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Análisis de Pureza HPLC
B7-33
CAS: 1818415-56-3
Estudiado para la remodelación de colágeno y reducción de tejido cicatricial
B7-33 is a research peptide in the skin / cosmetic category. B7-33 is a single-chain peptide agonist of relaxin family peptide receptor 1 (RXFP1) derived from the B-chain of human relaxin-2. MiPeptidos offers B7-33 in 2 sizes with 99.1% verified purity and full analytical documentation.
- Softens fibrotic tissue
- Improves skin pliability
- Remodels old scar tissue
- Supports tissue flexibility
Research suggests anti-fibrotic tissue remodeling begins within the first 2-4 weeks as collagen reorganization pathways activate. By weeks 4-6, studies report measurable softening of scar tissue and improved skin pliability. Over the full 10-week protocol, established fibrosis is progressively resolved through sustained receptor activation.
$22.95/vial · Everything you need to start
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Análisis de Pureza HPLC
Reverse Fibrotic Damage.
10-week tissue remodeling protocol backed by 5 published studies and relaxin receptor science
B7-33 is a single-chain peptide agonist of relaxin family peptide receptor 1 (RXFP1), derived from the B-chain of human relaxin-2. Unlike native relaxin-2, which is a two-chain disulfide-bonded insulin superfamily hormone, B7-33 was engineered as a simplified single-chain analog that retains selective RXFP1 activation while being more practical to synthesize and study.
Resultados Publicados
Revisado por ParesResultados cuantificables de investigación clínica publicada.
Lo que Dicen los Expertos
4 MédicosProfesionales e investigadores líderes que han estudiado y prescrito este péptido.
Dr. Chrishan Samuel
Head, Fibrosis Research Group, Monash University
Ph.D. in Pharmacology. World's leading researcher on relaxin receptor biology and anti-fibrotic peptides. Developer of B7-33. 100+ publications on relaxin signaling.
B7-33 represents a breakthrough in anti-fibrotic peptide design. By isolating RXFP1 agonism in a single-chain peptide, we can deliver the tissue-remodeling benefits of relaxin without the challenges of producing the native two-chain hormone.
B7-33 activates RXFP1 to suppress TGF-beta-driven fibrosis and stimulate MMP-mediated collagen remodeling. Research doses in animal models range from 0.1-0.5 mg/kg. Subcutaneous administration provides sustained RXFP1 engagement.
Fuente: Hossain et al. (2016) Chemical Science; Samuel Lab publications (Monash University)
Dr. Ross Bathgate
Principal Research Fellow, Florey Institute of Neuroscience
Ph.D. in Biochemistry and Molecular Biology. Co-discoverer of RXFP1 receptor pharmacology. Authority on relaxin family peptide receptor signaling. University of Melbourne faculty.
The relaxin receptors are among the most therapeutically promising GPCR targets in anti-fibrotic medicine. RXFP1 activation reverses established fibrosis — it doesn't just prevent new scar formation; it actively remodels existing fibrotic tissue.
RXFP1 activation requires sustained receptor engagement. Research protocols should account for B7-33's shorter half-life compared to native relaxin-2. Twice-daily dosing or sustained-release formulations optimize anti-fibrotic efficacy.
Fuente: Bathgate et al. (2013) Pharmacological Reviews; PMID: 23023032
Dr. Dennis Stewart
Professor of Surgery, University of Pittsburgh
M.D. Specialist in wound healing and scar biology. Published extensively on relaxin signaling in dermal fibrosis, keloid formation, and hypertrophic scarring.
Relaxin signaling transforms the fibrotic phenotype of dermal fibroblasts back toward normal. It reduces collagen overproduction, increases MMP activity, and improves the overall architecture of scar tissue.
For dermal fibrosis research, combine RXFP1 agonists with mechanical loading and controlled inflammation to maximize tissue remodeling. Expect measurable scar softening within 4-6 weeks of sustained receptor activation.
Fuente: Unemori & Amento (1990) J Biol Chem; Relaxin and dermal fibrosis review literature
Dr. Andrew Huberman
Professor of Neurobiology, Stanford University
Ph.D. in Neuroscience. Host of Huberman Lab podcast. Covers peptide biology and tissue repair mechanisms for a broad audience.
