Astressin B 10mg

Description

Astressin B 10mg Research-Grade Peptide

Disclaimer: Astressin B is not approved by the U.S. Food and Drug Administration (FDA) for human or veterinary use. It is intended strictly for laboratory and research purposes only.

What is Astressin B?

Astressin B is a synthetic cyclic peptide antagonist developed as a broad-spectrum blocker of corticotropin-releasing factor (CRF) receptors. It is a cyclic analog of astressin, engineered to antagonize both CRF receptor subtypes, CRF1 and CRF2, in preclinical research models. The compound was developed to serve as a pharmacological tool for investigating the physiological roles of the CRF signaling axis in stress-related, gastrointestinal, and neuroendocrine research systems.

Astressin B is distinguished from earlier CRF antagonists by its extended duration of action in preclinical models and its non-selective receptor profile, making it a research tool of particular interest in studies requiring sustained CRF pathway inhibition across both receptor subtypes simultaneously. Its cyclic peptide structure confers increased resistance to proteolytic degradation relative to linear CRF analogs under experimental conditions.

Astressin B is not an approved therapeutic compound. It is intended exclusively for qualified researchers operating in controlled laboratory environments. It is not a dietary supplement or consumer product and has no approved indications for human or veterinary use.

PROPERTIES OF ASTRESSIN B

Property	Details
CAS Number	CAS Number: Not universally registered in major chemical databases; compound identity confirmed by PubChem CID 73350132 (C₁₈₃H₃₀₅N₄₇O₅₅, MW 4043.7 Da)
Molar Mass	4043.7 Da
Chemical Formula	C₁₈₃H₃₀₅N₄₇O₅₅
Stability / Shelf Life	24 months when stored lyophilized at −20°C under recommended conditions
Synonyms	Astressin-B; cyclo(30-33)[D-Phe¹²,Nle²¹·³⁸,Glu³⁰,Lys³³]hCRF(12-41); non-selective CRF receptor antagonist
Storage Instructions	−20°C (lyophilized); protect from light, heat, and moisture
Amino Acid Sequence	Cyclic analog of hCRF(12-41) with D-Phe at position 12, Nle at positions 21 and 38, and a lactam bridge between Glu30 and Lys33
WADA Status	Not listed on the WADA 2026 Prohibited List

WORKING MECHANISM OF ASTRESSIN B

Astressin B is proposed to exert its observed activity through competitive antagonism at both CRF1 and CRF2 receptor subtypes in experimental models. CRF receptors are G-protein-coupled receptors (GPCRs) that activate adenylyl cyclase via Gs-protein coupling upon binding of endogenous CRF or urocortin ligands, leading to elevation of intracellular cyclic AMP (cAMP) and downstream activation of protein kinase A (PKA) signaling cascades. Astressin B has been documented in radioligand binding assays and functional cell-based studies to competitively displace native CRF ligands at both receptor subtypes, attenuating downstream cAMP accumulation in receptor-expressing cell preparations.

Mechanistically, Astressin B is thought to influence:

• Competitive displacement of CRF and urocortin ligands at CRF1 and CRF2 receptor binding sites, documented in radioligand competition binding assays with high affinity at both subtypes
• Attenuation of CRF-stimulated cAMP accumulation in CRF1 and CRF2 receptor-expressing cell preparations, consistent with competitive GPCR antagonism at the molecular level
• Suppression of CRF-induced HPA axis activation in preclinical rodent models, observed as reduced ACTH and corticosterone output following central or peripheral administration in experimental settings
• Inhibition of CRF-mediated gastrointestinal motility alterations, documented in rodent stress models examining colonic transit and visceral hypersensitivity under controlled laboratory conditions
• The extended duration of CRF pathway antagonism relative to linear CRF antagonists is attributed to its cyclic peptide architecture and increased resistance to proteolytic cleavage

The non-selective profile of Astressin B across CRF1 and CRF2 subtypes distinguishes it mechanistically from subtype-selective antagonists such as antalarmin (CRF1-selective) or antisauvagine-30 (CRF2-selective). All mechanistic findings are derived from in vitro binding assays and preclinical animal models only. Human receptor pharmacology data remain limited.

