Reactivos e instrumentos para inmunología, biología celular y biología molecular.

Busulfan [55-98-1]

Imprimir

Referencia NB-64-01086-500mg

embalaje : 500mg

Marca : Neo Biotech

Solicitar más información

Busulfan (Synonyms: Sulphabutin, Myleran, Busulphan)

Catalog No. T0923 Copy Product Info

Purity: 99.89%

Busulfan is an alkylating antineoplastic agent derived from dimethane sulfonate, with cytotoxic and immunosuppressive properties. It primarily acts by forming carbonium ions in vivo, which induce cross-linking between DNA strands or between DNA and proteins, leading to DNA damage, inhibition of DNA replication, and suppression of RNA transcription. In addition, Busulfan can inhibit thioredoxin reductase and induce apoptosis. It is commonly used as a myeloablative agent in preconditioning regimens for bone marrow transplantation and can also be used to establish anemia models.

Busulfan

Copy Product Info

Synonyms Sulphabutin, Myleran, Busulphan

Cas No. 55-98-1

Batch Information

Select Batch

Purity:99.89%

Appearance:Solid

Color:White

Resource Download

COA HNMR

Product Introduction

Bioactivity

Description	Busulfan is an alkylating antineoplastic agent derived from dimethane sulfonate, with cytotoxic and immunosuppressive properties. It primarily acts by forming carbonium ions in vivo, which induce cross-linking between DNA strands or between DNA and proteins, leading to DNA damage, inhibition of DNA replication, and suppression of RNA transcription. In addition, Busulfan can inhibit thioredoxin reductase and induce apoptosis. It is commonly used as a myeloablative agent in preconditioning regimens for bone marrow transplantation and can also be used to establish anemia models.
In vitro	Mice transplanted with busulfan exhibit slow and incomplete lymphoid engraftment. Mice treated with busulfan demonstrate a significant increase in apoptosis and a reduction in testicular weight. In NOD/SCID mice, busulfan treatment combined with irradiation achieves a detection sensitivity similar to that of limiting dilution assays. A dose-dependent lymphoid tissue reconstitution is provided in mice with 20 mg/kg to 100 mg/kg of busulfan. At 40 mg/kg, busulfan induces the maximum number of apoptotic cells while minimizing the number of necrotic cells.
In vivo	Busulfan, an alkylating agent that induces DNA damage through cross-linking DNA with DNA and proteins, triggers senescence in normal human diploid WI38 fibroblast cells via a cascade mediated by extracellular signal-regulated kinase (Erk) and p38 mitogen-activated protein kinase (p38 MAPK), independent of the p53-DNA damage pathway. Busulfan causes a transient reduction in glutathione levels, followed by a sustained increase in ROS production. The hypophosphorylation of Rb induced by Busulfan inhibits the expression of PCNA in testicular cells, preventing apoptosis of spermatogonial stem cells. Moreover, while Busulfan reduces the frequency of cobblestone area-forming cells, it does not significantly increase apoptosis in hematopoietic stem cells (HSC)-like cells and progenitor cells with similar phenotypes. Busulfan suppresses the hematopoietic function of HSC-like cells and progenitor cells through an apoptosis-dependent mechanism. Additionally, Busulfan-induced senescence in bone marrow hematopoietic cells correlates with a time-dependent increase in the expression of p16Ink4a and p19Arf.
Disease Modeling Protocol	Aplastic Anemia (AA) Model Modeling Mechanism： Busulfan combined with cyclophosphamide induces apoptosis (AA) through a dual damage mechanism: on the one hand, it directly destroys bone marrow hematopoietic stem cells/progenitor cells, inhibiting hematopoietic function; on the other hand, it activates inflammatory pathways, inducing high expression of RIP1 and RIP3 proteins in bone marrow cells and forming the RIP1-RIP3 necrosis complex, mediating necrotizing apoptosis of hematopoietic cells, while promoting the release of inflammatory factors such as IL-6, TNF-α, and FLT-3L, further aggravating the damage to the bone marrow hematopoietic microenvironment, ultimately leading to pancytopenia in peripheral blood and fatty degeneration of bone marrow hematopoietic tissue. Related Products： Busulfan (T0923) Modeling Method： Experimental Subject： Mice: ICR strain, male, 18–22 g, 6–8 weeks old Dosage and Administration Route： Intervention group: Nec-1 (necrotic apoptosis inhibitor) group received intraperitoneal injection of Nec-1 (2 mg/kg/day) prior to combined administration, followed by combined administration of Busulfan (20 mg/kg/day)+Cyclophosphamide (40 mg/kg/day) via intraperitoneal injection Control group: Intraperitoneal injection of an equivalent volume of physiological saline Dosing Frequency and Duration Model： Once daily for 12 consecutive days Validation： Hematological markers: Peripheral blood leukocytes (WBC), erythrocytes (RBC), hemoglobin (Hb), and platelets (PLT) were significantly decreased; bone marrow nucleated cell (BMNC) count decreased by 68.25%. Histological markers: Bone marrow hematopoietic tissue was replaced by adipose tissue, the hematopoietic area was reduced, the number of megakaryocytes and hematopoietic cells decreased, and the number of non-hematopoietic cells (adipocytes, endothelial cells) increased, accompanied by tissue edema, congestion, and focal necrosis. Cell death detection: Flow cytometry showed a significantly increased early apoptosis rate and mid-to-late apoptosis/necrosis rate of bone marrow cells. Fluorescent staining (Hoechst/PI) and scanning electron microscopy revealed apoptotic cells (cell membrane invagination) and necrotic cells (cell membrane blistering and swelling). Molecular markers: Western blot detected upregulated expression of RIP1 and RIP3 proteins in bone marrow cells (RIP3 began to increase from day 3 of drug administration, and RIP1 began to increase from day 9). Immunoprecipitation confirmed RIP1-RIP3. Complex formation; levels of IL-6, TNF-α, and FLT-3L were significantly elevated in bone marrow tissue supernatant (FLT-3L increased 4.46-fold). Precautions： Mice were euthanized by cervical dislocation, and one femur was surgically removed. After obtaining the femoral epiphysis, bone marrow cells were washed away with 1 ml of PBS to prepare a bone marrow cell suspension. References：Chen YF,et,al. The role of RIP1 and RIP3 in the development of aplastic anemia induced by cyclophosphamide and busulphan in mice. Int J Clin Exp Pathol. 2014 Dec 1;7(12):8411-20.
Synonyms	Sulphabutin, Myleran, Busulphan

