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Fig. 1 · Structure
Cat. No.
A11120
CAS No.
188062-50-2
Formula
C14H18N6O.H2SO4
Mol. Weight
384.4

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Abacavir sulfate

Cat. No. A11120 CAS 188062-50-2

Transcriptase inhibitor

Abacavir sulfate is a nucleoside analog reverse transcriptase inhibitor (NRTI); guanosine analog used to treat HIV and AIDS.

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Biological Activity

Target & Activity

Target Activity Value
HIV-1 reverse-transcriptase

In Vitro Studies

Abacavir alone did not activate QSR-TCR-transfected Jurkat cells tested with Abacavir-pulsed K562-HLA-B*57:01 cells. In B*57:01-KC, culture-supernatant IFN-γ and IL-1β levels were below the detection limit with or without Abacavir exposure. In the QSR-specific TCR system with K562-B*57:01 SAL, pulsing SAL with peptide plus Abacavir negatively impacted T cell recognition in the comparison with or without Abacavir. [1,2]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Abacavir alone and QSR-TCR activation

Cell-based study · Jurkat cells transfected with QSR-TCR; K562-HLA-B*57:01 [1]

In QSR-TCR-transfected Jurkat cells tested with Abacavir-pulsed K562-HLA-B*57:01 cells, the addition of Abacavir alone did not activate the Jurkat cells. TCR-mediated NFAT signalling was quantified by luciferase luminescence.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
TCR-mediated NFAT signalling was quantified by luciferase luminescenceReported result Abacavir (10 µg/mL) pulsed K562-HLA-B*57:01: The addition of abacavir alone did not activate QSR-TCR transfected Jurkat cells.[1]

Literature-Reported Treatment Conditions

Treatment concentration
10 µg/mL
Exposure duration
20–24 h; 6 h
Method
pulsed
Reported limits
Not stated in the sentences used: vehicle.
Methods and source locations

Compound reported in the paper: Abacavir

The paper names Abacavir without stating the salt or form; not verified as the sulfate form supplied as A11120. No dose conversion or lot validation.

Results > EBV specific TCRs are inhibited by abacavir (S57, S61, S62); Methods > Co-culture and luciferase reporter assay (S181, S184, S185, S188)

TCR-mediated NFAT signalling was quantified by luciferase luminescence: TCR-mediated NFAT signalling was quantified by luciferase luminescence; comparator: Jurkat with K562-B*57:01 — Results > EBV specific TCRs are inhibited by abacavir (S57, S61, S62)

Abacavir exposure and cytokine detection in keratinocytes

Cell-based study · B*57:01-KC [2]

In B*57:01-KC exposed to Abacavir at 100 μM for 12 h, culture-supernatant IFN-γ and IL-1β protein levels remained below the detection limit of 15.6 pg/mL. Levels were also below the detection limit without Abacavir exposure.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Protein levels of IFN-γ and IL-1β in the culture supernatantReported result Protein levels of IFN-γ and IL-1β in the culture supernatant of B*57:01-KC were below the detection limit (15.6 pg/mL) with or without abacavir exposure (100 μM, 12 h).[2]

Literature-Reported Treatment Conditions

Treatment concentration
100 μM
Exposure duration
12 h
Method
abacavir exposure
Reported limits
Not stated in the sentences used: vehicle.
Methods and source locations

Compound reported in the paper: Abacavir

The paper names Abacavir without stating the salt or form; not verified as the sulfate form supplied as A11120. No dose conversion or lot validation.

Results > HLA-B*57:01-expressing keratinocytes were immunologically activated by abacavir (S7)

Protein levels of IFN-γ and IL-1β in the culture supernatant: Protein levels of IFN-γ and IL-1β in the culture supernatant; comparator: without abacavir exposure — Results > HLA-B*57:01-expressing keratinocytes were immunologically activated by abacavir (S7)

Abacavir with peptide pulsing and T cell recognition

Cell-based study · QSR specific TCR with K562-B*57:01 SAL [1]

In the QSR-specific TCR system with K562-B*57:01 SAL, pulsing SAL with peptide plus Abacavir at 10 μg/mL negatively impacted T cell recognition. The comparison assessed the addition of Abacavir in the peptide-containing system.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
TCR-mediated NFAT signalling was quantified by luciferase luminescenceReported result 10 μg/mL of abacavir; QSR specific TCR with K562-B*57:01 SAL: pulsing of SAL with peptide plus abacavir negatively impacted T cell recognition.[1]

Literature-Reported Treatment Conditions

Treatment concentration
10 μg/mL
Exposure duration
20–24 h; 6 h
Method
pulsing of SAL with peptide plus abacavir
Co-treatment
Other interventions in this design: QSR peptide Either 10 μg/mL or 1 μg/mL. Compound effect isolated by the comparison: QSR specific TCR with K562-B*57:01 SAL, plus or minus ABC.
Reported limits
Not stated in the sentences used: vehicle.
Methods and source locations

Compound reported in the paper: Abacavir

The paper names Abacavir without stating the salt or form; not verified as the sulfate form supplied as A11120. No dose conversion or lot validation.

