Anti-Mouse/Human TYRP1/TRP1 (Clone TA99) – Purified in vivo GOLD™ Functional Grade

Anti-Mouse/Human TYRP1/TRP1 (Clone TA99) – Purified in vivo GOLD™ Functional Grade

Product No.: T745

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Clone
TA-99
Target
TYRP1/TRP1 (gp75)
Formats AvailableView All
Product Type
Hybridoma Monoclonal Antibody
Alternate Names
CAS2, CATB, GP75, OCA3, TRP, 5,6-dihydroxyindole-2-carboxylic acid oxidase, TRP1, TRP-1, catalase B, DHICA oxidase, glycoprotein 75, melanoma antigen gp75, MEL-5
Isotype
Mouse IgG2a k
Applications
ELISA
,
FA
,
ICC
,
IF Microscopy
,
IHC
,
in vivo
,
IP
,
RIA

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Antibody Details

Product Details

Host Species
Mouse
Recommended Dilution Buffer
Immunogen
SK-MEL-23 Melanoma cell line
Product Concentration
≥ 5.0 mg/ml
Endotoxin Level
< 1.0 EU/mg as determined by the LAL method
Purity
≥95% monomer by analytical SEC
>95% by SDS Page
Formulation
This monoclonal antibody is aseptically packaged and formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.2 - 7.4 with no carrier protein, potassium, calcium or preservatives added. Due to inherent biochemical properties of antibodies, certain products may be prone to precipitation over time. Precipitation may be removed by aseptic centrifugation and/or filtration.
State of Matter
Liquid
Product Preparation
Functional grade preclinical antibodies are manufactured in an animal free facility using only in vitro protein free cell culture techniques and are purified by a multi-step process including the use of protein A or G to assure extremely low levels of endotoxins, leachable protein A or aggregates.
Storage and Handling
Functional grade preclinical antibodies may be stored sterile as received at 2-8°C for up to one month. For longer term storage, aseptically aliquot in working volumes without diluting and store at ≤ -70°C. Avoid Repeated Freeze Thaw Cycles.
Regulatory Status
Research Use Only
Country of Origin
USA
Shipping
2 – 8° C Wet Ice
Additional Applications Reported In Literature ?
ELISA,
FA,
ICC,
IF microscopy,
IHC,
in vivo,
IP,
RIA
Each investigator should determine their own optimal working dilution for specific applications. See directions on lot specific datasheets, as information may periodically change.

Description

Description

Specificity
TA99 activity is directed against tyrosinase-related protein 1 (TYRP1/TRP1), a 75kDa differentiation-related human glycoprotein (gp75), formerly referred to as pigmentation- associated antigen (PAA).
Background
The pigment melanin is produced by specialized organelles called melanosomes that are present in melanocytes1. Melanosomes mature through four morphologically distinct stages, and it is in Stage II that melanin synthesis and deposition is initiated by enzymes including TYRP12.TYRP1/TRP1 (gp75) is a 75 kDa melanosomal membrane protein3,4 involved in melanin synthesis that is also the most abundant glycoprotein synthesized by pigmented melanocytes and melanomas5. In mice, TYRP1/TRP1 (gp75) is also known as the b (brown) locus and determines coat color6. Gene identity is 88% conserved between mouse and human. TYRP1/TRP1 (gp75) is glycosylated by addition and processing of five or more Asn-linked carbohydrate chains.

TA99 was generated by immunizing mice with whole cells of a darkly pigmented melanoma (SK-MEL-23) and fusing spleen cells with NS-1 cells for hybridoma production4. TA99 is reactive against mature melanosomes1. In normal tissues, TA99 reacts with elanin-containing cells in the basal layer of the epidermis as well as pigmented cells of the eye4. TA99 is widely used as a melanosomal marker.

