(±)bid

(±)-BI-D is an effective ALLINI(An allosteric IN inhibitor) that binds integrase at the LEDGF/p75 binding site (IC50: 2.4–2.9 μM).

Bid BH3 (80-99) is a biologically active peptide and a pro-apoptotic member of the 'BH3-only' (BOPS) subset within the BCL-2 protein family, crucial in apoptosis regulation. It interacts with Bcl-2, Bax, and Bak to initiate their activation or inactivation, inducing cell death. Bid translocates from the cytosol to the mitochondrial membrane as part of its mechanism. Pyroglutamyl (pGlu) peptides, which can arise from Glutamine (Q) or Glutamic acid (E) at the N-terminus, have a hydrophobic γ-lactam ring that enhances stability and provides resistance to gastrointestinal proteases. These peptides are recognized variants in peptide analyses, including HPLC purity assessments.

FAM-labeled Bid BH3 (80-99) is a biologically active peptide featuring a 5-FAM label at its N-terminus.

r8 Bid BH3, a biologically active peptide, is a pro-apoptotic member of the BH3-only subset within the BCL-2 family proteins, pivotal in regulating apoptosis. This compound exhibits lethality towards Bcl-2-expressing human leukemia cell lines, indicating its promise as a potential cancer therapeutic. The peptide is conjugated with poly-D-arginine (denoted by rrrrrrrr), enhancing cellular uptake.

Bid BH3 peptide, a small peptide derived from the Bid protein, binds to and activates the pro-apoptotic proteins Bax and Bak, leading to mitochondrial outer membrane permeabilization (MOMP) and cell apoptosis (apoptosis). This peptide is utilized in research on mitochondrial bioenergetics.

BI-6C9 is an inhibitor of tBid (Kd = 20 µM).BI-6c9 prevented MOMP and mitochondrial fission, and protected the cells from cell death.

OUN58101, also known as MDK-8101, also known as BI-D, is a RSV L-protein inhibitor. OUN58101 was first reported in patnet WO 2005042530. This product has no formal name at the moment. For the convenience of communication, a temporal code name was therefore proposed according to MedKoo Chemical Nomenclature (see web page: https://www.medkoo.com/page/naming).

Gossypol acetic acid (AT101), a polyphenolic compound isolated from cottonseeds, binds with Bcl-2, Bcl-xL, Mcl-1, and does not inhibit BIR3 domain and BID.

MLS-0053105, a chloromaleimide, functions as a selective inhibitor of BFL-1, exhibiting an IC50 of 0.4 µM against Bfl-1 F-Bid. Its inhibitory potency is over tenfold lower for Bcl-W, Bcl-2, and Bcl-XL, and it shows no activity against Bcl-B and Mcl-1.

BIO5192 hydrate is a selective and potent integrin α4β1 (VLA-4) inhibitor (Kd < 10 pM). The compound selectively binds to α4β1 (IC50 = 1.8 nM) over various other integrins and results in a 30-fold increase in mobilization of murine hematopoietic stem and progenitors (HSPCs) over basal levels[1][2].

Ensartinib (X-396) is a potent and orally active dual ALK MET inhibitor for the treatment of ALK-positive non-small cell lung cancer (NSCLC).

Purfalcamine is an orally active, selective Plasmodium falciparum calcium-dependent protein kinase 1 (PfCDPK1) inhibitor with an IC50 of 17 nM and an EC50 of 230 nM, exhibiting antimalarial activity by inducing developmental arrest of malaria parasites at the schizont stage[1][2].

(R)-(-)-Gossypol acetic acid (AT101 acetate), the R-(-) enantiomer of Gossypol acetic acid, binds with Bcl-2, Bcl-xL, and Mcl-1 with Ki values of 0.32 μM, 0.48 μM, and 0.18 μM, respectively; it does not inhibit the BIR3 domain or BID. [Phase 2]

YC-137 is a BCL-2 inhibitor, which selectively induces apoptosis of Bcl-2-overexpressing cells and disrupts its interaction with Bid BH3, thereby blocking the anti-apoptotic activity of Bcl-2.

GNE-8525 is a potent and selective pan-TRK inhibitor. GNE-8525 demonstrated potent antiproliferation activity with IC50 = 0.003 μM. In a tumor xenograft model derived from the KM12 cell line, GNE-8525 demonstrated in vivo antitumor efficacy when administered at ascending doses twice daily (bid) for 14 days in rats. Deregulated kinase activities of tropomyosin receptor kinase (TRK) family members have been shown to be associated with tumorigenesis and poor prognosis in a variety of cancer types. In particular, several chromosomal rearrangements involving TRKA have been reported in colorectal, papillary thyroid, glioblastoma, melanoma, and lung tissue that are believed to be the key oncogenic driver in these tumors.