Abbiotec LLC

Abbiotec LLC, established in 2007, is a biotechnology company focused on developing and commercializing next-generation antibodies and reagents for the life science research community. The company is headquartered in Escondido, California.

Product Portfolio:

Antibodies: Abbiotec offers a collection of polyclonal and monoclonal antibodies targeting various proteins, including CD markers, cell adhesion molecules, cytokines, hormones, protein kinases, receptors, and transcription factors.
Peptides: The company provides synthetic peptides, including substrates and active peptides, for use in assays related to ACTH, amyloid peptides, angiotensins, neuropeptides, and more.
Custom Services: Abbiotec offers custom polyclonal and monoclonal antibody production in various host species, as well as custom peptide synthesis with multiple modification options to suit specific research needs.

Browse Abbiotec LLC Products

14-3-3 (Ser58) Antibody

SKU: 252518|Size: 0.1 mL

14-3-3 Protein Antibody

SKU: 250447|Size: 0.1 mg

17a-Boldenone Antibody

SKU: 252286|Size: 0.1 mL

17a-Estradiol Antibody

SKU: 252287|Size: 0.1 mL

17a-Nortestosterone Antibody

SKU: 252288|Size: 0.1 mL

17a-OH-progesterone Antibody

SKU: 252289|Size: 0.1 mL

17a-Testosterone Antibody

SKU: 252290|Size: 0.1 mL

17a-Trenbolone Antibody

SKU: 252291|Size: 0.1 mL

17b-Boldenone Antibody

SKU: 252292|Size: 0.1 mL

17b-Estradiol Antibody

SKU: 252293|Size: 0.1 mL

17b-Nortestosterone Antibody

SKU: 252296|Size: 0.1 mL

17b-Testosterone Antibody

SKU: 252297|Size: 0.1 mL

17b-Trenbolone Antibody

SKU: 252300|Size: 0.1 mL

2,4-D Antibody

SKU: 251347|Size: 0.1 mg

2-amino benzimidazole sulphone Antibody

SKU: 252302|Size: 0.1 mL

20S Proteasome Antibody

SKU: 200179|Size: 0.1 mg

20S Proteasome Peptide

SKU: 350541|Size: 0.1 mg

293 Lysate

SKU: 450271|Size: 0.1 mg

2B- (A) Peptide

SKU: 350453|Size: 1 mg

2B- (S) Peptide

SKU: 350454|Size: 1 mg

3,4-Methylenedioxymethamphetamine Antibody

SKU: 252303|Size: 0.1 mL

3T3 (Balb) Lysate

SKU: 450269|Size: 0.1 mg

3T3 (NIH) Lysate

SKU: 450255|Size: 0.1 mg

4-Nitrophenyl AHD Antibody

SKU: 252305|Size: 0.1 mL

4-Nitrophenyl AMOZ Antibody

SKU: 252306|Size: 0.1 mL

4-Nitrophenyl AOZ Antibody

SKU: 252307|Size: 0.1 mL

4-Nitrophenyl SEM Antibody

SKU: 252308|Size: 0.1 mL

4E-BP1 (11G1) Antibody

SKU: 252682|Size: 0.1 mg

4E-BP1 (4B6G) Antibody

SKU: 252681|Size: 0.1 mL

4E-BP1 (9E1) Antibody

SKU: 252680|Size: 0.1 mL

4E-BP1 Antibody

SKU: 253533|Size: 0.1 mg

5'-nucleotidase cytosolic II Antibody

SKU: 250448|Size: 0.1 mg

5-HT-1A Antibody

SKU: 251494|Size: 0.1 mg

5-HT-1B Antibody

SKU: 251495|Size: 0.1 mg

5-HT-2A Antibody

SKU: 251427|Size: 0.1 mg

5-Lipoxygenase (Ser523) Antibody

SKU: 252519|Size: 0.1 mL

5-lipoxygenase Antibody

SKU: 251179|Size: 0.1 mg

8-OHdG Antibody

SKU: 251640|Size: 0.1 mg

A-20 Lysate

SKU: 450249|Size: 0.1 mg

A-779 Peptide

SKU: 350455|Size: 1 mg

A1BG (4B5) Antibody

SKU: 252985|Size: 0.1 mL

