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FasL, soluble (human) (recombinant) set

ALX-850-014-KI02 1 Set 778.00 USD
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Product Details

Alternative Name:APO-1L, CD95L, CD178, TNFSF 6
Application Notes:Kills Fas-sensitive cells at concentrations of >1ng/ml in the presence of cross-linking enhancer.
Species reactivity:Human, Mouse, Rat
Specificity:FasL binds to human, mouse and rat Fas (CD95).
Specific Activity:ED50: 1ng/ml (A20 cells)
Purity:≥95% (SDS-PAGE)
Contents:10µg of FasL, Soluble (human) (recombinant) (Prod. No. ALX-522-001) and 4x50µg of Enhancer for Ligands (Prod. No. ALX-804-034) which increases the biological activity (induction of apoptosis) by ~50-fold to a concentration range of 1-5ng/ml.
Formulation:FasL: Lyophilized. Contains PBS.
Enhancer: Liquid. In PBS, pH7.4, containing 50% glycerol. Contains no preservatives.
Reconstitution:Reconstitute FasL with 100µl sterile water. Further dilutions should be made with medium containing 5% fetal calf serum or carrier protein.
Concentration:FasL: 0.1mg/ml after reconstitution
Enhancer: 1mg/ml
Use/Stability:Stable for at least 6 months after receipt when stored at -20°C.
Handling:Avoid freeze/thaw cycles. After reconstitution, prepare aliquots and store at -20°C.
Shipping:Blue Ice
Long Term Storage:-20°C
Source:Produced in HEK 293 cells. The extracellular domain of human FasL (APO-1L; CD95L; CD178) (aa 103-281) is fused at the N-terminus to a linker peptide (26 aa) and a FLAG®-tag. Glycosylation of FasL, Soluble (human) (recombinant) is similar to natural human FasL.
Technical Info/Product Notes:FLAG is a registered trademark of Sigma-Aldrich Co.
UniProt ID:P48023
Regulatory Status:RUO - Research Use Only