The benefits of TA99 in cancer therapy are being investigated. In mouse, TA99 prevents outgrowth of B16F10 melanoma metastases5,7. In humans, TA99 is used for melanoma diagnosis5. Additionally, TA99 can target subcutaneous human melanoma xenografts in vivo5 and can induce neutrophil recruitment in tumor sites in a B16 melanoma mouse model8. TA99 also improves DNA vaccination against melanoma antigen gp1009. FcγR signaling is required for TA99 action5,9,10,11. TA99 has no impact on tumor outgrowth in established solid tumors12.

Antigen Distribution
TYRP1/TRP1 (gp75) is expressed by pigmented melanoma cells and cultured melanocytes. It predominantly localizes with melanosomes but can also be expressed on the cell surface. It is strongly expressed in B16F10 melanoma cells in vivo.
NCBI Gene Bank ID
UniProt.org
Research Area
Cancer

Leinco Antibody Advisor

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The TA-99 clone is a monoclonal antibody that targets tyrosinase-related protein 1 (TYRP1), also known as glycoprotein 75 (gp75). This protein is expressed on the surface of certain melanoma cells, such as the B16F10 cell line. Here are some common in vivo applications of the TA-99 clone in mice:

  1. Melanoma Models: TA-99 is used in mouse models of metastatic melanoma, particularly to study the efficacy of antibody-based therapies targeting gp75. It has been shown to effectively prevent lung metastases in models of B16 cells, which express gp75.

  2. Tumor Clearance Studies: The antibody is used to explore its effector functions, such as activating immune cells like natural killer (NK) cells and priming CD8+ T cells, which are crucial for antitumor activity.

  3. Evaluation of Immune Responses: TA-99 is utilized to assess the impact of modifications in antibody structure, such as fucosylation levels, on immune activation and tumor clearance. For instance, afucosylated variants of the antibody have enhanced binding to certain mouse Fc receptors, which can improve therapeutic efficacy.

  4. Preclinical Development: The TA-99 clone is also used in developing CAR-T cell therapies that target TYRP1/gp75-expressing cells, demonstrating its potential in targeted cancer treatments.

Overall, the TA-99 clone is a valuable tool in preclinical cancer research, particularly for studying targeted therapies in mouse models.

Commonly Used Antibodies and Proteins with TA-99 in the Literature

TA-99 is a well-characterized monoclonal antibody targeting tyrosinase-related protein 1 (Tyrp1, also known as TRP1 or gp75), primarily studied in murine melanoma (B16) models. Its combination with other antibodies, cytokines, and vaccines has been explored to enhance anti-tumor immunity and therapeutic outcomes.

Frequently Combined Agents

Agent TypeExample(s)Mechanism/Outcome with TA-99References
VaccinesTyrp1 DNA vaccine, gp100 DNA vaccineTA-99 synergizes with Tyrp1 and gp100 DNA vaccination, enhancing CD8+ T cell responses and tumor infiltration. Epitope spreading from gp100 to Tyrp1 is observed, indicating a broader immune response.
CytokinesIL-2TA-99 combined with IL-2 and T cell vaccines shows improved elimination of established tumors.
Checkpoint InhibitorsAnti-PD1A weekly regimen of anti-PD1, TA99-Neo2/15 (an engineered chimera), and DLnano-vaccines against gp100, Tyrp1, and Trp2 significantly extends survival in preclinical models.
Agonist AntibodiesAnti-4-1BB (CD137)Agonist anti-4-1BB antibodies synergize with TA-99, enhancing anti-tumor immunity by preventing activation-induced death of T cells.
Regulatory T Cell DepletionAnti-CD25 (for Treg depletion)TA-99 combined with anti-CD25 (to deplete Tregs) enhances anti-tumor effects, but timing is critical to avoid impairing effector responses.
TLR LigandsToll-like receptor ligandsCombination with immunostimulatory molecules like TLR ligands boosts innate and adaptive immune responses.
Engineered Fusion ProteinsTA99-Neo2/15 (antibody-cytokine fusion)TA99-Neo2/15, an antibody-cytokine chimera, is used with anti-PD1 and multi-antigen vaccines for improved outcomes.