Chemical Properties

Molecular Weight	246.30
Formula	C₆H₁₄O₆S₂
Cas No.	55-98-1
Smiles	CS(=O)(=O)OCCCCOS(C)(=O)=O
Relative Density.	1.35 g/cm3

Storage & Solubility Information

Storage

Shipping with blue ice/Shipping at ambient temperature.

Solubility Information

Ethanol: < 1 mg/mL (insoluble or slightly soluble)

DMSO: 50.00 mg/mL (203.00 mM), Sonication is recommended.

In Vivo Formulation

10% DMSO+40% PEG300+5% Tween-80+45% Saline: 3.00 mg/mL (12.18 mM)

Please add the solvents sequentially, clarifying the solution as much as possible before adding the next one. Dissolve by heating and/or sonication if necessary. Working solution is recommended to be prepared and used immediately. The formulation provided above is for reference purposes only. In vivo formulations may vary and should be modified based on specific experimental conditions.

Solution Preparation Table

DMSO

	1mg	5mg	10mg	50mg
1 mM	4.0601 mL	20.3004 mL	40.6009 mL	203.0045 mL
5 mM	0.8120 mL	4.0601 mL	8.1202 mL	40.6009 mL
10 mM	0.4060 mL	2.0300 mL	4.0601 mL	20.3004 mL
20 mM	0.2030 mL	1.0150 mL	2.0300 mL	10.1502 mL
50 mM	0.0812 mL	0.4060 mL	0.8120 mL	4.0601 mL
100 mM	0.0406 mL	0.2030 mL	0.4060 mL	2.0300 mL

Note : The dilution table applies only to solid products. For liquid products, please calculate the stock solution based on the stated concentration and/or density.

Usted podría estar interesado también en los siguientes productos:

Referencia

Descripción

Cond.

Precio Sin IVA

NB-64-00237-10mg

Pazopanib [444731-52-6]

10mg

NB-64-00408-50mg

Gemcitabine [95058-81-4]

50mg

NB-64-00274-50mg

Etoposide [33419-42-0]

50mg