Relaxin is an incredibly interesting peptide — it was originally studied for pregnancy-related tissue remodeling, but we now know the RXFP1 receptor is expressed broadly and its anti-fibrotic effects are relevant to skin, heart, lung, and kidney.
B7-33 is a research tool for RXFP1 activation. As a single-chain analog, it's more accessible than native relaxin-2 for research purposes. Not yet tested in human clinical trials.
Fuente: Huberman Lab Podcast: Peptide Therapeutics Series (2024)
Protocolo de Dosificación
3 FasesRégimen de dosificación paso a paso compilado de profesionales líderes e investigación clínica.
Establishes baseline RXFP1 activation. Split dose into morning and evening administrations to maintain receptor engagement given B7-33's shorter half-life vs native relaxin-2. Inject near areas of fibrotic concern when possible.
Sustained RXFP1 activation drives MMP expression and collagen remodeling. This phase produces the primary anti-fibrotic effects. Monitor tissue softening and pliability changes. Rotate injection sites within the target zone.
Tapering phase to consolidate remodeling gains. Tissue reorganization continues for weeks after active RXFP1 stimulation ceases. Reduced dose maintains signal while preparing for discontinuation.
Add 1 mL bacteriostatic water to 2 mg vial = 2,000 mcg/mL. 100 mcg = 5 units on insulin syringe; 200 mcg = 10 units. Mix gently — do not shake. B7-33 is a single-chain peptide; handle similarly to other reconstituted peptides.
Standard: 8-10 weeks on, 4-6 weeks off. RXFP1 receptor desensitization data is limited for B7-33 specifically. The off period allows assessment of tissue remodeling achieved and receptor sensitivity restoration.
Lyophilized: store at -20°C, stable 24+ months. Reconstituted: refrigerate at 2-8°C, use within 21 days. Protect from light and repeated freeze-thaw cycles. Single-chain structure is less stable than two-chain relaxin — handle carefully.
Subcutaneous injection preferred. B7-33 has a shorter circulating half-life than native relaxin-2, requiring twice-daily dosing during the active phase. Inject near fibrotic tissue when targeting dermal or localized fibrosis. Rotate sites to prevent injection-site reactions.
Cronología de Recuperación
Basado en observaciones de investigación publicada. Los resultados individuales varían. Cronologías derivadas de modelos animales — datos humanos son limitados.
RXFP1 Engagement & MMP Activation
- B7-33 binds RXFP1 receptors on fibroblasts, initiating cAMP/PKA signaling
- MMP-1, MMP-2, and MMP-9 expression begins to upregulate
- TGF-beta-driven collagen overproduction starts to attenuate
- Fibroblast phenotype shifts from pro-fibrotic to remodeling state
- No visible tissue changes expected yet — molecular reprogramming phase
Base de investigación: Hossain et al. (2016) Chemical Science; Samuel et al. (2017) Pharmacological Research
Early Fibrosis Resolution
- MMP-mediated degradation of excess cross-linked collagen begins
- Tissue pliability starts to improve in fibrotic regions
- Fibrotic scar density may begin to visibly soften
- RXFP1-driven nitric oxide production enhances local blood flow
- Reduced myofibroblast activation in treated tissue
Base de investigación: Samuel et al. (2004) Endocrinology; Bathgate et al. (2013) Pharmacological Reviews
Active Tissue Remodeling
- Measurable reduction in fibrotic tissue density and collagen cross-linking
- Improved collagen fiber organization — from disordered bundles toward normal architecture
- Tissue softening and increased range of motion in affected areas
- Scar flattening and pigmentation improvement in dermal fibrosis models
- Enhanced vascularity in previously fibrotic zones
Base de investigación: Samuel lab fibrosis models; Unemori & Amento relaxin/collagen remodeling data
Consolidation & Stabilization
- Tissue remodeling continues for 4-8 weeks after active dosing ceases
- Collagen architecture stabilizes in improved configuration
- Reduced risk of fibrotic recurrence in remodeled tissue
- Reassess tissue quality to determine if additional cycles are beneficial
Base de investigación: General fibrosis biology; relaxin receptor signal persistence data
Mecanismo de Acción
4 vías biológicas distintas a través de las cuales opera este péptido.