What are the Potential Research Observations of Astressin B?

The following research findings are based on articles retrieved from PubMed and are reported from preclinical and in vitro studies only. These findings do not constitute clinical evidence.

CRF Receptor Binding and Antagonism in Radioligand Assay Models:

Astressin B has been characterized in radioligand binding assays as a high-affinity competitive antagonist at both CRF1 and CRF2 receptor subtypes. Studies employing membrane preparations from receptor-expressing cell lines have documented concentration-dependent displacement of radiolabeled CRF at both subtypes, with reported Ki values in the sub-nanomolar to low nanomolar range in experimental binding systems. These in vitro characterization studies established Astressin B as a pharmacological reference tool for non-selective CRF receptor blockade in research models. Findings are from cell-based and membrane preparation systems and do not reflect clinical pharmacology. [Rivier et al., 2002] 

Stress-Induced HPA Axis Signaling in Rodent Models:

Astressin B has been investigated in rodent stress models examining CRF-mediated activation of the hypothalamic-pituitary-adrenal (HPA) axis. In preclinical studies, administration of Astressin B was associated with attenuation of stress-induced ACTH secretion and corticosterone elevation in rodent preparations under controlled experimental conditions. These observations have been used in laboratory frameworks examining the functional contribution of CRF receptor subtypes to neuroendocrine stress responses. Findings are from rodent models and have not been validated in clinical research settings. [Rivier et al., 2002] 

Gastrointestinal Motility and Visceral Sensitivity Research Models:
Astressin B has been employed as a research tool in preclinical studies examining CRF-mediated alterations in gastrointestinal function. In rodent models of stress-induced colonic motility, blockade of CRF signaling pathways was associated with inhibition of accelerated colonic transit and reduced visceral hypersensitivity responses under controlled laboratory conditions. These findings have contributed to investigations of the CRF signaling axis in gut-brain interaction research. Observations are from preclinical animal models and have not been replicated in clinical contexts. [Taché and Perdue, 2004] 

Hair Follicle Cycling Research in Preclinical Models:

Astressin B has been investigated in a preclinical mouse model examining the role of CRF receptor signaling in hair follicle cycling. In a study using a murine model of CRF over-expression associated alopecia, peripheral administration of Astressin B was associated with restoration of pigmentation and hair re-growth in affected animals under controlled experimental conditions. The proposed mechanism involved non-selective CRF receptor antagonism in skin and peripheral tissue. Findings are from a single CRF over-expressing mouse model and require independent replication before mechanistic conclusions can be drawn. [Wang et al., 2011] 

Note: Astressin B is not approved by the U.S. Food and Drug Administration (FDA) for human or veterinary use. It has no approved therapeutic indications. This compound is intended strictly for scientific research purposes only.

Safety Profile and Toxicological Considerations

Researchers have noted the following observations in experimental settings. Long-term safety data remain absent, and a complete toxicity profile has not been established in any biological system.

• No LD50 or standardized chronic toxicity data are available in the peer-reviewed literature for Astressin B
• No human pharmacokinetic, pharmacodynamic, or clinical safety profile has been established for this compound
• Inadvertent exposure risks are not characterized; no human safety data exists
• Given its broad CRF1 and CRF2 antagonism profile, off-target effects on stress axis regulation, autonomic function, and cardiovascular tone cannot be excluded based on available preclinical data
• Immunotoxicity, reproductive toxicity, and organ-level effects remain uncharacterized at the preclinical level beyond acute study observations
• Astressin B is a cyclic peptide susceptible to oxidation under aqueous conditions; solution stability must be accounted for in experimental design

WHY CHOOSE RCDBIO FOR ASTRESSIN B?

Each batch of Astressin B supplied by RCDbio undergoes independent third-party laboratory testing, with a batch-specific Certificate of Analysis (COA) available for researcher verification before experimental use.

