[1] The compound contains polyene, polyyne, and alcohol functional groups and is a structural isomer of oenanthotoxin, also found in water dropwort.

In humans, cicutoxin rapidly produces symptoms of nausea, emesis and abdominal pain, typically within 60 minutes of ingestion.

[8] This review included a case where a family of five used Cicuta extracts as a topical treatment for itching, resulting in the deaths of two children, a report that suggests that cicutoxin may be absorbed through the skin.

The toxicity of the plants depends on various factors, such as seasonal variation, temperature, geographical location and soil conditions.

[19] Though the overall yield was only 4% and the product was the racemic mixture, the synthesis has been described as "a significant accomplishment" given that it was achieved "without the benefit of modern coupling reactions".

[20] Outside of a plant, cicutoxin breaks down when exposed to air, light, or heat, making it difficult to handle.

1,4-diiodo-1,3-butadiene (9) is also a known compound and it is readily available by dimerization of acetylene accompanied by addition of iodine in the presence of platinum (IV) catalyst and sodium iodide.

Cicutoxin is a noncompetitive gamma-aminobutyric acid (GABA) antagonist in the central nervous system (CNS).

There is evidence that it has a long half-life in the body[citation needed], because of a patient who was submitted in a hospital after eating a root of a Cicuta plant.

[24] First signs of cicutoxin poisoning start 15–60 minutes after ingestion and are: vomiting, convulsions, widened pupils, salivation, excess sweating.

[22][23][25] Due to an overactive nervous system respiratory failure occurs which may cause suffocation and accounts for most of the deaths.

[18] Treatments used include the administration of activated charcoal within 30 minutes of ingestion to reduce the uptake of poison, maintaining open airways to prevent suffocation, rehydration to address the dehydration caused by vomiting, and administration of benzodiazepines that enhance the effect of GABA on the GABAA receptor[26][27] or barbiturates to reduce seizures.

Animals display similar effects of cicutoxin poisoning as do humans, but without vomiting (which can lead to increased lethality) – recorded symptoms include salivation, seizures, frequent urination and defecation, and degeneration of skeletal and cardiac muscles.

[24] Research studies on ewes has shown that skeletal and cardiac myodegeneration (damage of muscle tissues) only occur after a dose sufficient to induce symptoms of intoxication is administered.

Analysis of the animal's blood showed elevated serum enzymes that indicate muscle damage (LDH, AST and CK values).

The number and duration of seizures had a direct effect on the skeletal and cardiac myodegeneration and amount of serum change.

[24] Ewes given up to 2.5 times the lethal dose along with medications to treat symptoms of cicutoxin poisoning recovered, demonstrating that symptomatic treatment can be life-saving.

[25] It has also been investigated for antitumor activity, where it was shown that a methanolic extract of C. maculata demonstrated significant cytotoxicity in the 9 KB (human nasopharyngeal carcinoma) cell structure assay.