A1CF 293 Cell Lysate

SKU: 404649|Size: 0.1 mg

A2BP1 293 Cell Lysate

SKU: 402363|Size: 0.1 mg

A2M 293 Cell Lysate

SKU: 410350|Size: 0.1 mg

A431 Lysate

SKU: 450279|Size: 0.1 mg

A4GALT 293 Cell Lysate

SKU: 402258|Size: 0.1 mg

A4GNT 293 Cell Lysate

SKU: 406797|Size: 0.1 mg

A549 Lysate

SKU: 450278|Size: 0.1 mg

AAAS 293 Cell Lysate

SKU: 402152|Size: 0.1 mg

AADAC 293 Cell Lysate

SKU: 409500|Size: 0.1 mg

AADACL2 293 Cell Lysate

SKU: 403254|Size: 0.1 mg

AADAT 293 Cell Lysate

SKU: 406779|Size: 0.1 mg

AAMP 293 Cell Lysate

SKU: 409501|Size: 0.1 mg

AAMP Antibody

SKU: 252089|Size: 0.1 mg

AARS 293 Cell Lysate

SKU: 400598|Size: 0.1 mg

AARSD1 293 Cell Lysate

SKU: 405490|Size: 0.1 mg

AAT (2B12) Antibody

SKU: 252890|Size: 0.1 mL

AATF 293 Cell Lysate

SKU: 407465|Size: 0.1 mg

AATF Antibody

SKU: 251597|Size: 0.1 mg

ABAT 293 Cell Lysate

SKU: 400282|Size: 0.1 mg

ABCA4 Antibody

SKU: 253108|Size: 0.1 mL

ABCB5 293 Cell Lysate

SKU: 403116|Size: 0.1 mg

ABCB6 Antibody

SKU: 251592|Size: 0.1 mg

ABCB6 Peptide

SKU: 300116|Size: 0.1 mg

ABCB8 293 Cell Lysate

SKU: 407556|Size: 0.1 mg

ABCC3 293 Cell Lysate

SKU: 408598|Size: 0.1 mg

ABCD1 293 Cell Lysate

SKU: 410345|Size: 0.1 mg

ABCD2 293 Cell Lysate

SKU: 408174|Size: 0.1 mg

ABCD4 293 Cell Lysate

SKU: 408211|Size: 0.1 mg

ABCE1 293 Cell Lysate

SKU: 400966|Size: 0.1 mg

ABCE1 Antibody

SKU: 251983|Size: 0.1 mg

ABCF2 293 Cell Lysate

SKU: 401858|Size: 0.1 mg

ABCF3 293 Cell Lysate

SKU: 406353|Size: 0.1 mg

ABCG1 Antibody

SKU: 251599|Size: 0.1 mg

ABCG2 293 Cell Lysate

SKU: 408296|Size: 0.1 mg

ABCG8 293 Cell Lysate

SKU: 405838|Size: 0.1 mg

ABCG8 Antibody

SKU: 251985|Size: 0.1 mg

ABHD10 293 Cell Lysate

SKU: 402336|Size: 0.1 mg

ABHD11 293 Cell Lysate

SKU: 404352|Size: 0.1 mg

ABHD12B 293 Cell Lysate

SKU: 403690|Size: 0.1 mg

ABHD13 293 Cell Lysate

SKU: 405122|Size: 0.1 mg

ABHD14A 293 Cell Lysate

SKU: 406987|Size: 0.1 mg

ABHD14B 293 Cell Lysate

SKU: 405143|Size: 0.1 mg

ABHD2 293 Cell Lysate

SKU: 401837|Size: 0.1 mg

ABHD3 293 Cell Lysate

SKU: 404709|Size: 0.1 mg

ABHD4 293 Cell Lysate

SKU: 405886|Size: 0.1 mg

ABHD5 293 Cell Lysate

SKU: 402175|Size: 0.1 mg

ABHD6 293 Cell Lysate

SKU: 406068|Size: 0.1 mg

ABHD8 293 Cell Lysate

SKU: 405656|Size: 0.1 mg

ABI1 293 Cell Lysate

SKU: 401509|Size: 0.1 mg

ABI2 293 Cell Lysate

SKU: 401571|Size: 0.1 mg

ABIN3 Antibody

SKU: 254123|Size: 0.1 mg

ABL1 (7B11) Antibody

SKU: 252799|Size: 0.1 mL

ABL1 293 Cell Lysate

SKU: 407519|Size: 0.1 mg

ABL2 (1H1) Antibody

SKU: 252955|Size: 0.1 mL

ABL2 (1H1B) Antibody

SKU: 252698|Size: 0.1 mL

ABL2 293 Cell Lysate

SKU: 401882|Size: 0.1 mg

ABL2 Antibody

SKU: 251598|Size: 0.1 mg

ABLIM1 293 Cell Lysate

SKU: 407690|Size: 0.1 mg

ABO 293 Cell Lysate

SKU: 406112|Size: 0.1 mg

Recent Breakthroughs

Metabolomic insights into Lyme neuroborreliosis: Exploring cerebrospinal fluid for diagnostic clues.

Kuukkanen I, Pietikäinen A, Rissanen T, Hurme S, Kortela E, Hytönen J, Karonen M.