• Independent third-party laboratory testing per batch
• COA confirming compound identity and purity per lot
• Molecular identity confirmed against PubChem CID 73350132 (C₁₈₃H₃₀₅N₄₇O₅₅, MW 4043.7 Da) 
• RCDbio does not self-certify; all quality verification is conducted by accredited independent laboratories

Disclosure: Sponsored by RCDbio. This content is for informational purposes only and does not constitute an endorsement of any product for human use.

FREQUENTLY ASKED QUESTIONS

Is Astressin B approved for human use?

No. Astressin B is not approved by the FDA for any human or medical application. It is classified as a research-use peptide only and has no approved therapeutic indications in the United States or any other regulatory jurisdiction. It is intended exclusively for qualified researchers in controlled laboratory settings.

What distinguishes Astressin B from other CRF receptor antagonists used in research?

Astressin B is a non-selective CRF receptor antagonist, meaning it blocks both the CRF1 and CRF2 receptor subtypes in experimental models. This distinguishes it from subtype-selective compounds such as antalarmin, which targets CRF1 selectively, or antisauvagine-30, which targets CRF2 selectively. Additionally, the cyclic peptide architecture of Astressin B confers increased resistance to proteolytic degradation compared to linear CRF analogs, resulting in an extended duration of receptor blockade observed in preclinical models.

What receptor targets is Astressin B proposed to interact with in research models? 

Based on published radioligand binding and functional cell-based studies, Astressin B is characterized as a competitive antagonist at both CRF1 (CRHR1) and CRF2 (CRHR2) receptor subtypes. These receptors are GPCRs that couple to Gs proteins and regulate cAMP-dependent signaling cascades. Astressin B competitively displaces endogenous CRF and urocortin ligands at both subtypes in experimental binding systems, with reported affinity in the sub-nanomolar to low nanomolar range.

How should Astressin B be stored in a laboratory setting?

Lyophilized Astressin B should be stored at −20°C in a sealed, desiccated container protected from light, heat, and moisture. Reconstituted solutions should be prepared immediately before use and stored at 4°C for short-term use only, as cyclic peptides are susceptible to oxidation in aqueous conditions. Single-use aliquots are recommended before freezing to avoid repeated freeze-thaw cycles. Shelf life under recommended lyophilized storage conditions is reported at up to 24 months.

What preclinical models have been used in Astressin B research?

Published laboratory studies have employed rodent models, including mice and rats, across several research contexts. Models used include stress-induced HPA axis activation assays, CRF-stimulated colonic motility preparations, radioligand binding assays using receptor-expressing cell membrane fractions, and a murine model of stress-associated hair follicle cycling. All findings are from preclinical animal or cell-based experimental systems and do not represent validated human clinical data.

REFERENCES

Rivier JE, Rivier CL. Corticotropin-releasing factor peptide antagonists: design, characterization and potential clinical relevance. Front Neuroendocrinol. 2014;35(2):161-170. PMID: 24269930. https://pubmed.ncbi.nlm.nih.gov/24269930/ 

Taché, Y., & Perdue, M. H. (2004). Role of peripheral CRF signalling pathways in stress-related alterations of gut motility and mucosal function. Neurogastroenterology and Motility, 16(Suppl 1), 137–142. https://pubmed.ncbi.nlm.nih.gov/15066020/ 

Wang, L., Million, M., Rivier, J., Rivier, C., Craft, N., Stenzel-Poore, M. P., & Taché, Y. (2011). CRF receptor antagonist astressin-B reverses and prevents alopecia in CRF overexpressing mice. PLOS ONE, 6(2), e16377. https://pubmed.ncbi.nlm.nih.gov/21359208/ 

Disclaimer

Astressin B is exclusively for laboratory research purposes. RCDbio products are not intended to diagnose, prevent, treat, or cure any disease or medical condition. The Food and Drug Administration has not evaluated the statements on this page. Researchers must comply with all applicable local laws and regulations governing the use of research compounds. By purchasing, you agree to RCDbio Terms and Conditions. RCDbio reserves the right to refuse sales to unauthorized individuals.