Key Scientific Insights

  • Vaccine Combinations: TA-99 is often paired with DNA vaccines against Tyrp1 and gp100, resulting in enhanced CD8+ T cell infiltration and systemic reactivity against tumor antigens. The combination also induces epitope spreading, broadening the immune response beyond the original vaccine target.
  • Cytokine Augmentation: IL-2, a potent T cell growth factor, is used to amplify the effects of TA-99, especially in the context of adoptive T cell transfer and vaccination.
  • Immune Checkpoint Modulation: Anti-PD1 checkpoint inhibitors are combined with TA-99-based therapies to overcome immune evasion by tumors.
  • Agonist Antibodies: Anti-4-1BB antibodies prevent activation-induced death of T cells and further amplify the anti-tumor response initiated by TA-99.
  • Treg Depletion: Transient depletion of regulatory T cells (via anti-CD25) enhances the efficacy of TA-99, though the timing of depletion is crucial to avoid compromising effector T cell responses.
  • Innate Immune Stimulation: TLR ligands are used to activate innate immunity, complementing the adaptive response driven by TA-99.
  • Engineered Antibody-Cytokine Fusions: TA99-Neo2/15, an antibody-cytokine chimera, represents a next-generation approach, showing synergy with checkpoint blockade and multi-antigen vaccination.

Summary Table of Common Combinations

CombinationMain Outcome
TA-99 + Tyrp1/gp100 DNA vaccinesEnhanced CD8+ T cell response, epitope spreading
TA-99 + IL-2Improved tumor elimination in established disease
TA-99 + Anti-PD1Improved survival in preclinical models
TA-99 + Anti-4-1BBEnhanced T cell activation and anti-tumor immunity
TA-99 + Anti-CD25 (Treg depletion)Enhanced anti-tumor effect, timing-dependent
TA-99 + TLR ligandsBoosted innate and adaptive immunity
TA99-Neo2/15 + Anti-PD1 + VaccinesSignificantly extended survival

Conclusion

TA-99 is most commonly used in combination with DNA vaccines (Tyrp1, gp100), cytokines (IL-2), immune checkpoint inhibitors (anti-PD1), agonist antibodies (anti-4-1BB), Treg-depleting agents (anti-CD25), and TLR ligands to enhance anti-tumor immunity in preclinical melanoma models. These combinations aim to overcome tumor immune evasion, broaden antigen recognition, and sustain effective T cell responses. Engineered antibody-cytokine fusions like TA99-Neo2/15 represent an advanced strategy, showing promise when combined with checkpoint blockade and multi-antigen vaccination.

Key findings from scientific literature citing clone TA-99 focus on its use as a tool and therapeutic in immuno-oncology, specifically targeting tyrosinase-related protein 1 (TRP1/gp75) expressed in melanocytes and melanoma cells.

Essential findings include:

  • Target specificity and applications: TA-99 is a well-characterized mouse monoclonal antibody that recognizes human and mouse TRP1 (TYRP1, gp75), a glycoprotein involved in pigmentation. Its specificity has made it a standard marker for studying melanocyte biology and melanoma in laboratory research.

  • Cancer research and therapy: TA-99 has played a significant role in preclinical melanoma models, where it is used both for tumor detection (immunohistochemistry, Western blot) and as a therapeutic antibody. Notably, it has been foundational in assessing the immune response to melanoma, contributing to a better understanding of antibody-mediated tumor control.

  • Immunotherapy combinations: Experiments in mice show that combining TA-99 with immune-modulating strategies—such as immune checkpoint inhibitors or regulatory T cell depletion—enhances its anti-tumor effects. For example, TA-99 plus MEK inhibitor and immune checkpoint blockade led to improved therapeutic outcomes in melanoma models.

  • Mechanistic insights: Studies reveal that the efficacy of TA-99 in mobilizing adaptive immunity is tightly regulated by immune suppression (e.g., regulatory T cells, immune checkpoints). Effective combination therapies involve TA-99 and regulatory-targeted agents to overcome immune resistance.