Results > EBV specific TCRs are inhibited by abacavir (S57, S58, S65); Methods > Co-culture and luciferase reporter assay (S181, S184, S185); Fig. 9 legend (S231)

TCR-mediated NFAT signalling was quantified by luciferase luminescence: TCR-mediated NFAT signalling was quantified by luciferase luminescence; comparator: individual peptide epitopes without ABC — Results > EBV specific TCRs are inhibited by abacavir (S57, S65); Methods > Co-culture and luciferase reporter assay (S181); Fig. 9 legend (S231)

In Vivo Studies

In B*57:01-Tg, Abacavir administered p.o. increased epidermal p-IRE1α and XBP1 expression. Treatment with 4-PB suppressed the increase. [2]

Abacavir and epidermal protein expression

Animal study · B*57:01-Tg [2]

In B*57:01-Tg, Abacavir administered p.o. at 20 mg/body increased epidermal p-IRE1α and XBP1 expression at 3 h after administration. Treatment with 4-PB suppressed this increase.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
expression levels of phosphorylated IRE1α (p-IRE1α) and x-box binding protein 1 (XBP1) in the epidermisReported result 20 mg/body of abacavir p.o.; 3 h after abacavir administration: increased expression levels of phosphorylated IRE1α (p-IRE1α) and x-box binding protein 1 (XBP1) in the epidermis of B*57:01-Tg; 4-PB treatment suppressed the increase of p-IRE1α and XBP1 expression.[2]

Conditions shared by the study groups

Route
p.o.
Treatment course
3 h after abacavir administration
Vehicle
1% carboxymethyl cellulose aqueous solution
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Abacavir 20 mg/bodyvehicle20 mg/body of abacavir p.o.; 3 h after abacavir administration: increased expression levels of phosphorylated IRE1α (p-IRE1α) and x-box binding protein 1 (XBP1) in the epidermis of B*57:01-Tg; 4-PB treatment suppressed the increase of p-IRE1α and XBP1 expression.[2]
Abacavir 20 mg/body
Model: B*57:01-Tg
Methods and source locations

Compound reported in the paper: Abacavir

The paper names Abacavir without stating the salt or form; not verified as the sulfate form supplied as A11120. No dose conversion or lot validation.

Results > ER stress relief attenuated Abacavir-induced skin eruption in B*57:01-Tg (S35, S36); Materials and methods > Animals (S76); Materials and methods > Histology and immunohistochemistry (S113, S115); Fig. 4. legend (S182)

expression levels of phosphorylated IRE1α (p-IRE1α) and x-box binding protein 1 (XBP1) in the epidermis: expression levels of phosphorylated IRE1α (p-IRE1α) and x-box binding protein 1 (XBP1) in the epidermis; comparator: vehicle — Results > ER stress relief attenuated Abacavir-induced skin eruption in B*57:01-Tg (S35, S36); Fig. 4. legend (S182)

Abacavir 20 mg/body · Results > ER stress relief attenuated Abacavir-induced skin eruption in B*57:01-Tg (S35, S36); Fig. 4. legend (S182)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 188062-50-2
Applications Transcriptase inhibitor
Formula C14H18N6O.H2SO4
Molecular Weight 384.4
SMILES
C1CC1NC2=NC(=NC3=C2N=CN3[C@@H]4C[C@@H](C=C4)CO)N.OS(=O)(=O)O

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO Insoluble
Water 33 mg/mL (98.4 mM)
Ethanol Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Sooda A, Rwandamuriye F, Wanjalla CN, et al. Abacavir inhibits but does not cause self-reactivity to HLA-B*57:01-restricted EBV specific T cell receptors. Commun Biol (2022). PMID: 35173258 DOI: 10.1038/s42003-022-03058-9 Source material
  2. [2] Kazaoka A, Fujimori S, Yamada Y, et al. HLA-B*57:01-dependent intracellular stress in keratinocytes triggers dermal hypersensitivity reactions to abacavir. PNAS Nexus (2024). PMID: 38628599 DOI: 10.1093/pnasnexus/pgae140 Source material

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