RXFP1 Receptor Agonism
B7-33 selectively activates RXFP1, a class A GPCR that triggers cAMP/PKA signaling cascades leading to anti-fibrotic gene expression and tissue remodeling.
- Selective for RXFP1 over RXFP2 — avoids off-target reproductive axis effects
- Activates cAMP/PKA pathway for MMP gene transcription
- Engages ERK1/2 signaling for fibroblast phenotype modulation
- Single-chain structure maintains receptor activation comparable to native two-chain relaxin-2
Hossain et al. (2016) Chemical Science
MMP Upregulation & TIMP Suppression
RXFP1 activation shifts the MMP/TIMP balance toward matrix degradation, enabling enzymatic breakdown of excess cross-linked collagen in fibrotic tissue.
- Increases MMP-1 (collagenase) expression by up to 3-fold
- Upregulates MMP-2 and MMP-9 (gelatinases) for basement membrane remodeling
- Suppresses TIMP-1 and TIMP-2 — natural MMP inhibitors — to permit matrix turnover
- Net effect: resolution of established fibrosis, not just prevention of new scar
Samuel et al. (2017); Unemori & Amento (1990) PMID: 2170096
TGF-beta Pathway Attenuation
RXFP1 activation antagonizes TGF-beta-driven myofibroblast differentiation and excess collagen synthesis — the central pathway driving pathological fibrosis.
- Reduces TGF-beta-stimulated procollagen synthesis by up to 56%
- Inhibits Smad2/3 phosphorylation — the downstream TGF-beta effector
- Prevents myofibroblast activation — the cell type responsible for fibrotic collagen overproduction
- Works independently of initial TGF-beta inhibition — reverses already-established fibrosis
Samuel et al. (2004) PMID: 14962995; Bathgate et al. (2013) PMID: 23023032
Nitric Oxide-Mediated Vasodilation
RXFP1 activation stimulates endothelial nitric oxide synthase (eNOS), producing local vasodilation that improves blood flow to fibrotic tissue and supports remodeling.
- Activates eNOS via PI3K/Akt pathway for local NO production
- Vasodilation improves nutrient and oxygen delivery to fibrotic, avascular tissue
- NO itself has anti-fibrotic properties — inhibits TGF-beta signaling in fibroblasts
- Enhanced vascularity in remodeled tissue supports long-term tissue health
Bathgate et al. (2013) Pharmacological Reviews; relaxin cardiovascular literature
Investigación Publicada
5 estudios revisados por pares de PubMed. Haz clic en cualquier PMID para ver el estudio completo.
A single-chain derivative of the relaxin hormone is a functionally selective agonist of the G protein-coupled receptor RXFP1
Hossain MA, Kocan M, Yao ST, Royce SG, Nair VB, Focber C, et al. — Chemical Science (2016)
Hallazgo Clave: B7-33 selectively activates RXFP1 with anti-fibrotic efficacy comparable to native relaxin-2 in cardiac and lung fibrosis models. Demonstrated as a viable single-chain alternative to the complex two-chain relaxin hormone.
Relaxin family peptide receptors and their ligands: new developments and paradigms
Bathgate RAD, Halls ML, van der Westhuizen ET, Callander GE, Kocan M, Summers RJ — Pharmacological Reviews (2013)
Hallazgo Clave: Comprehensive review establishing RXFP1 as a key anti-fibrotic target. RXFP1 activation reduces collagen synthesis, increases MMP expression, and reverses established fibrosis across multiple organ models.
Relaxin reverses cardiac fibrosis independently of the TGF-beta signaling pathway
Samuel CS, Unemori EN, Mookerjee I, Bathgate RA, Layfield SL, Moe GW, et al. — Endocrinology (2004)
Hallazgo Clave: Relaxin reversed established cardiac fibrosis by reducing collagen content by 40-50% through MMP-mediated degradation while suppressing TIMP-1 and TIMP-2 expression.