  • Biotechnological innovations: TA99 has been linked to novel cancer immunotherapies such as antibody-cytokine fusion proteins and CAR-T cells targeting TRP1, broadening its translational potential for melanoma treatment.

  • Historical and technical context: Clone TA-99 was developed in the mid-1980s via hybridoma technology with the aim of generating antibodies reactive with melanoma antigens. It remains a reference antibody for TRP1 in research settings.

Summary Table: Key Applications and Findings for Clone TA-99

ApplicationKey Findings & Insights
Melanoma detectionUsed in immunocytochemistry and histology for TRP1/gp75 localization
Preclinical immunotherapyEffective in mouse models; stronger with immune checkpoint modulation
Antibody-based therapiesTested as unmodified antibody and as immunocytokine or CAR-T target
Mechanistic studiesReveals interplay between effector, regulatory immune cells, and tumor
Research reference toolStandard for TRP1/gp75 detection and melanoma studies

The collective literature indicates clone TA-99 is a pivotal reagent in melanoma biology and immunotherapy preclinical research, with significant evidence supporting its use as a therapeutic antibody, particularly in combination strategies.

Dosing regimens of the anti-tyrosinase-related protein-1 monoclonal antibody clone TA-99 vary by mouse model, experimental context, and the immunological background of the mice. Studies predominantly use C57BL/6 or specialized genetically engineered mice for melanoma and immunotherapy research.

Key differences in dosing regimens include:

  • Dose Amount and Frequency:

    • In typical C57BL/6 B16 melanoma models, TA-99 is administered at 200 µg per mouse intraperitoneally (i.p.) on days 5 and 7 or 5 and 9 after tumor inoculation. This two-dose schedule is supported by multiple studies focused on immune modulation and Treg depletion.
    • Other regimens utilize up to four doses at intervals determined by tumor or immune cell kinetics, especially in models designed to tolerate repeated dosing.
  • Routes of Administration:

    • Most commonly, TA-99 is delivered intraperitoneally (i.p.).
    • In models requiring rapid systemic exposure, intravenous (i.v.) injection is used, especially in metastasis models where B16-F10 cells are injected i.v. followed by TA-99 doses.
  • Specialized Mouse Models:

    • In knock-in mice expressing humanized IgG1 Fc regions (to model human FcγR biology and minimize immune clearance), repeated TA-99 administration is feasible without rapid clearance due to anti-drug antibody formation—unlike standard mice where anti-human IgG responses limit dosing.
    • In such models, four doses of a TA-99 hIgG1 variant are administered post tumor inoculation, enabling study of both efficacy and immunogenicity under chronic dosing.
  • Combination Therapy Contexts:

    • TA-99 is often given in combination with cytokines (e.g., IL-2, IFNα) or immune checkpoint inhibitors, altering dosing timing (often staggered or concurrent with other agents) and requiring careful schedule harmonization.
    • The combination with Treg depletion, for instance, sets TA-99 on days 5 and 7 after tumor cells, with adjunct therapy (e.g., anti-CD25 mAb) added at later time points.
  • Dose Range and Toxicity:

    • High single doses (300–1000 µg) have been associated with off-target effects (e.g., mouse depigmentation), and so lower doses (≤200 µg per injection) are used in most tumor and combination studies to balance efficacy and safety.
Mouse Model / ContextDose (per injection)Schedule (days after tumor)RouteNotes
C57BL/6 B16 melanoma (immunotherapy)200 µgDays 5 and 7 or 5 and 9i.p.Standard; sometimes combined with cytokines or Treg Ab
Human IgG1 knock-in mice4 doses (amount varies)Post B16-F10 inoculationi.v.Enables repeated/long-term dosing with Fc-variant
Toxicity / Depigmentation studies300–1000 µgNot specifiedNot specifiedLeads to depigmentation at high doses

Summary:
Most studies standardize on 200 µg i.p. on two separate days post-tumor inoculation for routine immunotherapy or tumor challenge models in C57BL/6 mice, whereas genetically engineered, humanized models support repeated or variant dosing regimens to study long-term effects and human-specific antibody variants. Combination protocols may further adapt the regimen to synchronize with other immune-modulating agents. High-dose applications are rare and primarily used for mechanistic or toxicity studies.

