Date published: 2026-4-1

1-800-457-3801

SCBT Portrait Logo
Seach Input

FANCB Inhibitors

Chemical inhibitors of FANCB function by interfering with the cellular processes that it facilitates, primarily the repair of DNA damage. Mitomycin C, Cisplatin, and Diepoxybutane all contribute to the formation of DNA crosslinks which can be particularly burdensome for the DNA repair machinery in which FANCB plays a critical role. These crosslinking agents directly challenge the Fanconi Anemia (FA) pathway through the introduction of lesions that FANCB is responsible for addressing. With an overwhelming presence of such crosslinks, FANCB is functionally inhibited as the repair mechanism it supports is overloaded. Similarly, Etoposide and Camptothecin exacerbate the amount of DNA breaks within the cell. Etoposide's stabilization of the DNA-topoisomerase II complex and Camptothecin's inhibition of topoisomerase I both lead to an increase in DNA breaks. FANCB, being a part of the complex network that repairs such damage, is functionally inhibited when the quantity of DNA damage exceeds the repair capacity of the FA pathway. Amsacrine and Teniposide, both topoisomerase II inhibitors, introduce a high frequency of DNA breaks which can saturate the FA pathway and in turn inhibit FANCB. The impaired function of FANCB is a result of the insurmountable DNA damage that it is tasked to repair. Bortezomib, while not directly interacting with DNA, disrupts proteostasis, affecting the cellular environment that is integral for FANCB's optimal function. By perturbing the balance of protein turnover, it can indirectly inhibit the FANCB protein's role in DNA repair. PARP inhibitors such as Veliparib, Olaparib, Talazoparib, and Rucaparib amplify DNA damage by preventing the repair of single-strand breaks. This escalation in DNA damage results in more complex double-strand breaks that challenge the FA pathway's repair capabilities. The functional inhibition of FANCB arises from the increased demand for repair that is imposed by these PARP inhibitors, thus overwhelming the FA pathway's finite resources and repair machinery.

Items 1 to 10 of 11 total

Display:

Product NameCAS #Catalog #QUANTITYPriceCitationsRATING

Mitomycin C

50-07-7sc-3514A
sc-3514
sc-3514B
2 mg
5 mg
10 mg
$66.00
$101.00
$143.00
85
(5)

Mitomycin C forms DNA crosslinks, thus inhibiting DNA replication and cell division. Since FANCB is involved in DNA repair via the FA pathway, crosslinking agents like Mitomycin C functionally inhibit FANCB by overwhelming the repair mechanism it facilitates.

Cisplatin

15663-27-1sc-200896
sc-200896A
100 mg
500 mg
$138.00
$380.00
101
(4)

Cisplatin induces DNA crosslinks that FANCB is responsible for repairing. Excessive crosslinks can saturate the repair capacity of FANCB, leading to its functional inhibition by overwhelming the FA pathway.

Etoposide (VP-16)

33419-42-0sc-3512B
sc-3512
sc-3512A
10 mg
100 mg
500 mg
$51.00
$231.00
$523.00
63
(1)

Etoposide stabilizes the DNA-topoisomerase II complex, leading to DNA breaks. FANCB's role in DNA repair suggests that increased DNA damage can overwhelm the FA pathway and inhibit FANCB's functionality through excessive substrate.

Camptothecin

7689-03-4sc-200871
sc-200871A
sc-200871B
50 mg
250 mg
100 mg
$58.00
$186.00
$94.00
21
(2)

Camptothecin inhibits DNA topoisomerase I, leading to DNA breaks. Overwhelming DNA damage can saturate FANCB's repair activity within the FA pathway, functionally inhibiting it due to excess DNA lesions.

Amsacrine hydrochloride

54301-15-4sc-214540
10 mg
$232.00
(0)

Amsacrine intercalates into DNA and inhibits topoisomerase II, leading to DNA cleavage. The resulting increase in DNA breaks can potentially overload FANCB's repair function, directly inhibiting its role in the FA pathway.

Teniposide

29767-20-2sc-204910
sc-204910A
25 mg
100 mg
$73.00
$235.00
6
(1)

Teniposide, a topoisomerase II inhibitor, increases DNA breaks. As FANCB is involved in DNA repair processes, the abundance of DNA damage can functionally inhibit FANCB by providing more damage than the FA pathway can effectively repair.

Bortezomib

179324-69-7sc-217785
sc-217785A
2.5 mg
25 mg
$135.00
$1085.00
115
(2)

Bortezomib, a proteasome inhibitor, can lead to the accumulation of damaged proteins and may indirectly inhibit FANCB by disrupting proteostasis and cellular homeostasis, affecting the cellular environment FANCB operates within.

Veliparib

912444-00-9sc-394457A
sc-394457
sc-394457B
5 mg
10 mg
50 mg
$182.00
$275.00
$726.00
3
(0)

Veliparib, a PARP inhibitor, can lead to the persistence of single-strand breaks which can collapse replication forks and become double-strand breaks, potentially saturating the DNA repair machinery including FANCB, leading to its functional inhibition.

Olaparib

763113-22-0sc-302017
sc-302017A
sc-302017B
250 mg
500 mg
1 g
$210.00
$305.00
$495.00
10
(1)

Olaparib, another PARP inhibitor, can also lead to an increased load of DNA damage by preventing the repair of single-strand breaks, indirectly inhibiting FANCB by effectively increasing the number of lesions for the FA pathway to repair.

Talazoparib

1207456-01-6sc-507440
10 mg
$795.00
(0)

Talazoparib is a highly potent PARP inhibitor that traps PARP-DNA complexes, leading to increased DNA damage. This can indirectly inhibit FANCB by amplifying the number of DNA lesions that exceed the repair capability of the FA complex.