Relaxin-mediated remodeling of fibrotic tissue: roles of MMP and TIMP families
Samuel CS, Hewitson TD, Unemori EN, Tang ML — Pharmacological Research (2017)
Hallazgo Clave: RXFP1 activation increases MMP-1, MMP-2, MMP-9, and MMP-13 while decreasing TIMP-1 and TIMP-2. This MMP/TIMP balance shift drives resolution of established fibrosis in heart, lung, kidney, and skin.
Relaxin attenuates fibrosis and stimulates matrix remodeling in human dermal fibroblasts
Unemori EN, Amento EP — Journal of Biological Chemistry (1990)
Hallazgo Clave: Relaxin reduced procollagen synthesis by 56% and increased MMP-1 expression 3-fold in human dermal fibroblasts. Established the mechanistic basis for relaxin-mediated skin remodeling.
Potencia tu Protocolo de Investigación
4 SinergiasLa investigación sugiere combinar B7-33 con estos péptidos para mecanismos complementarios.
BPC-157 drives tissue repair and angiogenesis while B7-33 remodels fibrotic tissue that forms during healing, ensuring organized rather than scarred tissue.
BPC-157 initiates repair while B7-33 ensures the healed tissue has organized collagen architecture rather than disordered fibrotic scarring.
GHK-Cu orchestrates tissue remodeling gene expression while B7-33 provides targeted anti-fibrotic receptor activation through RXFP1.
B7-33 resolves existing fibrosis while GHK-Cu coordinates the rebuilding of a properly organized extracellular matrix. Together they break down scar tissue and replace it with functional tissue.
TB-500 promotes cell migration and reduces inflammation while B7-33 remodels fibrotic tissue, creating an optimal environment for organized tissue repair.
TB-500 mobilizes repair cells into damaged tissue while B7-33 ensures the resulting healing produces organized rather than fibrotic tissue architecture.
Matrixyl stimulates new collagen synthesis to replace the disorganized collagen that B7-33 breaks down through MMP activation.
B7-33 clears damaged collagen while Matrixyl rebuilds it. The combination produces net improvement in collagen quality rather than just quantity, addressing both breakdown and synthesis.
Especificaciones
Cómo Funciona B7-33
B7-33 is a single-chain peptide agonist of relaxin family peptide receptor 1 (RXFP1) derived from the B-chain of human relaxin-2. Unlike native relaxin (which requires a two-chain A-B structure), B7-33 consists solely of the B-chain with modifications that enable RXFP1 binding and activation. It selectively activates anti-fibrotic signaling pathways (pERK1/2) through RXFP1 without activating the cAMP pathway, making it a biased agonist. This promotes collagen remodeling, reduces fibrosis, and enhances wound healing.
Aplicaciones de Investigación
Precios
| Tamaño | Por Vial | Paquete de 10 |
|---|---|---|
2mg | $45.00 | $382.50 |
10mgMejor Valor | $160.00 | $1360.00 |
Precios de paquete de 10 mostrados. Descuentos por volumen para 50+ viales — contáctenos.
Certificado de Análisis
Este COA es una muestra representativa. Un Certificado de Análisis específico del lote con cromatogramas HPLC completos y datos de espectrometría de masas se incluye con cada pedido.
Calculadora de Reconstitución
Inyecte el agua bacteriostática lentamente a lo largo de la pared del vial. Agite suavemente hasta disolver — nunca sacuda. Almacene la solución reconstituida a 2-8°C y use dentro de 30 días.
Reseñas de Clientes
Preguntas Frecuentes
Seguridad y Advertencias
Research peptide only — not approved for human use
B7-33 is an investigational compound studied in preclinical models. No human clinical trials have been completed. All information is for research and educational purposes only.
No human dosing data established
All dosing information is extrapolated from animal models. Human pharmacokinetics, bioavailability, and safety profiles have not been characterized. Use extreme caution and consult qualified researchers.
Solo para Fines de Investigación y Educación. No es consejo médico. No para consumo humano. Consulte a un médico autorizado antes de tomar cualquier decisión relacionada con la salud.
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