References & Citations

1 Thomson TM, Real FX, Murakami S, et al. J Invest Dermatol. 90(4):459-466. 1988.
2 Sitaram A, Marks MS. Physiology (Bethesda). 27(2):85-99. 2012.
3 Vijayasaradhi S, Doskoch PM, Houghton AN. Exp Cell Res. 196(2):233-240. 1991.
4 Thomson TM, Mattes MJ, Roux L, et al. J Invest Dermatol. 85(2):169-174. 1985.
5 Boross P, Jansen JH, van Tetering G, et al. Immunol Lett. 160(2):151-157. 2014.
6 Vijayasaradhi S, Houghton AN. Int J Cancer. 47(2):298-303. 1991.
7 Otten MA, van der Bij GJ, Verbeek SJ, et al. J Immunol. 181(10):6829-6836. 2008.
8 Chu D, Zhao Q, Yu J, et al. Adv Healthc Mater. 5(9):1088-1093. 2016.
9 Saenger YM, Li Y, Chiou KC, et al. Cancer Res. 68(23):9884-9891. 2008.
10 Murer P, Kiefer JD, Plüss L, et al. J Invest Dermatol. 139(6):1339-1348. 2019.
11 Bevaart L, Jansen MJ, van Vugt MJ, et al. Cancer Res. 66(3):1261-1264. 2006.
12 Benonisson H, Sow HS, Breukel C, et al. J Immunol. 201(12):3741-3749. 2018.
13 Vijayasaradhi S, Bouchard B, Houghton AN. J Exp Med. 171(4):1375-1380. 1990.
14 Bouchard B, Fuller BB, Vijayasaradhi S, et al. J Exp Med. 169(6):2029-2042. 1989.
15 Cui J, Arita Y, Bystryn JC. Pigment Cell Res. 8(1):53-59. 1995.
16 Kemp EH, Waterman EA, Gawkrodger DJ, et al. Br J Dermatol. 139(5):798-805. 1998.
17 Bin BH, Bhin J, Yang SH, et al. PLoS One. 9(8):e105965. 2014.
18 van Spriel AB, van Ojik HH, Bakker A, et al. Blood. 101(1):253-258. 2003.
19 Patel D, Bassi R, Hooper AT, et al. Anticancer Res. 28(5A):2679-2686. 2008.
20 Ly LV, Sluijter M, van der Burg SH, et al. J Immunol. 190(1):489-496. 2013.
21 They L, Michaud HA, Becquart O, et al. Oncoimmunology. 6(10):e1353857. 2017.
22 Pérez-Lorenzo R, Erjavec SO, Christiano AM, et al. Oncotarget. 12(2):66-80. 2021.
23 Tursi NJ, Xu Z, Helble M, et al. Front Immunol. 14:1072810. 2023.
24 Palmeri JR, Lax BM, Peters JM, et al. Nat Commun. 15(1):1900. 2024.
25 Albanesi M, Mancardi DA, Macdonald LE, et al. J Immunol. 189(12):5513-5517. 2012.
26 Dippel E, Haas N, Grabbe J, et al. Br J Dermatol. 132(2):182-189. 1995.
27 Dean NR, Brennan J, Haynes J, et al. Appl Immunohistochem Mol Morphol. 10(3):199-204. 2002.
28 Welt S, Mattes MJ, Grando R, et al. Proc Natl Acad Sci U S A. 84(12):4200-4204. 1987.
29 Zhao H, Eling DJ, Medrano EE, et al. J Invest Dermatol. 106(4):744-752. 1996.
Indirect Elisa Protocol
FA
ICC
IF Microscopy
IHC
in vivo Protocol
Immunoprecipitation Protocol
RIA

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