;281(5):R1401-10.

[6]. Radulovic J, et al. Modulation of learning and anxiety by corticotropin-releasing factor (CRF) and stress: differential roles of CRF receptors 1 and 2. The Journal of neuroscience : the official journal of the Society for Neuroscience. 1999 Jun 15;19(12):5016-25. [Content Brief]

[7]. Mackay KB, et al. Effects of a selective agonist and antagonist of CRF2 receptors on cardiovascular function in the rat. European journal of pharmacology. 2003 May 23;469(1-3):111-5. [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	0.2740 mL	1.3698 mL	2.7395 mL	6.8488 mL

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Antisauvagine-30

4 Cited Publications

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Antisauvagine-30

Publications Citing Use of MedChemExpress (MCE) Antisauvagine-30

All CRFR Isoforms