Ticks Tick Borne Dis

PMID:42001681

Free PMC article

Lyme neuroborreliosis (LNB), a disseminated manifestation of Lyme borreliosis (LB), arises when Borrelia burgdorferi sensu lato (Bbsl) spirochetes disseminate within the host and damage the peripheral nervous system and meninges, and in rare cases, also the parenchyma of the central nervous system (CNS). While early-stage LB is diagnosed clinically, accurate diagnosis of LNB requires cerebrospinal fluid (CSF) analysis, demonstrating pleocytosis and intrathecal synthesis of Bbsl-specific antibodies. There are, however, limitations in current LNB diagnostics, such as the unspecific nature of pleocytosis and post-treatment persistence of intrathecal antibodies necessitating the search for novel biomarkers. In this study, we employed untargeted ultrahigh-performance liquid chromatography coupled with tandem mass spectrometry (UHPLC-MS/MS) to profile small metabolites (<1500 Da) in CSF samples from subjects with definite acute LNB. Comparative analyses of metabolite profiles were performed between pretreatment subject samples (n = 63) and the following groups: (A) a subset of samples collected three weeks after treatment initiation from the same individuals (n = 36), (B) Bbsl antibody-negative subjects (non-LNB, n = 61), (C) subjects with other CNS infections (n = 21). Additionally, pretreatment LNB samples were compared between individuals with radiculitis (n = 40) and those without radiculitis (n = 23) (D). Out of 4222 molecular features (MFs) detected, 131 were prioritized based on statistical significance and magnitude of change for further detailed structural characterization. Altered metabolite classes included compounds from lysophospholipids [e.g., lysophosphatidylcholine (16:0), and lysophosphatidylethanolamine (18:0)], sphingomyelins [e.g., sphingomyelin (d18:1/14:0) and sphingomyelin d16:1/16:0)], sphingoid bases (e.g., d19:0 sphinganine, and 3-ketosphingosine), fatty acid amides (e.g., palmitoleamide and oleamide), cyclic phosphatidic acids [i.e., cyclic phosphatidic acid (16:0) and cyclic phosphatidic acid (18:2)], and amino acid metabolism (i.e., DL-glutamine, 5-hydroxytryptophan and DL-kynurenine). These findings underscore the potential of CSF metabolomics as a powerful complementary tool for diagnosing LNB and differentiating it from other CNS conditions. The identified metabolic signatures offer a foundation for future biomarker development and may enhance diagnostic precision, guide treatment strategies, and deepen our understanding of LNB pathogenesis.

Isotope Dilution NanoLC-MS/MS Quantitation of Methylglyoxal DNA-Protein Cross-Links: Formation and Repair in Human Cells.

Omondi RO, Barnes EM, Gurajala KC, Fisette G, Chaudray IA, Erber L.

Anal Chem

PMID:41995195

Free PMC article

DNA-protein cross-links (DPCs) represent a prevalent form of DNA damage that forms when cellular proteins become covalently trapped to DNA strands upon exposure to various endogenous and exogenous agents. Methylglyoxal is an endogenous metabolite that reacts with guanine and adenine bases in DNA and RNA, as well as cysteine, arginine, and lysine residues in proteins, generating advanced glycation end-products (AGEs), including DPCs. These modifications have been linked to human disease, including cancer, liver disease, diabetes, and neurodegenerative disorders. Herein, we present a mass spectrometry method for quantifying MGO-induced DNA-protein cross-links (DPCs) in human cells. We prepared an isotope 15 N 2 13 C 6 -dG-MGO-Lys internal standard and developed a quantitative liquid chromatography-tandem mass spectrometry (LC-MS/MS) method for detecting and quantifying the formation and repair of dG-MGO-Lys DPCs in cells. Genomic DNA was extracted, subjected to sequential protease and nuclease digestion, purified by offline high-performance liquid chromatography (HPLC), and analyzed by LC-MS/MS. The method's standard curve showed a strong linear relationship across a concentration range of 10-1000 fmol ( R 2 = 0.9994). The method achieved limits of detection (LOD) and quantification (LOQ) of 10 and 20 fmol, respectively. Inhibition of proteasome and SPRTN activity revealed that SPRTN functions as a predominant proteolytic enzyme in MGO DPC repair. Overall, this analytical approach can offer valuable insights into the relevance of DPCs in diseases linked to elevated MGO levels.

Label-Free High-Throughput Screening of CYP3A4 Inhibitors Using Acoustic Ejection Mass Spectrometry.

Rimmer MA, Wang J, Ranathunge TA, Shi Z, Li Y, Lee D, Chai SC, Lin W, Twarog NR, Ansari AZ, Shelat AA, Young BM, Chen T, Yang L.

