ddhCTP 100 mM Solution

Commodity name： ddhCTP 100 mM Solution
货号： OLV3028

Category:

Modified dNTPs

Email:

wangtongtong@cnorilife.com

Phone:

+86-15032236037

Request a quote now

Product Description

Technical Parameters
Purity	98%
Storage conditions	-20 ± 5℃
pH	8.0
Molecular formula	C ₉ H ₁₄ N ₃ O ₁₃ P ₃
Molecular weight	465.14
Specifications	1ml
Product abbreviation	ddhCTP 100 mM Solution
Chinese name	3'-Deoxy-3',4'-dihydro-CTP

Product Description

Tianjin Olive Biotechnology Co., Ltd. is proudly launching a highly significant modified nucleotide product—ddhCTP.

Perhaps the name ddhCTP still sounds quite unfamiliar to you, yet behind it lies an astonishing scientific saga. As we all know, after mammalian cells are infected by a virus, they release interferon, which in turn triggers a cascade of gene expressions—including the RSAD2 gene, which encodes viperin. Viperin is a molecule with broad antiviral activity, and its antiviral mechanism has been prominently featured in the internationally renowned journal Nature. Scientists have discovered that the viperin protein can catalyze the production of a remarkable small biomolecule—ddhCTP—which effectively inhibits viral replication within the body. ddhCTP is currently the only known naturally occurring antiviral small molecule produced by the body itself. It has attracted widespread attention for its broad-spectrum antiviral activity and lack of toxic side effects. Today, Olive Bio proudly announces that the ddhCTP molecule has been successfully synthesized artificially by our R&D team!

I. Antiviral Mechanism of ddhCTP

On the brutal battlefield of viral replication, the virus acts like a frenzied architect, striving to piece together individual nucleotide building blocks into a chain of genetic material. Under normal circumstances, the virus can use CTP as a nucleotide building block to synthesize its genome. Since ddhCTP shares a similar structure with CTP, the virus easily mistakes it for the correct building block and incorporates it into the genome. Yet, this is precisely where the ingenuity of ddhCTP lies. Once ddhCTP is incorporated, it functions like a steadfast guardian, blocking subsequent nucleotide building blocks from being added to the RNA chain. As a result, the RNA chain can no longer extend further—much like setting up an insurmountable “roadblock” along the path of viral replication. Through this chain-termination mechanism, ddhCTP effectively halts viral replication.

Specific experimental case:

1. Zika Virus Experiment: Researchers added different concentrations of ddhCTP to cell culture systems containing the Zika virus. As the concentration of ddhCTP increased, the replication rate of the Zika virus markedly slowed down. When the concentration reached a certain level, the amount of virus released decreased significantly. For example, in the control group, the number of Zika virus particles per milliliter of cell culture medium was 1,000 units; however, in the experimental group supplemented with high-concentration ddhCTP, the viral load dropped to fewer than 100 units, demonstrating a pronounced inhibitory effect.

2. Dengue Virus Assay: Primer extension assays revealed that ddhCTP (at concentrations of 0, 1, 10, 100, and 300 μM) exhibits concentration-dependent inhibition of the dengue virus (DV) RdRp. At the low concentration of 1 μM, a slight inhibition of full-length RNA synthesis was already observed; when the concentration reached 100 μM, the yield of full-length RNA was reduced by approximately 50%; and at the high concentration of 300 μM, full-length RNA synthesis was almost completely inhibited.

3. West Nile Virus Experiment: In a mouse model infected with the West Nile virus, mice were administered a treatment containing ddhCTP. Compared to untreated mice, the mice receiving the treatment showed a significantly reduced viral load in their bodies, and their survival rate was significantly improved. Meanwhile, histopathological examination of the mice revealed that organ damage was markedly alleviated in mice treated with ddhCTP.

II. The Difference Between ddhCTP and Existing Antiviral Drugs

1. Unique Mechanism of Action: Existing antiviral drugs typically work by inhibiting specific viral enzyme activities, blocking viral entry into cells, or interfering with viral assembly. In contrast, ddhCTP leverages its structural similarity to CTP to trick the virus into incorporating it into the genome, thereby halting the extension of the viral genetic material chain and fundamentally preventing viral replication.

2. Combining Targeted and Broad-Spectrum Activity—On the one hand, ddhCTP exhibits potent inhibitory effects against a variety of members of the Flaviviridae family, including Zika virus, dengue virus, West Nile virus, and hepatitis C virus, demonstrating a degree of specificity. On the other hand, although it shows limited efficacy against members of the small RNA virus family such as human rhinovirus C and poliovirus, this also highlights its specificity of action—it does not indiscriminately target all viruses. Compared with some broad-spectrum antiviral drugs, ddhCTP may have fewer side effects.

3. High safety: Many existing antiviral drugs may cause certain side effects in humans, affecting cell growth rates or viability, and even negatively impacting the host’s RNA and DNA polymerases. However, experimental results have confirmed that ddhCTP is safe; it does not adversely affect the host’s RNA and DNA polymerases. Moreover, overexpression of Viperin and the production of ddhCTP do not exert any detrimental effects on cell growth rates or viability.

Currently, viperin is the only human protein capable of producing a small molecule that can directly inhibit viral replication. Additionally, ddhCTP is the only known naturally occurring antiviral small molecule produced by the body itself. The synthetically produced ddhCTP offered by our company is undoubtedly a powerful and formidable tool in humanity’s ongoing battle against viruses.

Product Information