Product Literature References

The non-apoptotic function of Caspase-8 in negatively regulating the CDK9-mediated Ser2 phosphorylation of RNA polymerase II in cervical cancer: R. Mandal, et al.; Cell. Mol. Life Sci. 79, 597 (2022), Abstract;
Amplification of CD95 activation by caspase 8-induced endosomal acidification in rat hepatocytes: R. Reinehr, et al.; J. Biol. Chem. 283, 2211 (2008), Abstract; Full Text
Fas (CD95) induces macrophage proinflammatory chemokine production via a MyD88-dependent, caspase-independent pathway: W.A. Altemeier, et al.; J. Leukoc. Biol. 82, 721 (2007), Abstract; Full Text
p21CIP1/WAF1 controls proliferation of activated/memory T cells and affects homeostasis and memory T cell responses: C.F. Arias, et al.; J. Immunol. 178, 2296 (2007), Abstract;
CD1d-unrestricted human NKT cells release chemokines upon Fas engagement: M. Giroux and F. Denis; Blood 105, 703 (2005), Abstract; Full Text
Retinoic acid inhibits the proliferative response induced by CD40 activation and interleukin-4 in mantle cell lymphoma: M. Guidoboni, et al.; Cancer Res. 65, 587 (2005), Abstract; Full Text
The role of p53 and Fas in a model of acute murine graft-versus-host disease: S. Yada, et al.; J. Immunol. 174, 1291 (2005), Abstract; Full Text
Cutting edge: SDS-stable Fas microaggregates: an early event of Fas activation occurring with agonistic anti-Fas antibody but not with Fas ligand: P. Legembre, et al.; J. Immunol. 171, 5659 (2003), Abstract;
Intracellular localization of keratinocyte Fas ligand explains lack of cytolytic activity under physiological conditions: I. Viard-Leveugle, et al.; J. Biol. Chem. 278, 16183 (2003), Abstract; Full Text
An essential role for membrane rafts in the initiation of Fas/CD95-triggered cell death in mouse thymocytes: A.O. Hueber, et al.; EMBO Rep. 3, 190 (2002), Abstract; Full Text
Bcl-2 and Bcl-xL inhibit CD95-mediated apoptosis by preventing mitochondrial release of Smac/DIABLO and subsequent inactivation of X-linked inhibitor-of-apoptosis protein: X.M. Sun, et al.; J. Biol. Chem. 277, 11345 (2002), Abstract; Full Text
Caspase-10 is recruited to and activated at the native TRAIL and CD95 death-inducing signalling complexes in a FADD-dependent manner but can not functionally substitute caspase-8: M.R. Sprick, et al.; EMBO J. 21, 4520 (2002), Abstract;
Hepatic natural killer cells exclusively kill splenic/blood natural killer-resistant tumor cells by the perforin/granzyme pathway: D. Vermijlen, et al.; J. Leukoc. Biol. 72, 668 (2002), Abstract;
Induction of apoptosis in malignant pleural mesothelioma cells by activation of the Fas (Apo-1/CD95) death-signal pathway: J.H. 4th Stewart et al.; J. Thorac. Cardiovasc. Surg. 123, 295 (2002), Abstract;
Innate direct anticancer effector function of human immature dendritic cells. II. Role of TNF, lymphotoxin-alpha(1)beta(2), Fas ligand, and TNF-related apoptosis-inducing ligand: G. Lu, et al.; J. Immunol. 168, 1831 (2002), Abstract;
Multiple pathways of TWEAK-induced cell death: M. Nakayama, et al.; J. Immunol. 168, 734 (2002), Abstract;
Potentiation of Fas-mediated apoptosis by an engineered glycosylphosphatidylinositol-linked Fas: P. Legembre, et al.; Cell Death Differ. 9, 329 (2002), Abstract; Full Text
NF-κB signals induce the expression of c-FLIP: O. Micheau, et al.; Mol. Cell. Biol. 21, 5299 (2001), Abstract; Full Text
Three adenovirus E3 proteins cooperate to evade apoptosis by tumor necrosis factor-related apoptosis-inducing ligand receptor-1 and -2: C.A. Benedict, et al.; J. Biol. Chem. 276, 3270 (2001), Abstract; Full Text
Fas engagement induces the maturation of dendritic cells (DCs), the release of interleukin (IL)-1beta, and the production of interferon gamma in the absence of IL-12 during DC-T cell cognate interaction: a new role for Fas ligand in in: M. Rescigno, et al.; J. Exp. Med. 192, 1661 (2000), Abstract; Full Text
Fas ligand-induced c-Jun kinase activation in lymphoid cells requires extensive receptor aggregation but is independent of DAXX, and Fas-mediated cell death does not involve DAXX, RIP, or RAIDD: A. Villunger, et al.; J. Immunol. 165, 1337 (2000), Abstract; Full Text
Activation of Fas by FasL induces apoptosis by a mechanism that cannot be blocked by Bcl-2 or Bcl-x(L): D.C. Huang, et al.; PNAS 96, 14871 (1999), Abstract; Full Text

General Literature References

Apoptosis by death factor: S. Nagata; Cell 88, 355 (1997), Abstract;
Melanoma cell expression of Fas(Apo-1/CD95) ligand: implications for tumor immune escape: M. Hahne, et al.; Science 274, 1363 (1996), Abstract;
A role for CD95 ligand in preventing graft rejection: D. Bellgrau, et al.; Nature 377, 630 (1995), Abstract;
Fas ligand-induced apoptosis as a mechanism of immune privilege: T.S. Griffith, et al.; Science 270, 1189 (1995), Abstract;
Cytolytic T-cell cytotoxicity is mediated through perforin and Fas lytic pathways: B. Lowin, et al.; Nature 370, 650 (1994), Abstract;
Mature T cells of autoimmune lpr/lpr mice have a defect in antigen-stimulated suicide: J.H. Russell, et al.; PNAS 90, 4490 (1993), Abstract;

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