Anal Chem

PMID:41997578

Free PMC article

Label-free high-throughput screening (HTS) technologies have greatly accelerated early drug discovery by allowing direct measurement of biochemical activity without the need for chemical labels. Techniques like MALDI-TOF, RapidFire, desorption electrospray ionization, and acoustic-mist ionization mass spectrometry have shown strong analytical performance. More recently, acoustic droplet ejection mass spectrometry (AEMS) has emerged as a next-generation platform capable of analyzing over a thousand data points per hour. In this study, we thoroughly evaluated an AEMS workflow using cytochrome P450 3A4 (CYP3A4) as a model enzyme. Screening a library of 9702 compounds, this work represents the first successful label-free HTS campaign for CYP3A4 inhibitors in a 384-well format using AEMS. The result using nifedipine as a substrate was comparable to the widely used P450-Glo luminescence assay but with fewer inhibitor hits identifications. To further compare and parse differences between the methods and the substrates, 819 hits were retested using AEMS with luciferin isopropyl acetal, the same substrate used in the luminescence assay. The findings confirmed that both the assay method and the substrate influence which inhibitors were detected. Overall, this study established AEMS as a robust and reliable tool for CYP3A4 inhibitor screening. It offers high analytical precision, fewer false positives, compatibility with multiple substrates, and direct detection of metabolites, providing a practical way to validate hits and improve confidence in early drug discovery efforts.

Quantification of the Active Metabolites 4-Methylaminoantipyrine and 4-Aminoantipyrine of Dipyrone From Human Plasma by LC-MS/MS.

Schmidt S, Ihmsen H, Golditz T, Schüttler J, Wehrfritz A.

Int J Anal Chem

PMID:42004449

Free PMC article

Dipyrone (metamizole) is widely used as a nonopioid analgesic in perioperative and intensive care settings; however, its administration may be associated with severe adverse effects. In this study, we describe an analytical assay for the quantification of the active metabolites 4-methylaminoantipyrine (4-MAA) and 4-aminoantipyrine (4-AA) in human plasma using ultra-high-performance liquid chromatography coupled with tandem mass spectrometry (UPLC-MS/MS). In addition, the protein-unbound fractions of both metabolites were determined by ultrafiltration. Chromatographic separation was performed on a UPLC system using gradient elution, followed by MS/MS detection with an electrospray ionization source. The limits of detection for both metabolites were 100 ng/mL. Across the investigated concentration range (100-10,000 ng/mL), the relative error (%RE) ranged from -6.3% to +3.5%. Intra-day and inter-assay variability were below 10%. Method validation was conducted in accordance with the 2018 FDA Bioanalytical Method Validation Guidance, and all evaluated parameters met the required criteria for analytical accuracy and precision. The developed assay is suitable for monitoring dipyrone metabolites and may support the prevention of potential overdosing during prolonged analgesic therapy or in intensive care settings.

Metabolomics profiling of acute myelogenous leukemia patients to identify systemic differences associated with in vitro sensitivity to SYK inhibitors.

Brattås MK, Hatfield KJ, Paulsen Rye K, Reikvam H.

Metabolomics

PMID:41995902

Free PMC article

Introduction Acute myelogenous leukemia (AML) is a heterogeneous hematological malignancy. Despite therapeutic advances, high relapse rates and poor survival persist, underscoring the need for new treatment strategies. Spleen tyrosine kinase (SYK) is crucial for leukemic cell survival and proliferation, and SYK inhibition is being explored in AML therapy. Objective This study aimed to identify whether distinct baseline serum metabolic profiles can differentiate between AML patient samples exhibiting high versus low in vitro sensitivity to SYK inhibition. Methods Leukemic cells from 49 AML patients were evaluated for their in vitro antiproliferative response to SYK-selective inhibitors (entospletinib, RO9021) and dual SYK/FLT3 inhibitors (fostamatinib, TAK-659). Serum samples from the same patients were subjected to untargeted metabolomic profiling using liquid chromatography-mass spectrometry (LC-MS). Bioinformatic analyses were applied to identify metabolic signatures associated with differential drug sensitivity. Results Hierarchical clustering identified three drug sensitivity groups, i.e. high, intermediate, low. Untargeted metabolomics identified 1204 metabolites across major pathways. Comparative analyses revealed distinct metabolic differences between patients with high versus low sensitivity to SYK inhibitors. For dual SYK/FLT3 inhibitors, lipid metabolites consistently were more discriminative for drug response, while for SYK selective inhibitors the profiles were more heterogeneous. Pathway analyses highlighted alterations in amino acid, lipid, and xenobiotic metabolism, including arginine biosynthesis and glycine/serine metabolism, as potential determinators for effect of SYK inhibition. Conclusion This study highlights potential metabolite signatures associated with in vitro SYK-targeted therapy in AML. These findings support future research to identify potential serum biomarkers, guiding personalized SYK inhibition strategies in AML.